There in the foaming welter of email constantly flooding my in-box was an actual, real, good, sincere question from someone who didn’t understand how chromosome numbers could change over time — and he also asked with enough detail that I could actually see where his thinking was going awry. This is great! How could I not take time to answer?
So here’s the question:
How did life evolve from one (I suspect) chromosome to… 64 in horses, or whatever organism you want to pick. How is it possible for a sexually reproducing population of organisms to change chromosome numbers over time?
Firstly: there would have to be some benefit to the replication probability of the organisms which carry the chromosomes. I don’t see how this would work. How is having more chromosomes of any extra benefit to an organism’s replicative success? Yes, perhaps if those chromosomes were full of useful information… but the chances of that happening are non existent and fly in the face of ‘small adaptations over time’.
Secondly, the extra chromosomes need to come from somewhere. I’m not sure about this, but I believe chromosome number are not determined by genes, are they? There isn’t a set of genes which determines the number of chromosomes an organism has. So the number is fixed, determined by the sexually reproducing parents. Which leads me to believe that if the number does change, and by chance the organism is still alive and capable of sexual reproduction, that the number will start swinging back and forward, by 1 or 2, every generation, and never stabilising. The chances of this happening are also very very slim.
Let’s clear up a few irrelevant misconceptions first. Life probably started with no chromosomes — early replicators would have been grab bags of metabolites, proteins, and RNA that would have simply sloppily split in two, with no real sorting. DNA and chromosomes evolved as accounting and archiving tools: they were a way to guarantee that each daughter cell in a division reliably received a copy of every gene. Also, most living things now just have one ‘chromosome’, a loop of DNA, and perhaps a small cloud of DNA fragments. So to keep this simple we’re going to ignore all that, and consider only us diploid eukaryotes, where the question of chromosome numbers becomes a real issue.
Normally, I’d be scribbling madly on a whiteboard, so we’ll have to make do with some scribbles on the computer screen. Here, for instance, is a typical cartoon chromosome. It’s a string of DNA, and scattered along it we have sequences for genes, that I’ve labeled “A”, “B”, “C”, “D”, and “E”. I’ve also drawn a circular blob in the middle: that’s important. It’s not a gene, it’s a structure called the centromere, which gets all wrapped up in proteins to form a kinetochore. It’s a sort of anchor point; when the cell needs to move chromosomes around, as it does during cell division, it hitches motor proteins to the kinetochore and using drag lines called spindle fibers, tows it to a new destination.
I mentioned that this was a diploid organism — that just means that every chromosome comes in pairs. This cell would have a similar chromosome to the one that has the ABCDE genes on it; here I’ve draw it as containing the same genes, but in slightly different forms: abcde. This matters because during meiosis, when gametes (sperm and egg) are formed, the two chromosomes line up with one another and the cell machinery tows one chromosome to one daughter cell, and the other to the other daughter cell. It’s accounting; it makes sure each daughter gets a copy of all of the genes, one A or one a, one B or one b, etc., for instance.
For now, put the fact that there are two copies of each chromosome at the back of your mind and don’t worry about it. Let’s think about a single chromosome and ask what can happen to it.
Here’s something fairly common. An error in copying the DNA can lead to the loss of a piece of DNA. This happens with a low frequency, but it does happen — if we sequenced your DNA, we might well find a few bits missing here and there. We can get situations like this, where a whole gene gets lost.
Don’t panic! Remember that we have two copies of every chromosome, so while this one is missing the “D” gene, there’s that other chromosome floating around with a “d” gene. This is not necessarily bad for the individual, it just means he doesn’t have a spare any more.
Another kind of error that can happen with a low frequency is a duplication, where the machinery of the cell accidentally repeats itself when copying, and you get an extra copy of a piece of a chromosome, like so:
This person has two copies of D on this chromosome now (and remember that other chromosome, with it’s d gene — he actually has 3 copies in total now). This is not usually harmful: it gives the individual a little extra redundancy, and that’s about it. It can change the total amount of the D gene product in the cell, and if it’s a gene for which precise dosage is important, it can have visible effects…but in most cases, this is a neutral change.
You may have noticed that nothing has changed the chromosome numbers yet. Here’s a situation that can lead to the formation of a new chromosome: what if there is a duplication of the centromere, rather than a gene?
Remember, I told you that the centromere/kinetochore is where the cell attaches lines and motors to haul the chromosome to the appropriate daughter cell. In this case, two lines are attached; what if one tries to pull one centromere to the left, and the other tries to pull the other centromere to the right? Tug of war!
The end result is that the chromosome is broken into two chromosomes. I think this is a key concept that the questioner is missing: chromosome numbers really aren’t significant at all! You don’t need to add significant new information to create a new chromosome, and as I’ll show you in a moment, a reduction in chromosome numbers does not represent a loss of genetic information. Chromosome are disorganized filing cabinets, nothing more; we can shuffle genes around between them willy-nilly, and the cell mostly doesn’t care. A fission event like the one described above basically does nothing but take one pile of genes and split them into two piles.
But there are some important effects. This may not be an entirely neutral situation. Let’s bring back that abcde chromosome, and pair it up with our two new chromosomes, AB and CDE.
The accounting is accurate. This cell has two copies of the A gene, an “A” and an “a”, just like normal, and the two new chromosomes can still pair up efficiently with the old chromosome in meiosis, just like before. This is a healthy, functioning, normal cell, except for one thing: if it goes through meiosis to make a sperm or egg, it’s going to make a larger number of errors. There are three centromeres there, to be split into two daughter cells! Never mind what the Intelligent Design creationists tell you — the cell is really, really stupid, and it will more or less decide by eeny-meeny-miny-moe how to divvy up those chromosomes. If by chance the split is that one daughter gets AB + CDE, and the other gets abcde, both daughters have the full complement of genes and all is well. However, the split could also be that one daughter gets AB and nothing else, while the other gets CDE + abcde … and that’s no good. One is missing a whole bunch of genes, and the other has an overdose of a bunch.
The net result is that although this individual is fine and healthy, a significant number of his or her gametes may carry serious chromosomal errors, which means they may have reduced fertility. They aren’t sterile, though; some of their gametes will have the full complement of genes, and can similarly produce new healthy individuals who will probably have fertility problems. (Note: the significance of those fertility problems will vary from species to species. Organisms that rely on producing massive numbers of progeny so that a few survive to adulthood would be hit hard by a change that cuts fecundity; species that rely on producing a few progeny that we raise carefully to adulthood, like us, not so much. So you have to have sex 20 times to successfully produce a child instead of 5 times; that won’t usually be a handicap.)
So our two chromosome individual will have a reduced fertility as long as he or she is breeding with the normal one chromosome organisms, but those split chromosomes can continue to spread through the population. They are not certain to spread — they’re more likely to eventually go extinct — but by chance alone there can be continued propagation of the two chromosome variant. Which leads to another misconception in the question: something doesn’t have to provide a benefit to spread through a population! Chance alone can do it. We don’t have to argue for a benefit of chromosome fission at all in order for it to happen.
So we can have a population with a low frequency of scattered chromosomal variants, some carrying the rare two chromosome variant and others the more common one chromosome form. What if two individuals carrying the two chromosome variant breed? They can produce offspring that look like this:
How many centromeres are there? Four, not three. This is a situation the cell machinery can handle reliably, and this individual will consistently produce good gametes that accurately carry AB + CDE, nothing more, nothing less, and will have no reduction in fertility. Now we have a potentially interesting situation: individuals with the one chromosome situation have full fertility when breeding with other individuals with one chromosome; individuals with two chromosomes have full fertility when breeding with other individuals with two chromosomes; it’s when individuals with two different chromosome arrangements try to breed that fecundity is reduced. This is a situation where speciation is a possibility.
One last thing: what about reducing chromosome numbers? That’s easy, too. Here’s an organism with an AB chromosome, and a different chromosome with the genes MN on it. They can simply fuse in the region of the centromere.
This happens with a low frequency, too, and has been observed many times (hint: look up Robertsonian fusions on the web.) I think the key issue to understand here is that chromosome number changes are typically going to represent nothing but reorganizations of the genes — the same genes are just being moved around to different filing cabinets. This has some consequences, of course — you increase the chances of losing some important file folders in the process, and making it more difficult to sort out important information — but it’s not as drastic as some seem to think, and chromosome numbers can change dramatically with no obvious effect on the phenotype of the organism. These really are “small adaptations over time”, or more accurately, “small changes over time”, since there is no necessary presumption that these are adaptive at all.
I’ve discussed fusion events and how they relate to evolution before, and there’s an interesting difference in context there, too. My prior article was a response to Casey Luskin, an ignorant creationist who used his misunderstanding of genetics to foolishly assert the existence of a major problem, and that’s where we have a conflict: ignorance is not a problem, but stupidly using your ignorance to push invalid ideas is. This question in my mailbox is also ignorant — the fellow really doesn’t understand the basics of genetics — but it’s self-recognized ignorance that, in a good way, prompts him to ask a sincere question.
If you want to dig a little deeper, there are many ways genetic information can be rearranged on chromosomes, and this has opened the doors to some interesting evolutionary research. I’ve described how we can map the reshuffling of chunks of genetic information over time, a process called synteny mapping, which allows us to reconstruct ancestral chromosomes. A fish might have 42 chromosomes, and we might have 46, but we can still trace how the ancestral arrangement was scrambled in many different ways to generate the modern arrangements.
