Tandem repeats and morphological variation

Blogging on Peer-Reviewed Research
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All of us mammals have pretty much the same set of genes, yet obviously there have to be some significant differences to differentiate a man from a mouse. What we currently think is a major source of morphological diversity is in the cis regulatory regions; that is, stretches of DNA outside the actual coding region of the gene that are responsible for switching the gene on and off. We might all have hair, but where we differ is when and where mice and men grow it on their bodies, and that is under the control of these regulatory elements.

A new paper by Fondon and Garner suggests that there is another source of variation between individuals: tandem repeats. Tandem repeats are short lengths of DNA that are repeated multiple times within a gene, anywhere from a handful of copies to more than a hundred. They are also called VNTRs, or variable number tandem repeats, because different individuals within a population may have different numbers of repeats. These VNTRs are relatively easy to detect with molecular tools, and we know that populations (humans included) may carry a large reservoir of different numbers of repeats, but what exactly the differences do has never been clear. One person might carry 3 tandem repeats in a particular gene, while her neighbor might bear 15, with no obvious differences between them that can be traced to that particular gene. So the question is what, if anything, does having a different number of tandem repeats do to an organism?

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Luskin on gene duplication

Casey Luskin has to be a bit of an embarrassment to the IDists…at least, he would be, if the IDists had anyone competent with whom to compare him. I tore down a previous example of Luskin’s incompetence at genetics, and now he’s gone and done it again. He complains about an article by Richard Dawkins that explains how gene duplication and divergence are processes that lead to the evolution of new information in the genome. Luskin, who I suspect has never taken a single biology class in his life, thinks he can rebut the story. He fails miserably in everything except revealing his own ignorance.

It’s quite a long-winded piece of blithering nonsense, so I’m going to focus on just three objections.

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This last week in Biochemistry

It’s been quite busy last week. Despite the Neurobiology class didn’t meet that week, my other classes kept my hands full. I blame it on two exams and a paper due during the week of Homecoming.

Since I don’t have any new thoughts on Neurobiology, let’s see what can be dug up from my Biochemistry class. For the lab, I wrote my paper of Desulforedoxen. Its job is reducing sulfates. You can look it up at JMol using “1DHG” as the code.

I found this protein very interesting. In class, we had learned about the driving forces for tertiary structure in proteins: H-bonding, hydrophobic/Vanderwal’s, salt bridges, and disulfide bonds between Cystine residues. Upon examining Desulforedoxen, I learned that Cystines were capable of more than just S-S bonding. With four Cystines clustered nearby each other in the tertiary structure, an iron atom sits tetrahedrally bonded to the four sulfurs. While I bet it is a major player in tertiary structure, it just reeks of active site. Since the transition metal, and its neighboring sulfurs, have ‘D’ orbitals, this looks like it’s capable of something that can’t easily be performed in a test tube.

I’ll be a lot of you already know that this can happen in proteins. For me, it was learning it by observation instead of in lecture, that was fun. Moments like that have made it well worth it to go into biology. It’s also cool how such lesser-used amino acids have more than one purpose that they can serve in cells.

Note: the article I read about this protein said that it had iron bonded to the sulfur. When I looked it up in JMol, it was instead bonded to mercury. Weird. An abstract of the article I used can be found here. Anyways, just washing my hands so I don’t fall victim to the inconsistencies-lynch-mob. Have a nice day.

Basics: Master Control Genes and Pax-6

Blogging on Peer-Reviewed Research

One concept that is sometimes used in developmental biology is the idea of the “master control gene” or “master switch” — a single gene whose expression is both necessary and sufficient to trigger activation of many other genes in a coordinated fashion, leading to the development of a specific tissue or organ. It’s a handy concept on which to hang a discussion of transcription factors, but it may actually be of rather limited utility in the real world of molecular genetics: there don’t seem to be a lot of examples of master control genes out there! Pax-6 is the obvious one, a gene that initiates development of the eye, and other genes may be mentioned in certain stem cell pathways, but even in the eyes of vertebrates, for example, eye development is more complicated than a single switch, and similarly, many other developmental processes seem to use multiple or redundant regulatory controls — the cases where we have a single gene bottleneck are either rare or poorly represented in the literature.

They’re still at least pedagogically useful, though — it’s a simple case of imposition of a specific developmental pathway on a patch of tissue.

