Last week, I wrote a bit about maternal genes, specifically bicoid, and described how this gene was expressed in a gradient in the egg. Bicoid is both a transcription factor and a morphogen. The gene product regulates the activity of other genes, controlling their pattern of expression in the embryo. Today I thought I’d get more specific about the downstream targets of bicoid, the gap genes.
In my previous comments about maternal effect genes, I was talking specifically about one Drosophila gene, bicoid, which we happen to understand fairly well. We know its sequence, we know how it is controlled, and we know what it does; we know where it falls in the upstream and downstream flow of developmental information in the cell. So today I’m going to babble a bit more about what bicoid is and does, and how it works.
In developmental biology, and increasingly in evolutionary biology, one of the most important fields of study is deciphering the nature of regulatory networks of genes. Most people are familiar with the idea of a gene as stretch of DNA that encodes a protein in a sequence of As, Ts, Gs, and Cs, and that’s still an important part of the story. Most people may also be comfortable with the idea that mutations are events that change the sequence of As, Ts, Gs, and Cs, which can lead to changes in the encoded protein, which then causes changes in the function of the protein. These are essential pieces in the story of evolution; we do accumulate variations in genes and gene products over time.
If you’ve read this outrageous WaPo op-ed that basically says you can’t expect moral behavior from scientists who are glorified baby-killers, you might appreciate this rebuttal at the Give Up Blog. The foundation of the fundiecrat anti-science article is that 1) Hwang Woo Suk was bad, therefore all stem cell/cloning research is tainted, and 2) alternative techniques (most of which they don’t seem to understand) and adult stem cells will give us all the answers we need.
Which actually leads into this week’s “ask a science blogger” question:
Last week, I received some delusional e-mail from Phil Skell, who claims that modern biology has no use for evolutionary theory.
This will raise hysterical screeches from its true-believers. But, instead they should take a deep breath and tell us how the theory is relevant to the modern biology. For examples let them tell the relevance of the theory to learning…the discovery and function of hormones…[long list of scientific disciplines truncated]
Dr Skell is a sad case. He apparently repeats his mantra that biology has no need of evolution everywhere he goes, and has never bothered to actually crack a biology journal open to see if biologists actually do use the theory. In my reply to him, I did briefly list how evolution is used in every single one of his numerous examples, but today I’m going to focus on just the one I quoted above: hormones.
One of many open questions in evolution is the nature of bilaterian origins—when the first bilaterally symmetrical common ancestor (the Last Common Bilaterian, or LCB) to all of us mammals and insects and molluscs and polychaetes and so forth arose, and what it looked like. We know it had to have been small, soft, and wormlike, and that it lived over 600 million years ago, but unfortunately, it wasn’t the kind of beast likely to be preserved in fossil deposits.
We do have a tool to help us get a glimpse of it, though: the analysis of extant organisms, searching for those common features that are likely to have been present in that first bilaterian; we’re looking for the Last Common Bilaterian by finding the Least Common Denominators among living species. And one place to look is among the flatworms.
PvM at the Panda’s Thumb has already written a bit about this issue in the article “Human Gland Probably Evolved From Gills”, but I’m not going to let the fact that I’m late to the party stop me from having fun with it. This is just such a darned pretty story that reveals how deeply vertebrate similarities run, using multiple lines of evidence.
The diagram above shows the early cleavages of the embryo of the scaphopod mollusc, Dentalium. You may notice a few peculiarities: the first cleavage is asymmetric, producing a cell called AB and a larger sister cell, CD. Before the second division, CD makes a large bulge, called a polar lobe, and it almost looks like it’s a three-cell stage—this is called a trefoil embryo, and can look a bit like Mickey Mouse. The second division produces an A, a B, a C, and a D cell, and there’s that polar lobe, about as large as the regular cells, so that it now resembles a 5-cell embryo. What’s going on in these animals?
Maternal effect genes are a special class of genes that have their effect in the reproductive organs of the mutant; they are interesting because the mutant organism may appear phenotypically normal, and it is the progeny that express detectable differences, and they do so whether the progeny have inherited the mutant gene or not. That sounds a little confusing, but it really isn’t that complex. I’ll explain it using one canonical example of a maternal effect gene, bicoid.
The fugu is a famous fish, at least as a Japanese sushi dish containing a potentially lethal neurotoxin that was featured on an episode of The Simpsons. Fugu is a member of the pufferfish group, which have another claim to fame: an extremely small genome, roughly a tenth the size of that of other vertebrates. The genome of several species of pufferfish is being sequenced, and the latest issue of Nature announces the completion of a draft sequence for the green spotted pufferfish, Tetraodon nigroviridis, a small freshwater species.