Wow. Thank you for answering a zillion questions in one fell swoop!
Thanks PZ! I asked my biology teacher the same question in high school but she couldn’t tell me. Not that I was trying to disprove evolution or anything, I was just curious! Ever since then I’ve always had a mild curiosity about this very question but never got around to digging up the answer. Now (15 odd years later) I finally know!
Superb!
Now THAT was a great answer, PZ! And it disproves the notion that you’re an old poopy-head who just wants to make fun of the sincere god-bots. You treat others as they treat you; a respectful and intelligent question gets a response in kind, whereas a threatening, abusive letter filled with cant and deliberate gets either chucked, or held up for contempt.
Just to repeat: great answer — thorough, thought-provoking, and clear. Why the hell couldn’t the National Geographic specials have stuff like you just did, instead of the pretty, but vapid and (mostly) dumbed-down stuff they produce?
I’ve just started reading Relics of Eden, by Daniel Fairbanks. It describes these kind of things very well for a layman like me, and I have been writing down parts of it that I know will be very good ammunition for my debates with IDers and creationists.
Thank you, I’ve wonder the same thing for a long time. I’m sure I’ll recover to normal or increased levels of “self-recognized ignorance” after I’ve thought about this awhile.
Thanks for addressing this topic. This has been something I have been wondering about since I learnt some basic genetics at school.
hurrah *much applause*
This is one of the questions that I had always wondered about but never taken the time to look up. Thanks for answering it.
And remember, it actually takes good working replication machinery even to keep chromosome numbers the same over generations.
In cancer cells, aneuploidy, the “wrong number” of chromosomes, is very common. Yet cancer cells are notorious for surviving, and even adapting through darwinian selection. Even many normal cells in our bodies can be aneuploid.
The fact is that it is all too easy to change chromosome numbers, and what is amazing is how meiosis usually manages to keep the right number. Selection has to weed out many changes in chromosome number, while occasionally a change in numbers is either beneficial, or perhaps simply neutral yet able to give rise to a new species. The fusion that gave rise to our chromosome 2 may be an example of the latter.
Glen D
http://tinyurl.com/2kxyc7
Excellent.
Oh SNAP!
Kudos to whomever asked this question, your answer PZ helped me understand how the process works. Thanks again.
Wow. That was marvelously lucid. Thank you:)
Some examples: Humans have 1 fewer chromosome than the rest of the great apes – our chromosome #2 is recognisably the fusion of 2 of the ape chromosomes (now called 2A and 2B).
Horses have 64 chromosomes, donkeys have 62 – they can interbreed, and the result is almost always sterile, no idea whether the success rate is lower than normal.
As I understand it, plants do this far more often than animals – including by simply doubling up – i.e. the child plant has 2x the chromosomes (and evolution can then create differentiation, assuming that the plants are fertile (domesticated wheat) or just by slow mutation even if they’re not, but helpful humans propagate cuttings (banana).
(.)(.)
As a long time lurker, time to stick my head above the parapet and say ‘brilliant’. Thanks for a great explanation.
Awesome! I hadn’t actually wondered about that–I’d assumed arrangements were made. (I guess that makes me a dogmatic believer in evolution, like the creationists are always accusing us of being? Except that I’ve always known the answers to these questions existed, if I cared to look for them.) Nonetheless, this is a very cool thing to know.
One thing I’m wondering about, though: what’s the likelihood that several organisms within a species would have a break in the same place? Is it happening when the cousins get to breeding mostly? Or is that “same place” an oversimplification, where there’s various nonsense to either side of the break? Or is there something about certain segments of DNA that make them more likely to sprout an extra centriole? Or is it just a large numbers fallacy–it’s going to happen, because there are a huge number of trials?
That was refreshing, thanks :)
That’s what I like about this blog! It is at the same time very entertaining and very educational. Creationists have actually done me a favor: I would never have learned so much about biology if it hadn’t been for their making claims out of ignorance. Thanks once again, PZ!
Very descriptive, thanks PZ.
Ah! Written so even a physicist can understand it.
Thanks, unnamed emailer!
I seem to recall reading about a species of fern that has a ridiculously large number of chromosomes, like on the order of 20,000 or so… but I can’t seem to find the name of it now. Does anybody know anything about this, or was this a lie I read on wikipedia?
A THEORY IN CRISIS!!!!!!
I believe there are examples of balanced translocations being dominant in populations of Drosophila on some islands. If the translocation break points don’t wreck genes, the duplicated translocation can be perfectly viable, an least in the balanced form. I don’t have the time to go into the details (they are in many genetics books), but this is a pretty straight forward way that two populations can lose the ability to interbreed.
And I used to think that Hu Chromossome 2 was an ape Robertsonian, but then they had to go find a telomere or centromere in there somewhere…
that was such a nice nice hypothesis until it ran into a little data….
-d
I once wrote a pair
Of Haikus, related, but
Willing to fuse–please
Don’t ask me how one
Limerick now replaces
The Haikus in twos
*****
I once wrote a pair of Haikus
Related, but willing to fuse
Please don’t ask me how
One limerick now
Replaces the Haikus in twos
(OT– http://digitalcuttlefish.blogspot.com/2008/04/i-just-love-xkcd.html )
I wish you were my prof, PZ!
Yay! Learning!
One of the arguments more learned creationists have raised is that the great apes have 48 chromosomes, but humans have only 46. How could humans have possibly evolved from the same phylogenetic ancestor as we have? One answer is in a great paper:
Hillier LW, and lots of others.
Generation and annotation of the DNA sequences of human chromosomes 2 and 4.
Nature. 2005 Apr 7;434(7034):724-31.
Apparently, in the course of our evolution, two ancestral primate chromosomes fused to make chromosome 2 in humans, an illustration of the point PZ Myers makes toward the end of his nifty piece. Added beauty is a stretch of telomeric TTAGGG repeats –inside– the chromosome. So, not only does this find support the idea that we evolved from a common ape ancestor, it also shows just how it must have happened.
Chromosomal numbers can vary within the same species. This number is very plastic. Mice colonized Madeira 1000 years ago and the 6 populations all have varying karyotypes. This is fast in evolutionary terms.
Same thing is observed in Tunisian mice. The latter are thought to be undergoing speciation, driven in part by karyotypic differences and lower fitness in hybrids.
Your smackdowns of creationists are fun, but stuff like this is priceless for us laypeople. Have you considered putting these in a book?
Ahhh, always a good day when gains new understanding before lunch. Even if it is from the gooier, more icky sciences. =)
Seriously though, very enlightening, many kudos PZ.
Lovely dip into the refreshing pool of knowledge. Besides helping the general public, stuff like this helps people like me see easier ways to explain things than I can come up with myself. Thanks!
Rarely do I ever get that deep into biology, precisely because its specifics are not easily explained. Thanks for the detail – I can now say I understand at least one involved concept in biology.
(Though I finally got my brain around the explanation, it took just enough time to confirm that my choice to enter philosophy and anthropology was the correct one…)
Great post, PZ!
And Cuttlefish, I am always in awe of your mad skilz, but that is astoundingly inventive! Perhaps there are other biological phenomena you could represent in concrete poetry…
Happy, happy, joy, joy.
Every now and then somebody puts real information in front of me, and I unwittingly learn something. Rarely so elegantly presented, however. Thank you. I’ll show this to my wife when she gets off work.
There’s an interesting twist on the breakage fusion business pointed out in a nice paper (full text available) — that since female meiosis is asymmetric (two cell divisions produce only one egg and some polar bodies, so some chromosomes get thrown away) there is competition between chromosomes for getting into the egg. If you have one breakage, or one fusion, you will have an odd number of total centromeres (like PZ drew above). It turns out there is a slight preference for the ‘extra’ centromere to either go to the egg, or to the first polar body – different ways for different organisms. This is why if you look at mammalian karyotypes, you will see that they are either all-metacentric (centromeres near the middle) like humans, or all-acrocentric (telomeres near one end) like many mice, but never a mixture of both, as would be expected if inheritance were random. That’s chromosome evolution put into high gear by a ‘selfish’ phenomenon.
Excellent. I often wondered about this too. And I’ve heard the same assertions from idiots thinking that chromosomes make speciation impossible.
One answer that I give is to repeat the line that they often use: “interspecies hybrids are usually sterile”. As in the horse donkey example, as in ligers and tigons, as in many others. But there was an important word in there. They are usually sterile. Not always.
The more you post like this, the more I consider going to Minnesota to finish my bio degree.
Hint: Move to Arkansas. We need the education.
One thing I found of interest when I looked some of this stuff up for a discussion on a Christian webforum I inhabit is the frequency of fusions in humans, right now.
Something like 1 in a 1000 human individuals in the general population have a Robertson translocation, in which different chromosomes are fused into a single larger chromosome. Details are available in Changes to Chromosome Structure (pdf file); fact sheet 7 from the Australian Centre for Genetic Education.
There is probably no real effect for such individuals, until they try to have children, when they are likely to have some difficulty with fertility.
I passed this information on without the depth of education that a biologist would bring to the subject. Posts like this one here are a great help.
Wow PZ, that was great!
There are other mechanisms for changing numbers that I didn’t discuss: polyploidy and alloploidy, for instance. This post only describes a few of the ways we can get variations. Don Kane also mentioned translocations, which are sneaky ways for a chromosome to gradually scramble itself around, piece by piece.
