Since work is quite frantic lately, and my attention span has gone on holiday, I’ve decided to do something I haven’t done before and just say a few words about papers that caught my interest today without actually reading them. Each of these is probably worth a full-blown meandering of its own, but I know I wouldn’t ever get to them at this rate. Better read their abstracts and give some quick thoughts than let them sink unnoticed into the murk of my “papers” folder!
(1) How many genomes do we (not) have?
Reference: Ali Abbasi A & Hanif H (2012) Phylogenetic history of paralogous gene quartets on human chromosomes 1, 2, 8 and 20 provides no evidence in favor of the vertebrate octoploidy hypothesis. Molecular Phylogenetics and Evolution, in press (doi: 10.1016/j.ympev.2012.02.028)
(How many papers have authors with alliterating names? :D)
In the circles I move in, it’s pretty much canon that the ancestors of living vertebrates doubled their entire genomes twice. It’s still debated exactly when these duplications occurred, but few people doubt that they did. This so-called 2R hypothesis is supported by things like our possession of several (quite often, four) copies of genes that are singletons in our closest living relatives (read: lancelets*), and more importantly, that whole big chunks of lancelet chromosomes can be matched to chunks of four different vertebrate (mainly, human) chromosomes. Genes that are close to one another in lancelets are often also close together in vertebrates.
The relationship is not perfect – in well over 500 million years of evolution, genes inevitably get lost and bits of chromosome scrambled. And, thus, there is always room to question the 2R scenario, which is what this paper clearly does. They propose that those four-gene families originated at all sorts of different times, from small local duplications and rearrangements. If they are right, this is a very important result. It basically uproots every bit of speculation ever proposed on how the genome duplications contributed to the evolution of vertebrates, which, far as I can tell, is a hell of a lot of speculation. Not having read the whole paper, I would still put my money on 2R, but who knows what the future holds? Maybe we are facing a minor paradigm shift?
(2) The segmentation clock also ticks in insects!
Reference: Sarrazin AF et al. (2012) A segmentation clock with two-segment periodicity in insects. Science, advance online publication (doi: 10.1126/science.1218256)
The evolutionary history of segmentation is one of my random interests, and from my point of view, the above is a good reason to squee in a most fangirlish way. Segmentation is the construction of a body from repeating units. In its purest form, which isn’t that common in modern animals, the animal is essentially made up of identical repeated blocks containing a copy of each key organ like kidneys, nerve centres, limbs and muscles. (Even in the most perfectly segmented creatures, head and tail ends form something of an exception. Ragworms make a nice example.) More commonly, only some components are repeated, and they are repeated with slight differences along the body. Vertebrates’ spine and associated muscles are a good example, and so are the defining traits of arthropods, their jointed exoskeletons equipped with repeated pairs of appendages.
Although traditionally it has been thought that arthropod and vertebrate segmentation have independent origins, parts of the genetic machinery are shared between both groups (as well as segmented worms). Various “segmentation genes” are active in distinct stripes in our embryos, marking out future segments even before we can see the segments themselves. In vertebrates, cells periodically switch “segmentation genes” on and off, and this combined with the growth of the embryo produces a dynamic stripey pattern of gene expression. While segments and stripes of gene expression are darn obvious in arthropods, this is the first time anyone has confirmed that some arthropod segmentation genes actually oscillate like their vertebrate counterparts do, as opposed to, say, the cells expressing them moving about. Whether this is a spectacular example of convergent evolution or evidence of a shared ancestral heritage, I couldn’t say, but it’s really cool either way.
(3) Old genes are entrenched, new genes are redundant after all?
Reference: Chen WH et al.(2012) Younger genes are less likely to be essential than older genes, and duplicates are less likely to be essential than singletons of the same age. Molecular Biology and Evolution advance online publication (doi: 10.1093/molbev/mss014)
So, this claims to resolve a conundrum I wasn’t even aware of before. Gene duplication is thought to be important for the evolution of new functions because two copies of a gene mean there is a backup if one of them fails at its original function. Hence, theory goes, duplicate genes are much less restricted in the evolutionary paths they can take. Apparently, studies in mice have contradicted this common wisdom by claiming that duplicate genes are just as likely to be indispensable as genes without backup copies. However, Chen et al. are saying that this is wrong, confounded by gene age. Since new genes are less likely to be essential than old genes (which had more time to evolve interactions with the rest of the genome), and mouse duplicates are on average older than mouse singletons, the two effects end up cancelling out. When they factor in gene age, duplicates are indeed less essential than loners. One of the central tenets of current thinking about (genetic) novelty stays in the ring for another round…
(4) Is reducing complexity easier than increasing it?
Reference: Harjunmaa E et al. (2012) On the difficulty of increasing dental complexity. Nature advance online publication (doi: 10.1038/nature10876)
How complexity increases in evolution is more than a breeding ground for creationist incredulity, it’s also quite interesting for bona fide evolutionary biologists. Looking at the development of mouse teeth, Harjunmaa et al. notice that increases and decreases in the complexity of tooth shapes require different sorts of mess-ups. Simpler-than-normal teeth are common in mutants and easy to make in experiments. More complex teeth – i.e. those with more cusps – are rarely if ever seen in natural mutants. Turns out they are perfectly possible – you just need to manipulate several genetic pathways at the same time to produce a clear result.
Can this be generalised? Is greater complexity usually harder to achieve? When does this apply and when does it not? I’ve recently read papers that explore how complexity increases easily and completely by chance (I have a half-written post about them languishing on my hard drive, FWIW). Are the rules different for different levels of organisation? The aforementioned complexity-by-chance papers analyse the molecular level: one is about the architecture of gene switches, the other about a protein machine. Teeth are pretty large pieces of life with thousands upon thousands of such machines participating in their production. Does that make a real difference, or is what I’m seeing just coincidence? Dunno, but it’s fascinating to think about!
Heh, it looks like I took rather bigger “bites” of these news than I planned to. I kind of managed to write the equivalent of a full-blown meandering anyway. The only difference is that I didn’t painstakingly reference this one. I hope that doesn’t mean that half of what I wrote off the top of my head is wrong 😀
*Lancelets are now not considered our closest relatives. Unbelievable as that may seem, that honour goes to sea squirts and their ilk. However, the sea squirt bunch are ridiculously weird in all sorts of respects, and their genomes are jumbled beyond recognition. So… not so great if you want to learn anything about our ancestors.