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The Hox code

Blogging on Peer-Reviewed Research

The Hox genes are a set of transcription factors that exhibit an unusual property: they provide a glimpse of one way that gene expression is translated into metazoan morphology. For the most part, the genome seems to be a welter of various genes scattered about almost randomly, with no order present in their arrangement on a chromosome — the order only becomes apparent in their expression through the process of development. The Hox genes, on the other hand, seem like an island of comprehensible structure. These are all genes that specify segment identity — whether a segment of the embryo should form part of the head, thorax, or abdomen, for instance — and they’re all clustered together in one (usually) tidy spot.

Within that cluster, we see further evidence of order. Look at just the Drosophila part of the diagram below: there are 8 Hox genes in a row, and their order within that row reflects the order of expression in the fly body. On the left or 3′ end of the DNA strand, lab (labial) is expressed in the head, while Abd-B (Abdominal-B) is expressed at the end of the abdomen.

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Schematic of relationship between Drosophila and mouse Hox genes. Hox genes are shown as colored boxes in their order on the chromosome. Orthologous genes between Drosophila and mouse, and paralogous mouse genes are shown color-coded.

Knocking out individual Hox genes in the fly causes homeotic transformations — one body part develops into another. These genes are early actors in the cascade of interactions that enable the development of morphologically distinct regions in a segmented animal — the activation of a Hox gene from the 3′ end is one of the earliest triggers that leads the segment to develop into part of the head.

Now look at the mouse part of the diagram above. We vertebrates have Hox genes that are homologous to the fly Hox genes, and they’re also clustered in discrete locations with 3’→5′ order reflecting anterior→posterior order of expression. There are differences — the two most obvious that we have more Hox genes on the 5′ side (these correspond to expression in the tail—flies do not have anything homologous to the chordate tail), and vertebrates also have four banks of Hox genes, HoxA, HoxB, HoxC, and HoxD. This complicates matters. Vertebrates have these parallel, overlapping sets of Hox genes, which suggests that morphology could be a product of a combinatorial expression of the genes in the four Hox clusters: there could be a Hox code, where identity can be defined with more gradations by mixing up the bounds of expression of each of the genes.

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Axis formation in spider embryos

Blogging on Peer-Reviewed Research

Some of you may have never seen an arthropod embryo (or any embryo, for that matter). You’re missing something: embryos are gorgeous and dynamic and just all around wonderful, so let’s correct that lack. Here are two photographs of an insect and a spider embryo. The one on the left is a grasshopper, Schistocerca nitens at about a third of the way through development; the one on the right is Achaearanea tepidariorum. Both are lying on their backs, or dorsal side, with their legs wiggling up towards you.

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There are differences in the photographic technique — one is an SEM, the other is a DAPI-stained fluorescence photograph — and the spider embryo has had yolk removed and been flattened (it’s usually curled backward to wrap around a ball of yolk), and you can probably see the expected difference in limb number, but the cool thing is that they look so much alike. The affinities in the body plans just leap out at you. (You may also notice that it doesn’t seem to resemble a certain other rendition of spider development).

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Wait until the creationists try to wrap their little minds around artificial life … oops, too late

Here’s some exciting news: Artificial life likely in 3 to 10 years. It is exciting but not surprising at all — but of course we’re going to be able to assemble entirely artificial life forms soon. It’s just a particularly complicated kind of chemistry, and it’s more of a deep technical problem than anything else. I wouldn’t be quite so specific about the date — there are also all kinds of surprises that could pop up — but I’m optimistic, and I think the overall assertion is supported by the increasing rate of accomplishment in the field.

But of course, in addition to the usual suggestions from interested followers of science that I should mention this cool article on the blog, I’ve gotten a few from creationist complainers (Already! See what my email is like?) Expect to hear more outrage from the religious right as this story develops in the coming years, which might be a good thing … they’re going to have to spread themselves thin to fight all the interesting work coming out of biology, and evolution won’t be the only target anymore. Anyway, here’s one of my creationists, expressing his unhappiness in odd directions.

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Your mama’s soul doesn’t love you

If it existed, it might also be profoundly autistic and … diabetic? So science cannot disprove the existence of a soul, but one thing we’re learning is how much valued human properties such as love and attachment and awareness of others are a product of our biology — emotions like love are an outcome of chemistry, and can’t be separated from our meaty natures.

The latest issue of BioEssays has an excellent review of the role of the hormone oxytocin in regulating behaviors. It highlights how much biochemistry is a determinant of what we regard as virtues.

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