This is great. I envy your students. None of my biology professors ever explained this question so clearly, and although I’ve had a general notion of it, I’ve always still been a bit confused. (Bad me for not doing the research to clear up any confusion, I know.) Now I understand much better. Thanks, PZ!
I’ve wondered about this recently, thanks, this is a really good answer
Great great great post – thanks again PZ for a fine post!! An additional point is that depending on the literature source you read, somewhere between 1 in 600 to 1 in 1000 people carry a balanced translocation (the numbers vary depending on the type of study performed). That is, one chunk of a chromosome has switched places with another – no gain or loss of genetic material, but instead the re-shuffling that PZ discussed above. Such people are perfectly normal, and may never be aware that they carry a balanced translocation. Or, they may have a history of infertility or spontaneous abortions, or have a child or children with congenital anomalies. This is why it is standard practice to have chromosome analysis performed as part of a reproductive-issues work up, or if a child is born with anomalies. Chromosome rearrangements in humans (well, all animals with chromosomes) are neither common nor rare.
BTW – Cuttlefish is a poetry ROCK STAR. Love the fusion!
If it hasn’t been done already, this needs to be sent to Wilkins as a “Basics of Science” post.
Great answer. The question asked about selective advantage and your answer (accurately) says that there needn’t be a necessary selective advantage to propagate through the population. However, there is a potential selective advantage (and disadvantage) to having material scattered across several chromosomes (for a diploid eukaryote). With only one chromosome, all of your material is in one cabinet, inherited wholesale from parent to child, child to grandchild. You’ll necessarily have an exact copy of one of your ancestors chromosomes (leaving aside meiotic recombination), bringing both the good and the bad copies of genes along. Splitting up your genetic material into chromosomes that can be inherited independently means you will get a mixture of the grandparental genes. You won’t be an exact genetic copy. This allows increased mixing and matching of genetic material, potentially improving the chances of a beneficial combination of genes.
Of course more chromosomes also means more record keeping. More centromeres and telomeres to handle during duplication and meiosis/mitosis. I think the jury is still out on whether there might be some optimum number of chromosomes (rhinos have 84!).
Interestingly, most avian species have numerous microchromosomes. Up to 25% of the DNA (and 50% of the coding sequence) is not in conventional chromosomes but rather in a pool of smaller chromosomes. In these microchromosomes, recombination and mutation rates are significantly higher than in standard chromosomes, which may have significant impacts on their evolution.
There is interesting research into the origin of these microchromosomes and chromosome number in general. Nakatani Y et al (2007 – Genome Research 17:1254) suggest that microchromosomes may represent an ancestral vertebrate state where fusions have produced the 20-30 large chromosomes found in most vertebrate clades.
True. I personally know 2 people who have altered karyotypes, balanced. They were picked up on the basis of a family history of fertility problems and miscarriages. These weren’t severe though, one of the ancestral families ended up with 6 kids.
Wow, a post from PZ Myers about science, on Scienceblogs of all places!
Great post, PZ!
But one critical point: perhaps you could have included a little more about what the *evidence* is for what you’ve just said. I can just hear the creationists saying “But how do YOU know?” I think that one general problem with the way science is often taught is that it is taught in abstraction from the evidence for/context of discovery of the claims being presented to the student. Although you usually do a pretty darn good job of not making that mistake.
Here’s something to ponder: how many big bang doubters have you met that could name one single piece of alleged evidence for the big bang? I sure haven’t met any.
Not surprisingly, those who are aware of the evidence believe, those who aren’t, don’t.
I wish you were my prof, PZ!
The archive here makes him everybody’s prof.
Dig in – it’s the best part of the place.
Not least because the prof can really employ multimedia.
I recommend “How to make a vulva”. I won’t link to it directly because I have no idea whether the comments are worksafe in the land of patriarchal womb-control ;-)
Thanks PZ, this was a wonderful read.
I’m a long time lurker, occasional commenter.
This kind of stuff is so much cooler than just saying “Goddidit.”
Thankyou for this, P-Zed. It’s always a treat to learn something from an expert without having to become an expert first.
Honestly, if more people were able to communicate technical concepts like you communicate this one, I doubt we would have nearly as much problems getting people to accept sound science and reject nonsense.
It’s such a pleasure seeing a pro on top of their game. Well done, sir.
That was a beautifully concise explanation! Well done.
I’m given to sentimentality on occasion, and PZ’s mini-lecture brought me back to the class on genetics and heredity I took way back in 2001. The instructor was Dr. Mike Harrington here at the U of A, and he shared PZ’s talent for clarity as well as a sense of humour. (Plus, he wrote some of the best exams I’ve ever had the pleasure of taking–yes, you read that correctly: a well-written exam can be a pleasure for a prepared student.)
Man, I loved that class. Now I feel like quitting my job and going back to school.
Wow… that’s all I can say. That was an amazing explanation. Good job!
I wish I were smart enough to understand all this stuff, but I read a few paragraphs and my brain does a short circuit. Bzzzt. But even not understanding what you are saying, I realize you have an infinitely better argument for evo than the creos.
Weird, my post deleted all my spacing between sentences.
Cuttlefish, this is honestly your best yet!
I bow in awe.
Great post, great thread.
Regarding the reduction of chromosome numbers in Humans vis a vis the great apes, some work by Simon et al. several decades ago uncovered some circumstantial yet intriguing evidence that the process was specifically influenced by the mother. I don’t have the text handy, but one section I recall rather clearly said something to the effect “Mama, don’t take my Chromosome away.”
Sorry, the link to the listing of articles is stripped from my bad html.
This is it:
http://pharyngula.org/articles.html
There is plenty of evidence for this. Take some of the human genetic illnesses. Some of these involve extra chromosomes, and yet they are people who function, albeit in these cases with varying degrees of handicap.
It’s clear that some mutations like this aren’t noticed because the effects aren’t extreme. If they lead to an advantage, you would get the growth of organisms with extra chromosomes.
Nick
@Raven:
karyotypes:
AAAAAAAAAAAAAAhhhhhhhhhhhhhh!
lol.
Boomer, I did a quick google search and found indications that the species is Ophioglossum reticulatum, which apparently has 630 pairs (1260, a bit less than your recollection of 20000, but still ridiculous consider that animals seem mostly to be in the double digits). Note, this is after about 5 seconds of looking by a nonbiologist, so it’s possible that I’ve missed something. The website I found is http://www.vivo.colostate.edu/hbooks/genetics/medgen/basics/minmax_chromos.html
Thanks, PZ. I enjoy reading such explanations. That’s one reason why I visit this site regularly.
Nice post! This will make a fantastic addition to the things I send to brash, ignorant creationists. I can’t wait until the creationists read it. I’m sure their response will looks something like this …
PZ Myers has admitted that, on the subject of evolution: “Chance alone can do it.”
Lucid lesson! I really wasn’t interested in this subject, but, I started reading and I was hooked on learning more.
Nothing original in my comment, I just want to chime-in and say how fantastic and accessible that explanation was. I just got a biology lesson from a professor for free (complete with whiteboard illustrations)! If people really do learn something new every day, this will probably be the most interesting thing I’ll learn this week (now that the John Adams miniseries is concluded). Thanks PZ!
OK, I’m officially in love with Cuttlefish! Haiku to limerick? Let me catch my breath….
(OP Kudos)
What an excellent post. Thanks PZ.
(snark)
Where are Nisbet and Mooney? This is a frame they should really see.
(Comment Kudos)
Cuttlefish, that was brilliant, and inspiring seeing as my timestamp math says you did it in less than an hour.
This is very illuminating indeed … However: What about species that have holocentric chromosomes (i.e., no centromeres?). Many insects, for example, are notoriously variable in chromosome numbers, and often with no correlation to their phylogenetic history. And they have holocentric (or holokinetic) chromosomes.
There is one part of this explanation that I don’t understand.
When there is a single chromosome with two centromeres, the chromosome is split when one part (AB) is pulled in the opposite direction of the other (CDE). However this would produce one cell with the chromosomes (AB) and (abcde) and another with (CDE) and (abcde). I imagine these cells wouldn’t do that well, but even worse in the case of gametes we would have 4 cells with (AB), (abcde), (abcde) and (CDE).
So how do we go from a cell splitting a single chromosome into two different cells, to the state with a cell containing (AB) (CDE) and (abcde).
Thanks PZ
Very interesting, neutral mutations propagating, then a benefit for reproduction of two chromosome offspring which could lead to speciation. Great stuff, keep on posting science stuff I learn so much from reading your posts.
Good biology lesson! Here’s a followup question: How does the cell pair homologous chromosomes during meiosis? Are centromeres unique (tagged, somehow) to the chromosome pair?
The whole idea of chromosome number goes much deeper. Basically prokaryotes and the vast majority of eukaryotes are haploid. If they reproduce sexually, the zygote is the only diploid stage. Only animals and the sporophyte generation of plants are routinely diploid (dikaryon in basidiomycetes). What’s the advantage of being diploid? It allows you to be heterozygous for one thing, and meiosis allows for recombination of parental genotypes. So ultimately this leads to your point, more chromosomes allows for more gene combinations, more variation upon which selection can act. With the exception of the rattlesnake ferns, which have some very high chromosome numbers (paleopolyploids?), there must be some optimal range (1 to 4 dozen) of chromosome number to accomplish this efficiently.
What I find fascinating is the implication that divergence of species would occur most readily when an individual with a chromosome split or fusion becomes a member of a small isolated (in-breeding) group. The likelihood of such a mutation gaining any traction in a large population would be quite small. So island populations in particular would be prone to divergence.
