Today was more context and a bit of a caution for my developmental biology course. I warned them that we’d be primarily talking about animals and plants (and mostly animals at that), but that actually, all of the general processes we’re describing are found in bacteria and other single-celled organisms — that in a lot of ways, microbiology is actually another developmental biology course. Yes, I went there: developmental biologists tend to be imperialists who see all the other sciences as mere subsets of the one true science. Of course, you could also take that as developmental biology being a synthetic discipline that steals bits and pieces from everywhere…
So the primary lessons today were reviews of stuff these students should have gotten in cell and molecular biology, with bits of biochemistry and microbiology thrown in. We talked about genes getting switched on and off, and the example I used was the classic: the lac operon in E. coli. What? You don’t know about it? It’s a beautiful system, in which the bacterium switches on the genes needed for digesting the sugar lactose only when the sugar is available in the environment. I showed this nice little 3 minute video:
Switching genes on and off? That’s development! It gets a little more intricate in multicellular animals, but all of the fundamental logic is right there in E. coli: activators and repressors, positive and negative feedback, the boolean logic of gene regulation. I also mentioned that when we’re reading Carroll’s Endless Forms Most Beautiful, he’s going to make a big deal out of exactly this kind of regulation, but I want them to remember that it’s not unique to butterflies or fruit flies or frogs, it’s a common theme in all kinds of diverse cells.
We then talked about cell signaling. How does a cell know which genes are supposed to be off and on? It interacts with its environment (as in the lac operon) or its neighbors to make decisions about activity. To illustrate that, we went through quorum sensing and biofilms — again, cell signaling is not unique to animal development, it was all worked out in principle in single-celled organisms. I gave them a little foreshadowing and mentioned that we’d be discussing Sonic Hedgehog and Notch and Delta later in the course, classic examples of signaling in multicellular systems, but in bacteria we have things like hapR and AHL signaling.
Finally, I raised the issue of a phenomenon we’ll be talking about on Wednesday: patterning. Why aren’t your arms growing from your hips, why don’t you have fingers on your feet instead of toes, why are your eyes paired and on the front of your head? Because there is positional information in the embryo that can be read by cells and tissues and lead to development of appropriate structures in their proper places. But once more, this is not unique to multicellular animals. A paramecium, for instance, is not a generic blob, but has a definite shape and orientation; it has organelles in predictable places, and is covered with a nearly crystalline lattice of cilia with specific axes of orientation. I showed them choanoflagellates and pointed out that these protists, representing a multicellular precursor, had a specific shape and a collar organ in a specific functional location: how do they know how to do that?
That’s the question we’ll be asking next. I warned them too that I won’t be lecturing at them on Wednesday, so they’d better have their morning coffee. I’m expecting them to read a review paper on positional information in embryos (pdf), and I’m going to make them explain it all to me for a change.
Kerszberg M, Wolpert L (2007) Specifying Positional Information in the Embryo: Looking Beyond Morphogens. Cell 130(2):205–209.