I stay away from large multicellular features because we have no idea how they work. Ok, maybe some idea, but the state of the field is pathetic. Evo-devo has great potential, but the developmental biologists (eg. Sean Carroll), while being good at developmental biology, fail to comprehend evolutionary biology. The evolutionary biologists, on the other hand, don't seem to get development or how genes work. In any case, it's big and complicated and desperately needs several major paradigm shifts before we get anywhere, so I focus on cellular and molecular features. And I have stories to tell.
Take the eukaryotic genome, for example. As Mike Lynch put it: "The epitome of un-intelligent design". Many an adaptive excuse have been proposed for introns, for example. "They allow greater flexibility in genetic [exon] shuffling, allowing complexity" etc. Problem is, complexity is not evolution's "goal". It does not strive there. Increase in complexity is a by-product. And it is not necessarily adaptive. Same thing with introns: bacteria get away with extremely streamlined small genomes (and are wildly successful at the same time, much more so than eukaryotes); furthermore, the few introns bacteria have are self-splicing, meaning they politely remove themselves immediately after transcription, through RNA enzymatic activity – thus suggestive of their role as genetic parasites. Basically, spliceosomes were a bit of an afterthought – I don't have space to go into the story here, but feel free to ask
– and the eukaryotic introns lost their self-splicing ability – and exploded. All over the genome. Presumably before the last eukaryotic cenancestor. So what promoted this sudden explosion of introns? One major factor that changed during the switch from prokaryotic to eukaryotic domains was a dramatic reduction in effective population size. Why does this matter? Drift is weaker in larger populations, and thus selection is more dominant there (in bacteria). The idea is that unicellular eukaryotes have a much smaller effective population sizer and thus notably less selective force acting on their genomes, letting loose intron multiplication (result of mutational bias, essentially – in the form of transposition, duplications, etc – and there ARE documented cases of recent de novo intron formation...). Introns are slightly deleterious (but mostly neutral), so loosen selection a little and they go crazy. Curiously, organisms where there has been a strong selection against large genome sizes, like intracellular parasites (eg. microsporidia), have reduced their intron populations to a tiny handful (and some of those may have been exapted to essential functions). I think one species, Encephalitozoon cuniculi, has something like 17 introns IIRC. Nucleomorphs - relict highly-reduced eukaryotic nuclei of secondary plastid symbionts) also have a highly reduced intron count, just like the microsporidia. Thus suggests selection doesn't really like them too much, but tolerates them when its weakened by small effective population size.
See, isn't this so much richer than "oh, introns are there because they must be good for something...oh, they enable more gene variety/novelty, which is good, because then eventually it made us! =D" ?
For a nice summary by someone who gets this stuff much better than I do, I strongly recommend M Lynch 2007 PNAS "The frailty of adaptive hypotheses for the origins of organismal complexity", with an accompanying colloquium talk here: http://sackler.nasmediaonline.org/2006/ ... lynch.html (I like this guy: he bridges population genetics and molecular genetics/genomics, and soon, cellular biology – topics that are apparently forbidden to ever meet by some non-existent law somewhere...) I'd like to know what you think
I also have a bit of a series on my blog: http://skepticwonder.fieldofscience.com ... 0evolution start with part I. Am also in the process of writing Mike Lynch's seminar talk from a couple weeks ago... The problem with the adaptationist program (sensu Gould & Lewontin 1979) is that anyone can make a story to explain anything. Any story sounds great. Those kinds of stories are, for the most part, untestable – and therefore not science. This gives people the impression evolution is a simple storytelling exercise, and that anyone can do it given an ability to explain why something would be good. At that point, these hypotheses are not even wrong – the very framework is flawed. Evolutionary biology IS an experimental science – we can make predictions and test them out, especially in the realm of evolutionary mechanisms. While the path of evolution is important (and quite scientific – see the complexity of modern phylogenetic techniques!), the process is also essential to the complete theory. People seem to think the process stopped being developed since Darwin – I beg to differ. Eg., you can experimentally test effects of bare drift (without selection) through so-called 'mutation accumulation' experiments, where a single member of a selfing population are picked at random, allowed to generate a large-ish population and picked again, etc for 50 generations. Effects are dramatic, and interestingly, percolate even to the behavioural and morphological levels (this was done in several model systems, the more striking results in the nematode C.elegans). This, in my view, is real evolutionary science. (selection can be measured too)
It takes great discipline to do good theory in evolutionary biology. Sad to say, most people lack it. Especially science writers.