I’ve often wondered why we don’t have just one chromosome, and your explanation even offers an inkling why that would be unlikely.
Thanks for your patience.
And now I’m waiting for the inevitable question: “But have you OBSERVED this?”.
I want to see some of your post-Expelled hate-mails, too. Hopefully, from someone who had never heard of you before this weekend. The more basic errors these emails contain, the better.
Case Luskin recently returned (in typically obtuse manner) to the subject of the fused ape chromosomes 2A&2B.
Intelligent Design 101: Casey Luskin on Human Chromosomal Fusion
He argues that the similarities are caused by common design, but of course he doesn’t mention the degenerate centromere and vestigal telomeres (i.e. evidence of dysteleology), and he also doesn’t manage to mention the potential biological importance of looking at the genes surrounding the fusion point (PGML/FOXD/CBWD) for changes that may have led to the origins of modern human abilities.
But he has this silly scenario which he explores at the end of the podcast. To paraphrase – imagine, a population of future humans derived from modern H. sapiens. These future humans (“the double fuser people” or DFP) have inherited a new chromosome fusion which is fixed in the population (i.e. reached 100% frequency, they now have 44 chromosomes – 22 pairs).
Modern H. sapiens are extinct, all their knowledge is unavailable and DFP humans are starting again from scratch. The DFP humans compare themselves with surviving chimps. These future DFP humans would think they had a common ancestor with chimps, but with 2 chromosomes fusions in between.
However, Luskin argues that this inference would be logically invalid, as the second hypothetical fusion event took place in modern H. sapiens, and has:
Is Luskin being intentionally dense? In his scenario either of the fusion events could have taken place at almost any arbitrary generation in the history of the population – between the last common ancestor with the outgroup (chimps in this case) and long enough before the karyotype is tested to fix the variant across the population.
In his own scenario, if ‘the double fuser people’ humans got hold of a modern human karyotype and thought “perhaps we share a common ancestor with this organism, except for a single chromosome fusion event”, they would be completely correct.
I second the comment at #30 about a book – why not, at the very least, put a collection of your ‘science’ posts together, similar in vein to Science Blogging Anthology – or at least have your own chapter in the next edition? Are you listening, Coturnix? :-)
That was really, really good.
Great. I already throw more details at the freshman than they want, and you give me a few more to rattle around and spill out.
On the question of big chromosome numbers, here’s an info page – don’t know how authoritative it is, but I’m betting moreso than Wikipedia:
http://arbl.cvmbs.colostate.edu/hbooks/genetics/medgen/basics/minmax_chromos.html
@ #71
A little hard to explain without the use of pictures but here goes.
The chromosome during mitosis will be two pieces of almost identical, tightly coiled, double stranded DNA, held together at the centromere. The spindle fibers attach to one piece of DNA and at the proper time pull the two apart. With two centromeres if both spindles grabbed the same piece of DNA there would be no break. If however they each attach to opposite strands the break will occur.
So in this case we have chromosome ABCDE (with two centromeres) copying for mitosis. So there are two identical pieces of DNA held together at the centromeres. We’ll call one ABCDE and the other A’B’C’D’E’. If the spindle attaches on the ABCDE strand at one centromere and the A’B’C’D’E’ strand at the other, when separated (and broke) one resulting daughter cell will end up with AB and C’D’E’ while the other one ends up with A’B’ and CDE resulting in no net imbalance of information.
I hope that I didn’t confuse you more.
I particularly like the “SNAP!” and “FUSE!” bits. I imagine your students do, too.
PZ gave a great explanation but he could’ve made it even greater if he drew the replicating chromosomes as X’s rather than lines
Cool stuff PZ! I’d been wondering about this for years. Many thanks.
Thank you. If I had had science teachers with your interpretive abilities, maybe I would have studied a hard science rather than history (though I love history).
My understanding is that even though chromosomes can snap or fuse, the information encoded upon them remains (relatively) unchanged? Does this mean that the position of the gene on the chromosome does not really matter? Cool.
To #59:
“Mama, don’t take my Chromosome away.”
One of the common causes of Down’s is improper segregation of Ch 21 in females.
The idea is that because female meiocytes (look that word up!) are formed in the early months of gestation, they are about 20 years old when there is the first possibility of them being used (should be used?), and as late as 45 or even 50 years old.
Women in their 20s have about a 1/3000 chance of a Down’s kid; in their 40s it’s more like 1/50. Those old chromosomes git suck….
Interesting to think about how old you really are. In my case, the maternal set of chromosomes for my early divisions, I remember them well, was some time in 1927….
My big grin for the day, thanks PZ.
So I take it this means that organisms which become isolated in contained environments will speciate more quickly than those in large mixing populations? (because the oddballs’ offspring are contained together).
I do know that colour and coat and size variations jump up like dandelions as soon as an animal is taken into domestication. Look at hamsters , only kept as pets since the 1930s.
Noni
@#81
Thanks for the explanation drew, but I’m still a little confused. It seems to me that you are saying both homologous chromosomes would have to have the double centromere for this to occur, which would then make sense. However, I don’t think that’s what PZ said. He seems to have your A’B’C’D’E’ notated as abcde, and his abcde remains intact and single centromered throughout the process. Is this correct?
Not only are cells really, really stupid, they are rather egotistical as well and don’t like sharing their ice cream cones.
Really, I thought your microtome-sharp wit was only reserved for the bible types and spared us flakey folks who occaisionally entertain the possibility that cells might be smarter than just bags of goo. I really wonder if that silly notion fits in the same category with Creationism. Okay maybe it fits in the same big fat “wrong” category, but still.
I enjoyed your very lucid writing anyway, even if it was for me a bit of a bullet with butterfly wings, metaphoricaly speaking.
#5 boomer
I just finished it yesterday–it’s good all the way through!
http://www.cbc.ca/news/viewpoint/vp_savory/20080311.html is an article on science vs. creationism, featuring Fairbanks.
http://www.cbc.ca/technology/technology-blog/2008/03/your_interview_daniel_fairbank.html is a page for comments on the article, though there don’t seem to be any there yet.
http://search.barnesandnoble.com/Relics-of-Eden/Daniel-J-Fairbanks/e/9781591025641 is the Barnes&Noble page for the book.
Chapter 1 of the book explains the fusion of chromosomes 2A and 2B to form human chromosome 2. In includes a full-page DNA sequence showing the fusion site–two partial telomeres joined, with a flip–all the surrounding telomeres, and a bit more for context.
Appendices 1 and 2 are heavy-duty stuff, “The Story of NANOG and Its Pseudogenes” and “The Nine Inversions”, the latter being a detailed discussion of the nine places where portions of the human or chimpanzee genome (in chromosomes 1, 4, 5, 9, 12, 15, 16, 17, and 18) are inverted relative to their common ancestors.
I particularly enjoyed Appendix 3, From Darwin to the Human Genome : A Brief History. It’s about the people, and what they did.
There’s a nice description of “Rosalind Franklin, a physicist with a superb talent for x-ray diffraction.”
Thank you for the explanation.
I learned in high school and college (1950s and 60s) that I had 48 chromosomes. I find out now that apparently I’ve lost two of them. Does that happen to everyone when they get old?
Dan Freiberg
Thanks PZ. It’s been a while since my freshman biology class. For us non-scientist loving scientists, it’s nice to get a refresher now and then. As I was reading through, I kept thinking “Oh yeah! That’s right. I totally forgot about that.”
Keep up the good work.
I don’t always read your science posts, but for whatever reason I read this one. I’m not sure what it is, but you’ve obviously done something right!
I was under the impression that a driving theory that the numbers could change by the HERV ?
http://www.ncbi.nlm.nih.gov/pubmed/7831772
Todays APOD has a rather nice family photo of phage family
http://antwrp.gsfc.nasa.gov/apod/ap080421.html
I wonder if the secret lies with mitochondrial DNA?
http://sci.odu.edu/biology/directory/greenwood.shtml
anyway, good post
And the subject of a lovely essay by Stephen Jay Gould in Bully for Brontosaurus which, by coincidence, I was reading yesterday.
*applause*
Very nice, accessable descriptions, PZ. The paragraph about ignorance was a fitting coda in light of Luskin and the other recent rant. It’s been said before, but ignorance is not usually a failing or an insult. Everyone is ignorant about a huge number of things, but the way one reacts to ignorance is the important part. When you recognize the limits of your knowledge in an area of importance or personal interest, and that ignorance leads to an honest search for more information, then ignorance becomes a motivator of personal and cultural improvement.
The problem comes when ignorance is coupled with arrogance, as “willful ignorance” – when a person insists that their own unfounded opinions are of greater worth than the evidence, which of course will be selectively ignored and fallaciously opposed in order to maintain an unaltered opinion.
#88
Not quite.
I think your problem is that you’re forgeting the DNA duplicates before all of this starts.
So we’re dealing with a diploid organism here so there is 1 pair chromosomes. This pair will have roughly same genes but different alleles (most likely), i.e. similar but not identical. So one we’ll call (as PZ does) ABCDE, and the other we’ll call abcde. ABCDE mutates into a chromosome with two centromeres. When they ready for mitosis they’ll make copies of them selves we’ll denote by the prime(‘). So going into the cycle the cell will have ABCDE with its copy A’B’C’D’E’ joined at the two centromeres, and abcde joined with its copy a’b’c’d’e’ at its only centromere. So lowercase will look like an X, while uppercase will look like an X with two crosses. Now there are spindles that attach to the centromeres, the other end stretches to the edge of the cells, one pulls right one pulls left separating the two strands to opposite sides of the cell just before the cells split.
