Hey, I’m teaching a genetics class this term, and someone is taking one. I’m going to be spending part of my day setting up flies for an upcoming lab…this looks awfully familiar.
I mulled over some of the suggestions in my request for basic topics to cover, and I realized that there is no such thing as a simple concept in biology. Some of the ideas required a lot of background in molecular biology, others demand understanding of the philosophy of science, and what I am interested in is teetering way out at the edge of what we know, where definitions often start to break down. Sorry, I have to give up.
Seriously, though, I think that what does exist are simple treatments of complex subjects, so that is what I’m aiming for here: I talk a lot about genes, so let’s just step way back and give a useful definition of a gene. I admit right up front, though, that there are two limitations: I’m going to give a very simplified explanation that fits with a molecular genetics focus (pure geneticists define genes very differently), and I’m going to talk only about eukaryotic/metazoan genes. I tell you right now that if I asked a half dozen different biologists to help me out with this, they’d rip into it and add a thousand qualifiers, and it would never get done. So let’s plunge in and see what a simple version of a gene is.
I’ve just read the article on the parthenogenetic Komodo dragons in Nature, and it’s very cool. They’ve analyzed the genetics of the eggs that have failed to develop (the remainder are expected to hatch in January) and determined that they were definitely produced without the aid of a male.
We analysed the parentage of the eggs and offspring by genetic fingerprinting. In the clutches of both females, we found that all offspring produced in the absence of males were parthenogens: the overall combined clutch genotype reconstructed that of their mother exactly. Although all offspring were homozygous at all loci, they were not identical clones. Parthenogenesis was therefore confirmed by exclusion (clutches had different alleles from potential fathers) and by the fact that the probability of obtaining a clutch of homozygous individuals after sexual reproduction was very low (P<<0.0001). Sungai’s resumption of sexual reproduction confirmed that parthenogenesis was not a fixed reproductive trait (that is, it is facultative) and that asexual reproduction is likely to occur only when necessary.
That line about “all offspring were homozygous at all loci, they were not identical clones” might need a little more explanation. Mama Dragon is heterozygous at some loci, but the meiotic mechanism that produces a diploid egg means that one cleavage (most likely the second meiotic cleavage) was suppressed, so both homologous chromosomes in the resultant ovum were derived from the same replicated DNA strand. They are not clones of the mother, because they are all homozygous while she was heterozygous; they are not identical, because which of each of the paired homologous chromosomes was passed on to an individual is random.
(I’m a little confused by the statement that they offspring are homozygous at all loci, though; that would imply that there was no crossing over at all in meiosis I, which doesn’t sound right. There ought to be reduced heterozygosity but not complete homozygosity, unless reptiles are weirder than I thought.)
The other useful snippet of information is that sex determination in these reptiles is of the WW/WZ type, where the females are the heterogametic sex. Since all of the progeny of parthenogenesis are homozygous, they are all of the homogametic genotype, and therefore male.
Parthenogenesis can also bias the sex ratio: in Varanus species, females have dissimilar chromosomes (Z and W), whereas the combination ZZ produces males10, so the parthenogenetic mechanism can produce only homozygous (ZZ or WW) individuals and therefore no females.
This has theological implications, obviously. We can now understand how a female could give rise to a male by parthenogenesis: Mary Mother of God must have been a heterogametic reptoid. David Icke will be so pleased.
Watts PC, Buley KR, Sanderson S, Boardman W, Ciofi C, Gibson R (2006) Parthenogenesis in Komodo dragons. Nature 444:1021-1022.
I’ve been writing a fair amount about early pattern formation in animals lately, so to do penance for my zoocentric bias, I thought I’d say a little bit about homeotic genes in plants. Homeotic genes are genes that, when mutated, can transform one body part into another—probably the best known example is antennapedia in Drosophila, which turns the fly’s antenna into a leg.
Plants also have homeotic genes, and here is a little review of flower anatomy to remind everyone of what ‘body parts’ we’re going to be talking about. The problem I’ll be pursuing is how four different, broadly defined regions of the flower develop, and what that tells us about their evolution.
Oh happy day, the Sea Urchin Genome Project has reached fruition with the publication of the full sequence in last week’s issue of Science. This news has been all over the web, I know, so I’m late in getting my two cents in, but hey, I had a busy weekend, and and I had to spend a fair amount of time actually reading the papers. They didn’t just publish one mega-paper, but they had a whole section on Strongylocentrotus purpuratus, with a genomics mega-paper and articles on ecology and paleogenomics and the immune system and the transcriptome, and even a big poster of highlights of sea urchin research (but strangely, very little on echinoderm development). It was a good soaking in echinodermiana.