When the cell divides the two daughter cells will each get a copy of abcde, that are identical to each other, they’ll separate with no problem. The only problem will come when trying to separate the one with two centromeres.
For the purpose of visualization perhaps think in colors, Let’s make ABCDE red and A’B’C’D’E’ blue. The left side of the cell attaches to the red strand at centromere 1 and the blue strand at centromere 2, and likewise the right strand attaches to blue at c1 and red at c2. At the proper phase the threads will start to pull and it’s going to create a lot of mechanical stress on the DNA molecules, and they’ll break. So each daughter will get part blue and part red.
So you’ll end up with two daughter cells each containing one small chromosome AB, another small chromosome CDE, and a large (original size) chromosome abcde.
I hope I’m helping but I may be confusing you more.
PZ: Great article! Have you decided what you’re going to present at the Denver AG?
And the smallest chromosome number is one, in males of a species of Australian ant. Nicely done presentation.
Neat! I never knew that. See kids, you can learn things by reading the Internets.
So if I’m understanding you correctly, since changes in chromosomal numbers is a factor that can lead to speciation, speciation itself is a consequence of both accident and divergence from other populations due to adaptation. Am I crazy, or do I actually have that right?
Also, I’ve seen complaints from some creationists that science textbooks, etc. use too many illustrations and not enough photos. Given the power of modern microscope technology, I’d say that’s a useful criticism. How about adding in some photos of chromosomes or metaphase to help illustrate what you’re talking about? There are many beautiful examples.
PZ, could you add more detail about how the chromosomes line up, and how daughter cells normally end up with a complete set of them rather than one getting two chromosome 1s and the other getting two chromosome 2s? Then, why does the situation in 7chrom.jpg make that not work?
Now THIS is what the internet is for. For me anyway. Thanks!
speciation itself is a consequence of both accident and divergence from other populations due to adaptation.
Essentially, that’s the gist of it, yes.
Chromosomal duplication is just one avenue of generating new diversity of genetic material (there are many others), which of course ends up producing new phenotypes selection can act on.
Then it becomes even more complicated, as selection doesn’t always have a strong effect on the direction traits can take within a given population.
often, just drift can shape which phenotypes we see in a population as well.
It entirely depends on what kinds of selection pressures a given population is under, and it’s relative size and level of isolation.
In some populations, selection pressure on some traits is so low that they “drift”, and so much of the variation in phenotypes we see is just the result of what we call neutral theory:
http://en.wikipedia.org/wiki/Neutral_theory_of_molecular_evolution
If you have a grasp of the fact that there are many sources of potential variation (like chromosomal duplication, point mutations, horizontal gene transfer, etc.), and that selection can be highly variable as a mechanism for effecting the observed phenotypes within a given population, you have a pretty good grasp of the modern theory of evolution.
@#88
You are correct, I did make a notational error, thanks for clearing that up, yet I still think something isn’t quite right here. It’s my understanding that this type of duplication error (that is doubling of the centromere) would only happen in, well, duplication. So you don’t have a cell that just starts out with a chromosome containing two centromeres, you start out with a cell with both homologous chromosomes having one centromere each. Then, when mitosis begins ABCDE (with its single centromere) has some replication error and produces A’B’C’D’E’ (with two centromeres). This leads to the problem I described above.
Thanks for taking the time to explain this, I hope we’re nearly done. :)
Chromosomal duplication is just one avenue of generating new diversity of genetic material (there are many others), which of course ends up producing new phenotypes selection can act on.
I should modify that as well to include that the “of course” part is a gross oversimplification of how genes interact with the environment itself, whether we are talking during development, or even before. One things we have certainly learned over the last 30 years (and PZ will certainly stress) is the rather large role environment can play on development. We know from mapping the human genome (and other things) that there isn’t a one-to-one correspondence between gene and phenotype like I learned when I was young. Hence, the entire evo-devo field.
Epigenetics also rather complicates the whole issue.
http://www.pbs.org/wgbh/nova/sciencenow/3411/02.html
all that said, what you said was essentially correct.
It’s just that in actuality, there is a lot going on behind what appears as such a simple statement.
:)
Posted by: Scooty Puff, Jr.
…oh, and one more thing to remember…
“Scooty Puff, Jr. suuuuccckkkksss!”
Fry recommends the Scooty Puff, Sr.: The Doombringer.
I seem to recall learning in high school Bio that there are some organisms (plants? insects? I can’t remember) with an interesting pattern of chromosomal inheritance — they alternate generations with N chromosomes with generations with 2N chromosomes.
Could you maybe talk about that?
PZ, thanks once again for your extraordinary public service. Your efforts are appreciated by many!
Yeah, well, the bible ain’t got no photos or illustrations ‘t’all, and them creos ain’t questionin’ it none.
Now I’m no expert, but PZ’s post is a produced-for-mass-consumption (though eloquent) explanation of a few fundamentals in cell biology. And this is what creationists manage to befuddle so completely and consistently. It is hard to come away thinking anything other than they criticize what they are stridently unwilling to understand. And why with them it is more effective to ridicule than to reason.
This is a great article. I’m here for the education in the science and the belly laughs as you destroy the creationist loonies.
Keep it up.
I think that’s true sometimes, Spaulding, but it’s also true that photorealistic illustrations can include too much unnecessary detail which distracts from the main pedagogical purpose of the illustration. It depends on what you’re trying to communicate, in what context, and to what audience. Schematics, properly used, can reduce an illustration to its essentials, and remove the distraction of unnecessary detail.
I don’t know what the creationists you mention are complaining about, but given all the anti-science and anti-education I’ve read from them, I’d venture to guess they perceive the use of a carefully-crafted schematic drawing emphasizing teaching points as more “biased” than a photo full of noise.
Some of the criticisms of the Expelled cell video are a case in point–there is simply too much going on for non-specialists to watch and extract the salient features the illustrators want to concentrate on in real time. So the XVIVO illustrators pick and choose particular features from photorealistic images to include, and others to leave out.
(The fact that the Expelled video included the same set of features the XVIVO video did, and excluded the same set of features the XVIVO video did–well, at the very least, it looks like plagiarism, although establishng the facts of the matter may have to await a court case, if there is one. But it gets back to the fact that photorealistic images can contain too much information, if the pedagogical point trying to be made risks getting lost in the noise of realistic detail, and that illustrators can select features for emphasis, which may serve the teaching better than the undifferentiated detail can serve it.)
More praise over here, that was a wonderful explanation – I vote for more uses of the virtual whiteboard.
I also second the vote for a book. This reminded me of reading “The Extended Phenotype” only in a tone as if PZ was writing it and I realized I would buy a book of that in a second.
Thanks PZ!
#109:
You’re mostly talking about haploid vs. diploid generations – they’re not generations in the general sense, but a reproductive pattern most obvious in plants like ferns, where you have child independent organisms that reproduce asexually alternating with sexual generations.
But really, every multicellular organism does this. Humans have a haploid state as well, the egg and sperm. The haploid has simply been reduced, like in flowering plants. I don’t know of any multi-cellular organism without meiosis.
What’s stranger is that some organism do gender determination by chromosome number – the common pattern is that males get N, and females get 2N. The males are unfertilized eggs, so they are more closely related to their mothers than the females, leading to all kinds of breeding complexities in social insects.
@#106:
Just wondering if this is a meiosis mitosis ambiguity. If we are talking about changes that are getting passed on to offspring, we are most likely talking about meiosis. Quick and dirty meiosis: the DNA gets duplicated (error produces two centromeres in ABCDE), homologous pairs divide, the break occurs, and you should have gotten 2 haploid cells with duplicated DNA, which then go on to divide up that duplicated DNA. But, with the two centromeres, you get 3 “chromosomes” once the break occurs in the first division. Since you can’t divide 3 evenly 2 ways, you have a couple possibilities. You can have the AB/CDE and abcde in the daughter cells, or AB/abcde and CDE, or CDE/abcde and AB. Both of the second cases will probably mean the kid won’t survive. The first case however, would give rise to a change in chromosome number with no ill effects as you still have all the genes, and in the right amounts. The only thing is that the child would have both AB and CDE pairing with an ABCDE chromosome from the other parent. That COULD get by and survive in a population. Eventually, you might get one of these heterozygous individuals (AB/CDE for one, and the whole ABCDE for the other) mating with another heterozygous individual, in which case some of their children (1/4) would have 2 fragments matching up with 2 fragments, and thus would have increased their chromosome number.
Hope that helped.
And prompts you to write a sincere answer. The most excellent kind of framing indeed! What the ‘good-framing-agitators’ (frame botherers?) keep missing is that the agitprop of the creationists is never a sincere search for knowledge and there is no frame capable of piercing that. When someone has a legitimate, sincere question, the good scientists like PZ can produce the most composed, the most collected, the most AMICABLE of responses.
The fire-breathing is reserved for the willful and wanton ignorance peddlers.
Wow, I really should proof read my posts better. In my 3 examples, the 2nd two cases can lead to some pretty interesting outcomes (increase and decrease in gene dose), but I focused on the first since it is the simplest.
Awesome.
I’m 113 posts in, and not a single creationist troll has opted to chime in. Why is that? Could it be that when the science lessons begin the creationists hit the road?
PZ,
That was a wonderful explaination of how the number of chromosones may change. Thank you. I am a Christian and wanted you to know we don’t all hate you! Thanks again.
-Randy
I can’t say how nice it is to see a thread where people just exchange information instead of butting heads. Too bad it’s bed time here, I’d love to see more, but it’ll have to wait for tomorrow. Just wanted to say “Thanks” and “Keep it up” to the commenters as well :)
938MeV
Not necessarily. That’s one way it could happen, another way could be if the centromere existed in the middle of a transpable element and was reinserted into the chromosome. But I think you’re right in that a replication error is probably the most likely event. Also remember that the spliting of the double centromered chromosome doesn’t necessarily have to happen on the same mitotic event as the replication error.
There is another error you’re making with regard to the DNA replication itself, and I should note that with the way I explained it I could carry partial responsibility. I used ABCDE and A’B’C’D’E’ for ease of notation and being able to explain it to you, but you’re not going to have original and copy. The original chromosome is divided equally between the daughters, so in my two copies ABCDE and A’B’C’D’E’ both contain half new material and half original material.
Also of note, I’m explaining it here as it would pertain to mitotic cell division, this is going to be partly different in the case of meiotic division which gives rise to sex cells where it would almost certainly exert a greater effect on progeny. And in that case The daughter cells of which there are (eventually) 4 would each contain 1 chromosome instead of 1 pair. Biology is a little messy and can be difficult to explain sometimes.
We covered this a little in my intro to human evolution class, but not in any detail at all, so it’s nice to have the extra information. It’s very clear and succinct. Thank you!
whoa, you should do updates like this more often.
@#117
I see what you are saying, but the issue I have is right after the “DNA gets duplicated (error produces two centromeres in ABCDE).” Let’s let * stand for a centromere
We start out with:
(AB*CDE and ab*cde)
DNA replication with error producing centomere doubling:
((AB*CDE, AB**CDE) and (ab*cde, ab*cde))
Now concentrating on just AB**CDE, the cetromeres attach to the spindle, randomly both centromeres may pull the chromosome in the same direction leaving us with an unbroken AB**CDE in one cell (scenario A):
cell 1 cell 2
(AB*CDE) (AB**CDE)
Or (and here is the crux of the problem), the centromeres may pull in different directions, causing the break in AB**CDE to form AB*/*CDE giving us (scenario B):
cell 1 cell 2
(AB*CDE, AB*) (*CDE)
or
(AB*CDE, *CDE) (AB*)
My point is if, as PZ presents it, it is the action of the centromeres being pulled in the different directions that causes the actual break in the chromosome, then we can’t get (scenario C) where we end up with:
cell 1 cell 2
(AB*CDE) (AB* *CDE)
because this is the scenario where both centromeres are pulled in the same direction, and thus the chromosome doesn’t snap. Yet, scenario C is where the rest of the explanation that PZ offers goes on from.
Do you see my confusion?
This is probably all just an artifact of the explanation PZ gave was simplified for mass consumption, but I do want to understand and I certainly don’t want to be caught with my pants down when some creationist tells me that increase in chromosome # prevents speciation.
some commentators here express mild embarassment at taking a biologist’s word for some aspect of biology. Its great that they want to know more, but I think there is nothing to be ashamed of if someone accepts evolution “on faith” (faith in the scientific community, in this case). All the sciences are now at a point that the details become too complicated for most non-specialists, but that does not prevent us from believing that “superconductivity is a quantum phenomenon on a classical scale” or any other startling and (in its details) extemely complicated physical phenomenon. PZs explanation was great, but I just wanted to point out that evolution is only controversial because some religious nuts find it hard to swallow. Otherwise, it is mainstream science and laymen should feel reasonably comfortable with taking it “on faith”, just as they take other scienctific facts “on faith”….its great that so many want to know the details, but there is no special reason why THESE details should be on everyone’s fingertips, just as there is no particular reason why the mathematical treatment of the wave function should be on every person’s fingertips..
Thanks PZ,
Interesting, the creationists are rather scarce in the comments section of a post like this.
Now that’s what I call a productive question. It evoked a fascinating, clear explanation, a number of interesting digressions and refinements, links to lots or related information, and a hilarious conceptual tour de force from the beloved and respected Cuttlefish.
Made my day!
Excellent! Thanks, PZ!
@#127:
Ah, now I’ve figured out where the problem in communication is. The duplicated AB*CDE NORMALLY forms an X shaped pair (the two left arms being ABCDE and the two right being A’B’C’D’E’). The crossing point of the X is the SHARED centromere. If the centromere was doubled, the resultant tetrad would look like two X’s stacked on top of each other (TWO crossing points). You would not have one set of arms on the tetrad having one centromere, and the other set with two, with the tetrad only crossing at one point, and a free centromere hanging off on one of the loose arms.
Hope it makes more sense now.
This post kicks ass. At times like this, I almost wish I went into biology instead of comp sci…almost…
I don’t believe this was a creationist. You gave yourself away: no “Comic Sans” font.
:p
Pretty nice article! I’ve thought for a while that in some sense Downs folks (trisomy 21 et misc) were like a “first draft” of a potential subspecies.
Another good and related question is, how does DNA evolve “vertically”? IOW, I get about ACTG sequences being changed and selected, but how does DNA evolve to be longer (roughly but not dependably correlated with “advancement”) with time as well of course as adapted at the same time?
AHA! You said “mechanisms!” And as we all know, you can’t have a mechanism without a mechanic!
Sorry. There was too much smart in this thread and I was feeling left out. Had to inject some stupid.
@#132
That makes sense, as long as both ABCDE and A’B’C’D’E’ _both_ have double centromeres, (for this illustration let’s have AB*C*DE): Sorry about the .s instead of spaces, but the posting software has mangled my beautiful ascii art.
A….A’
.B..B’
..**
.C..C’
..**
.D..D’
E….E’
Otherwise, why wouldn’t you have the dangling centromere? If we start out with a AB*CDE and have a replication error to make A’B’*C’*D’E’ wouldn’t it be:
A….A’
.B..B’
..**
.C..C’
.D…*
E…..D
…….E
Don’t we need two double centromeres chromosomes to line up, in order to make the double X as above?
And if we have a dangling centromere my objection above stands. But to not have a dangling centromere, we need to have a cell _start_ with a chromosome with double centromeres, before replication. And how would that happen?
Thanks for sticking with this and explaining the a few of the details.
From PZ’s post:
He who knows not, and knows that he knows not, is a student. Teach him.
He who knows not, and knows not that he knows not, is a fool. Shun him.
That, I think, sums up the difference between this questioner and a creationist. My thanks to both the questioner and PZ for one of the best posts I’ve ever read on Pharyngula; like many others commenting here, I learned a lot from it.
llanite Dave noted
Sure. And it demonstrates that it’s not about the science for them. ‘Course, we all knew that.
PZ, that was simple enough even for me. Can you label it as one of the “Basics” posts everyone was going to do last year?
Firemancarl [#12], “Kudos to whomever asked this question” is not quite right. “Kudos to her” is right. But when you replace “him” or “her” with a clause, the whole clause is the object of “to” but within the clause, “Wh…” is the subject of “asked” so it’s “Who”: “Kudos to whoever asked this question.”
Then, you just have to remember that “kudos” is a Greek singular meaning “glory” and you’re home free.
@#138:
Do be honest, I don’t know exactly why you can’t have a dangling centromere. There are some vague notions floating around in my brain, and I seem to remember being told why it wouldn’t happen. But I do not have my good reference material handy (in another country in fact) and couldn’t find anything good in a brief perusal of the net. So I will not insert a quite likely wrong answer into this conversation and will hope someone else knows.
This post is the perfect example of how I got hooked on this site years ago. Thanks PZ!
I’m with Milo. Beautiful!
Thanks again PZ…
This makes me wonder though: here is a perfect example of a relative ignoramus (me) learning new details (and very clearly!!!) from an expert (in this case, PZ).
What I want to know is why – W-H-Y – some folks, who are every bit as ignorant as I am in biology, can’t seem to digest this abundantly clear and crisp example of what biologists in fact know? WHY can’t they even TASTE, let alone SWALLOW DOWN this material, just to see if it MAKES ANY SENSE?
Never mind. I already know the answer to those rhetorical questions. It’s because these details don’t reinforce the Big Idea that some god-thang is behind it all, WHATEVER the detailed mechanisms involved.
Isn’t it funny? How many times have we been accosted by ID’ers chastising us for having what they characterize as “closed minds”?
But there’s something else. WHY should I be so easily willing to defer to an expert in the science in order to update my knowledge? And WHY are the religiously-inclined so unwilling to accept the very same evidence?
The difference must be in the psychological foundation between these…and it must be due to whatever cultural forces cultivate it from early childhood. Mighty powerful stuff. It’s been said before, but the systematic RESTRICTION of a child’s natural curiosity – whatever the culture – is tantamount to a kind of child abuse. In life-long effect, it’s every bit as outrageous as the worst physical abuse imaginable.
Spaulding [#102],
There’s one exception to creationists complaining when drawings are used instead of photos: Dembski’s Flagellum.
I thought this a very clear explanation — and I’m curious about whether the person who asked the original question also thinks so. Are they satisfied now, or do they still have issues? For all I know, they’ve already shown up in Comments.