Fascinating stuff…read this paper in PNAS, Evidence that the adaptive allele of the brain size gene microcephalin introgressed into Homo sapiens from an archaic Homo lineage, or this short summary, or John Hawks’ excellent explanation of the concepts, it’s all good. It’s strong evidence for selection in human ancestry for a gene, and just to make it especially provocative, it’s all about a gene known to be involved in brain growth, and it’s also showing evidence for interbreeding between Homo sapiens and Neandertal man.
The short short explanation: a population genetics study of a gene called microcephalin shows that a) it arose and spread through human populations starting about 37,000 years ago, b) this particular form of the gene (well, a small cluster of genes in a particular neighborhood) arose approximately 1.1 million years ago in a lineage distinct from that of modern humans, and c) the likeliest explanation for this difference is that that distinct lineage interbred with modern humans 37,000 years ago, passing on this particular gene variant that was then specifically selected for, a process called introgression.
The work looks sound to me, and I’m convinced. The one thing to watch for, though, is that there will be attempts to overreach and couple possession of this gene to some kind of intellectual superiority. We don’t know what this particular variant of the gene does yet! All we can say at this point is that some abstract data shows that a particular allele spread through the human population at a rate greater than chance would predict, that the gene itself has as one of its functions the regulation of brain growth, but that it is highly unlikely that that particular function is affected by the variant. Whatever it does, I expect the role is more along the lines of subtle fine-tuning rather than simply making people smart.
Here’s an annoying case of political correctness run amuck.
…the Human Genome Organisation (HUGO) Gene Nomenclature Committee…is renaming a number of genes that have potentially offensive or embarrassing names.
The shortlist of 10 genes -Â including radical fringe, lunatic fringe and, bizarrely, Indian hedgehog –Â was compiled in response to physicians’ worries about “inappropriate, demeaning and pejorative” names.
The problem arose because most of the genes were initially discovered in fruitflies, and their names were then transferred to the human versions of the genes, which were discovered later…when applied to the human versions of the genes, many of these names become uncomfortable.
While no one wants to curtail the creativity of fruitfly geneticists, it will be important to ensure that, in the future, no joky names are adopted for human genes where they might cause offence. Other quirky names in the fruitfly genome include headcase and mothers against decapentaplegia (MAD).
Darn prissy physicians. They’ve got no sense of humor. Will they try to rename one-eyed pinhead next? How about half baked? The zebrafish geneticists are just as amusing, you know.
I’d like to know what the physicians are concerned about, anyway. It’s not as if they’re going to be informing patients that their illness is caused by a broken frizzled gene, nor is it going to be somehow better or easier if they rename it “Wnt Receptor X-17” or something similarly dry and empty. I hope whoever started this knows a good proctologist who can do a stick-ectomy.
And seriously, there ought to be something like the priority rules of taxonomy to prevent random gomers from running around changing names just because they don’t like them.
Did the internet get stupider while I was away this past week? I mean, it’s gratifying to my ego to imagine the average IQ of the virtual collective plummeting when I take some time off, but I really can’t believe I personally have this much influence. Maybe the kooks crept out in my absence, or maybe it was just the accumulation of a week’s worth of insanity that I saw in one painful blort when I was catching up.
What triggers such cynicism is the combination of Deepak Chopra, Oliver Curry, and now,
William Tucker. Tucker wrote a remarkably silly piece in the American Spectator in which he drew deeply faulty conclusions from human genetics to support a thesis rife with misogyny and foolish chauvinism on human evolution. It was like a piece on evolutionary psychology written by someone who didn’t know any genetics at all.
Hang on to your hats—we’re going to see a factoid from one magazine article balloon up into a declaration of the superiority of the male species (I use “species” here both ironically and mockingly).
You may have heard about that odd hothead mutation in Arabidopsis that seemed to be violating a few principles of basic genetics—there was an unexpectedly high frequency of revertants that suggested there might be a reservoir of conserved genetic information outside the genome. Reed Cartwright proposed an alternative explanation, that gamete selection could skew the results. Now the latest reports suggest that the bias was an artifact of foreign pollenization (which I think is interesting in itself. Life is damned good at sneaking its genes in wherever it can.)
Anyway, if that’s all gobbledygook to you, Scientific American has put up a lucid summary of the hothead affair. It’s an example of good science, where the observations and hypotheses are hammered out and refined to get a best explanation.
Carl Zimmer brings up another essential point about the HAR1F study: it was work that was guided by evolutionary theory. The sequence would not have been recognized in the billions of nucleotides in the genome if it hadn’t been for an analysis directed by the principles of evolution.
Wells’ diatribe was amazingly wrong. I looked at it again and there could be another half-dozen essays in just picking up apart the stupidity in it.