938MeV,
Now I think I get where you’re coming from, and you’re right. It could happen that way. Probably immediately nothing goes wrong…Because only one strand has the second centromere sequence it probably wouldn’t form up the joint and it would hang off like your little ascii thing suggests. That’s not really a problem. Don’t forget that the proteins involved in all this probably wouldn’t form it up properly because they depend on the context of having both sides in the pocket…it’s all about conformation. In other words, since the coresponding “leg” doesn’t have the centromere sequence, the one that does will probably just super coil up like the rest of the DNA with probably a few extra proteins bound to it unstably because they can’t form up the proper conformation without their “match”
That means that the problem wouldn’t establish itself until the next generation (be it next set of replications in mitosis or next individual in meiosis). Which means that replication would start up with the double centromere sequence being present from the start.
Mark, #103:
When the chromosomes are duplicated, they are linked together by a complex of proteins called the cohesin complex. I like to visualize this as a rubber band binding the two sister chromatids into a single pile.
There are structures called spindle set up at opposite ends of the cell. Each centrosome has a complex called a kinetochore, which attaches to a fiber that’s connected to only one spindle pole. When pairs of sister chromatids are attached to opposite spindle poles, the cohesin complex is dissolved (the rubber band is cut), and the sister chromatids are pulled to opposite sides of the cell.
There’s a more technical (and probably better) explanation here in Molecular Cell Biology, 4th ed. Figure 13-18 is particularly useful.
Noting how many recent commenters have said how polite and troll-free this post is, as it was driven by an honest question, I wonder – PZ, did the original questioner ever respond to your answer here? What did s/he have to say about it?
Excellent! Takes me back 50 years when I learned my science from reading Isaac Asimov. A clear explanation in a conversational tone plus a simple schematic, and all with humor. PZ, when you retire from teaching university students, could you write a few science texts for teenagers (and those adults who function as adolescents when it comes to science)? You could really do science education a great service and this blog proves that you have the verbal flow for it. What a pleasure that was to read!
hey, some dude (who has probably escaped his dungeon cell, and hasn’t figured out that the next step is an IP ban), just to make you happy…
Fuck You!
You’re a world-class asshole who is even beyond being called a demented fuckwit.
congratulations.
#114 thalarctos , et. al.:
I absolutely agree that a diagram can often be more didactically useful than a photo. However, there are numerous situations where the photos are both beautiful and useful. Illustrating ion channels in a college textbook might be done with illustrations, but talking about extinct species, microorganisms, etc., can be compellingly done with photos of fossils and specimens, rather than drawings. Yeah, obviously the images are already there for people who want to do a Google search, and nobody is demanding photos of The Fossil of Jesus; but if using more photos makes some people slightly less hostile towards science, and gives everyone beautiful textbooks, I don’t see a downside.
Except of course, for heavier, more expensive books. But that’s not an issue on the internet!
And the nitwit some dude had to show up just after a comment mentioning Asimov, who taught me at least as much as any three of my favorite teachers! I was reliving a chapter from “Only a Trillion.” I think it was titled “The Abnormality of Being Normal. Now comes an exception to the rule. Dammit, boy!
Dude, your timing is crude
But you’ll not spoil my mood!
You’re not only rude
But potential squid food!
Now to the forgetting and ignoring. No forgiving this fool . . .
Hey, Ichthyic:
FUCK OFF, LOSER
Hey, Ichthyic:
FUCK OFF, LOSER
It would be remiss of me to not say, “Thank you, thank you very much” to PZ, the masked questioner and (nearly) all of the above commenters. This has been a true delight; enlightening, entertaining and educational. Who could want for more?
Well…uh…erm…HERRING AND GRUEL AND PORRIDGE AND MILK!
Well…uh…erm…HERRING AND GRUEL AND PORRIDGE AND MILK!
…and lions and tigers and bears?
PZ, can you get in your way-back machine and travel to 1998 to teach my genetics class? Because then it might actually have made sense.
*Waits patiently for brain to flood with tasty info from the past*
i doubt very seriuosly that genes control the number of chromosomes, they may precipitate a change in chromosome number but that would be causal.
One cool application of this stuff: Making beer
See, hops that are diploid produce enormous numbers of seeds, which are exceptionally bitter, and making beer from these plants produces bitter beer. But for lager, you need a smoother taste. Unfortunately, it’s hard to get the seeds out.
Luckily, science has the answer! By treating diploid plants with chemicals, you can produce tetraploid plants, which behave in exactly the same way as diploid plants. Bummer. But if you breed them with diploid plants… you get triploid plants, and they produce hardly any seeds at all!
Yay for science/beer/beery science/sciency beer!
Hi, I thought I ought to comment as I was the one who asked the original question.
Yes, this post answers my query and I enjoyed reading it very much. Thank you PZ Myers.
My ignorance stems from the fact that I am a (very young) philosopher, and pretty much trust the sciences to get it right without getting involved much. I write almost exclusively on natural selection, so perhaps my ignorance of genetics is a bit shameful. I see that a few people have recommended the book “Relics of Eden” which I intend to pick up now.
Thanks again.
Science Beer…
Brilliant!
Ah, Benjamin! See what you have done! Single handedly* you have sent a soft breeze of accord to gently smooth the normally raised hackles that are a familiar feature of this blog! You have caused a hush to fall upon the loud voices and brought back, if only fleetingly, a sense of wonder that unites us in our joy of learning. And all it took was an honest question and humble implication that you would really, really like to have an honest answer. Wow, Ben. Way cool. Go well and return often.
*Ok, PZ helped some.
(Now back to our regularly scheduled free for all.)
E Pluribus Unum
Polyploidy was mentioned in a comment by PZ. This happens when cell division is normal except the cell does not physically divide in two, resulting in a cell with twice the normal number of chromosomes. This is quite frequent in plants but much less so in animals. Lurker mentioned bananas. These are interesting in that in a normal diploid (having a pair of each chromosome) the chromosomes doubled to make a tetraploid. This then crossed with the original to give plants with three sets of chromosomes, the cultivated bananas. At meiosis (the cell division that gives rise to the egg cells and pollen) when the number of chromosomes is halved, the three sets causes great confusion resulting in very few viable egg cells and pollen grains. This is part of the reason why you never find a seed in a banana. It also causes major headaches for people trying to breed disease resistence into bananas.
Truly a wonderful post & the comments thread is the icing on the cake.
@ 116: no multicellular organisms without meiosis – what about things like rotifers with their amictic eggs? I remember seeing a headline in our local paper a year or few ago, for an article on rotifers: No sex for millions of years! (It was unfortunately juxtaposed with a photo of the researcher profiled in the story…)
That was the best, most lucid
geneticsscience post I’ve ever seen. Bravo!Thanks! Although having studied biology myself, molecular genetics is not my speciality (fossils are), so I am not always certain about all the issues. At least now I won’t be embarassed by a creationist stumping me with this! :-)
Here’s a thought:
PZ and Cuttlefish team up for a book. Biology made accessible for us lay-folk, interspersed with Cuttlefish’s poetry.
You’re welcome.
Brilliant, PZ! Very very clear, even to a non-scientist like myself. Also, I feel even more smug about the fact that I Googled Robertonian fusions only yesterday. Bwah.
Re: chromsomes with two centroemeres being pulled apart.
In most cases, one of the two centromeres is inactivated–or so it seems. Recent work seems to suggest that in reality, centromeres are not equally efficient at assembling the kinetochore, which is that part of the centromere where the spindle attaches. In essence, one centromere gets the job done before the other can interfere.
…the sock puppet love fest continues…
PZ,
brilliant stuff, thanks! Have you considered taking up teaching? I think you might be good at it.
This question in my mailbox is also ignorant — the fellow really doesn’t understand the basics of genetics — but it’s self-recognized ignorance that, in a good way, prompts him to ask a sincere question.
Slate magazine’s “Explainer” column routinely thanks not only the experts who answer questions, but the questioners as well. An excellent practice, to my mind, so: thanks, dude, for giving PZ a chance to increase not only your knowledge but mine as well.
Finally, Cuttlefish @25: I’ve always loved your stuff, but this one has me gasping like a landed rockcod, gobsmacked by sheer technical brilliance.
Some Dude, we don’t need updates on your love life
however, for anyone who wants to know about mine, I had a date tonight, and it went extremely well.
Thanks both to PZ and to the person who asked the original question. This was something I wanted to know too but wouldn’t have dared ask.
Very enlightening. It reminded me of Przewalski’s horses, which have a different number of chromosmes than domesticated horses. http://nationalzoo.si.edu/animals/asiatrail/fact-phorse.cfm
Re 103, 149,
That makes sense for mitosis; after DNA replication, the two sides just remain associated. I was asking about how homologous chromosomes are associated with each other in meiosis. The only thing I can think of is that all the chromosomes are opened up, so individual nucleotides on one chromosome can stick to complementary nucleotides on another. After that, I could see the process you described working, but still want to know what prevents both chromosomes from attaching to fibers connected to the same spindle.
Thank you,PZ. I always enjoy your science posts, you are truly an excellent teacher.
Benjamin, everyone’s ignorant about lots of things. There’s NOTHING shameful about honestly seeking more information! Good question, educational response. Everyone wins.
25: :-o
:-o
:-o
:-o
:-o
[someone please close my jaws, I’m drying out]
73:
No, the crossing-over is what connects the pairs, and crossing-over can only happen between very similar chromosomes, i.e., those of the same pair. Crossing-over involves DNA strands partly separating and joining up with those of the other chromosome, see comment 178.
85:
Precisely.
(Unless there happens to be an enhancer or silencer close by.)
91:
No, you simply forgot to unlearn everything you were taught that long ago. :-) At that time, it hadn’t been noticed yet that the X and Y chromosomes are a pair. So it was thought that everyone had two X and two Y chromosomes, and that the missing ones had simply been overlooked so far (which was plausible at that time). Also, something tells me nobody had yet looked at what karyotype women have. :-)
101:
Behind “and”, add “/or”.
136:
By gene duplications, and by the proliferation of junk. Which is why it’s not even roughly correlated to anything interesting except cell size.
161:
You don’t need to doubt. It’s already known that chromosome number is not controlled at all except by how well meiosis and fertilization work.
167:
Yes, the bdelloid rotifers don’t do meiosis. They get away with it by being tetraploid (which lets them repair their DNA easily) and by somehow having got rid of transposable elements.
To add to the love fest, deservedly so by the way, PZ, excellent article.
And Cuttlefish, WOW, just WOW, I am humbled. How do you do it?
“Here’s something fairly common. An error in copying the DNA can lead to the loss of a piece of DNA. This happens with a low frequency, but it does happen — if we sequenced your DNA, we might well find a few bits missing here and there. We can get situations like this, where a whole gene gets lost.
Don’t panic! Remember that we have two copies of every chromosome, so while this one is missing the “D” gene, there’s that other chromosome floating around with a “d” gene. This is not necessarily bad for the individual, it just means he doesn’t have a spare any more.”
http://en.wikipedia.org/wiki/Cri_du_Chat
Just the loss of a small portion of band 15 of chromosome of the short arm of chromosome 5 can have devastating effects so it really depends on what genetic material is missing.
“Cri du chat syndrome is due to a partial deletion of the short arm of chromosome number 5. Approximately 80% of cases results from a sporadic de novo deletion, while about 10-15% are due to unequal segregation of a parental balanced translocation where the 5p monosomy is often accompanied by a trisomic portion of the genome. The phenotypes in these individuals may be more severe than in those with isolated monosomy of 5p because of this additional trisomic portion of the genome. Most cases involve terminal deletions with 30-60% loss of 5p material. Fewer than 10% of cases have other rare cytogenetic aberrations (eg, interstitial deletions, mosaicisms, rings and de novo translocations). The deleted chromosome 5 is paternal in origin in about 80% of the cases.
Loss of a small region in band 5p15.2 (cri du chat critical region) correlates with all the clinical features of the syndrome with the exception of the catlike cry, which maps to band 5p15.3 (catlike critical region). The results suggest that 2 noncontiguous critical regions contain genes involved in this condition’s etiology. Two genes, Semaphorine F (SEMA5A) and [delta catenin] (CTNND2), which have been mapped to the critical regions are potentially involved in cerebral development and its deletion may be associated in CdCS patients. Also the deletion of the telomerase reverse transcriptase (hTERT) gene localized in 5p15.33 should contribute to the phenotypic changes in CdCS.
“and chromosome numbers can change dramatically with no obvious effect on the phenotype of the organism.”
I think that also depends on exactly what genetic information is being reorganized. For example, Down syndrome (trisomy 21)
http://en.wikipedia.org/wiki/Down_syndrome
involves the duplication of the entire 21st chromosome (so there are 3 copies of chromosome 21 instead of 2) certainly has severe phenotypic effects. The same is true for the following genetic diseases which are all trisomies (addition of a 3rd chromosome):
Edwards syndrome (trisomy 18)
http://en.wikipedia.org/wiki/Edwards_syndrome
Patau syndrome (trisomy 13)
http://en.wikipedia.org/wiki/Patau_syndrome
On the other hand, some trisomies involving the sexual chromosomes (X and Y) can be relatively benign:
XXX syndrome
http://en.wikipedia.org/wiki/XXX_syndrome
Klinefelter’s syndrome (XXY)
http://en.wikipedia.org/wiki/Klinefelter_syndrome
XYY syndrome
http://en.wikipedia.org/wiki/XYY_syndrome
So the statement that chromosome numbers can change without any obvious effects is too sweeping. There are many cases where even the addition of a single chromosome has devastating effects.
Best post EVER, even though PZ obviously has a diploid-centric view of the universe… Now, plants, plants are just kinky, chromosomally speaking.
Cuttlefish, all other poets must bow down before you in awe. Truly, you performed a feat that will be studied by future generations of comp-lit types.
#184:
The relatively benign nature of trisomies in sex chromosomes (or even a monosomy: XO) is due the tiny size of the Y chromosome and the inactivation of all but one X chromosomes (http://en.wikipedia.org/wiki/Barr_body). Notice that there is no clinical conditions corresponding to trisomy 1 for instance, that kid wouldn’t even make it to being born.
My understanding is that even though chromosomes can snap or fuse, the information encoded upon them remains […] unchanged? Does this mean that the position of the gene on the chromosome does not really matter?
Precisely.
(Unless there happens to be an enhancer or silencer close by.)
Okay. I thought I understand. What the hell is an enhancer or a silencer and how could they affect the effectiveness of the gene as it relates to chromosomal position? Does this mean that the proximity of a gene to another set of instructions can either turn the gene off or, conversely, turn the gene on? And, following the same idea, if a snap pulls a gene away from a silencer, that gene can become active again? Do I have that right? (Keep in mind, I’m a liberal arts major (and a practicing historian)).
Thanks for this helpfully clear explanation. I’ve long wondered about this, and whether chromosomal fusion would involve an “evolutionary leap” in terms of the resulting organism’s characteristics. Thank you for taking the time to explain this subject in a way that those who are not biologists/geneticists can understand!
What a lovely explanation. Clear as a bell.
thank you.
Thanks for the explanation. However, what selective advantages could fusion of chromosomes provide since humans have a fused chromosome 2? Or does this boil down to chance events?
(Disclaimer: I’m not a creationist, but just wanted to ask this in case my creationist friends pressure me for an explanation)
Thanks very much, PZ. I would have had to do much background research to answer that question. Your explanation was lucid, thorough and very readable.
Thanks, PZ, for the crystal-clear and fascinating explanation (I’d long wondered about this). I should come here more often.
Thanks PZ for a great lesson in genetics. A lot of other people are willing to share their knowledge too. Keep it up.
Relatedly, a pretty good and very relevant review just came out about this in the Journal of Cellular Biochemistry: Centromeres in cell division, evolution, nuclear organization and disease
So when are you going to add a category called “Basics”?
A fantastic post, which I need to print out and save. If I understand it correctly (at first pass), then, re: the Chromosome 2 discovery in Hiller et al, is that what must have happened is one of the original chromosomes of our common ancestor with chimps lost a telomere during replication and that prompted its binding/fusing with its neighbor, correct?
I’ve just found this (late as usual to the best parties – sigh) …
My first thought after digesting this was as follows … if there are any animators among the regular posters here on PZ’s blog, turn this article into a quality animation pro bono and mail him the result. Because it deserves it. Don’t forget to embed appropriate copyright notices in case Dembski tries to rip it off though!
If I had decent artistic skills, I’d be tempted to do this myself. Trouble is, any effort I came up with would look as if Salvador Dali cut loose with Adobe ImageReady whilst smoking weapons-grade hallucinogens …
A fantastic post indeed
How can chromosome numbers change?
great explanation
chromosome numbers can change
I wasn’t the one asking the question, but I am one that has serious doubts. So yes, this is how chromosome numbers could increase.
I still believe we have no evidence of this process actually happening.
Suppose this theory were in fact true and the main mechanism for increasing chromosome numbers. With thousands and thousands of mammal species living today, we’d then expect to find “same” species among mammals with different number of chromosomes.
Well, we found some. Problem is, if these are a result of chromosome change, it is known to be fusion, not fission or polyploidy.
So honestly, if you ask me, this is a theory that is nice in theory only, but without proof of it to have happened with evolution of mammal species.
Call me ignorant or stupid. At least I don’t believe everyhing I been told without real physical proof!
LOL
Ok,I call you ignorant and stupid !
Well PH Tran, what do you propose instead that can account for the different numbers of chromosomes that we observe in different species? Keep in mind that evolution has been demonstrated beyond all reasonable doubt, so keep common ancestry in mind in any answer you give.
Regardless of the drive-by trolls commenting on year-old threads(Potato,Tran??),I like to go back in time and read through them nevertheless,brings back memories LOL.
Oh look, the creo troll is engaging in cargo cult citation requesting!
Here’s a few:
http://www.genetics.org/content/159/3/1179.short
http://humrep.oxfordjournals.org/content/21/6/1484.full
http://www.ncbi.nlm.nih.gov/pubmed/7116675?dopt=Abstract
http://www.nature.com/jhg/journal/v36/n1/abs/jhg19918a.html
http://www.ncbi.nlm.nih.gov/pubmed/1183067?dopt=Abstract
Oh, here is link to the 1999 article:
http://www.talkorigins.org/origins/postmonth/jan99.html
I did link to it. On top of my composite article
http://creavsevolu.blogspot.com/2009/08/karyogrammata.html
I give a clickable index of internal links, and the link to the 1999 article is just below the level you come to by clicking “Update on Chromosome Numbers” here:
http://creavsevolu.blogspot.com/2009/08/karyogrammata.html#update