Last time, I criticized Ann Gauger’s Evolution News and Views article “A Simple Transition to Multicellularity — Not!” for asserting that the requirement for kinesins in Volvox inversion implied a requirement for novel genes in the evolution of multicellularity. In a similar vein, Dr. Gauger presents programmed cell death and sex as problems for this transition:
The somatic cells commit suicide by a process known as apoptosis — programmed cell death — that I wrote about here. This process involves a minimum of several novel genes as well.
Where does this assertion that programmed cell death in Volvox “involves a minimum of several novel genes” come from? Programmed cell death (PCD) occurs in many unicellular eukaryotes, including Chlamydomonas reinhardtii. Furthermore, two types of metacaspases, genes involved in PCD in many algae and plants, are found in both Chlamydomonas and Volvox.
The Volvox and Chlamydomonas genomes are virtually identical in terms of gene content, so it would be very surprising if the genetic basis of PCD were dramatically different. If Dr. Gauger has identified novel PCD genes in Volvox, she should present these results at the Volvox meeting this summer…early registration is still open!
Finally there is the not so small matter of sexual reproduction. Getting two kinds of reproductive cells, eggs and sperm, requires triggering a new set of regulatory genes to change the pattern of gene expression, so as to produce the two cell types. And more than that — going into stasis, recovering from stasis, and going from diploid to haploid again requires yet more regulation. (Volvox normally has only one set of chromosomes — they are haploid — but after fusion of egg and sperm they are diploid — having two sets of chromosomes.)
As with kinesins and PCD, Dr. Gauger fails to mention that Chlamydomonas also has sex. In fact, the genetic basis of sex is quite similar among Chlamydomonas, Volvox, and other volvocine algae.
The pattern here is to assert a requirement for novel origins of traits that are shared between Volvox and its unicellular relative, Chlamydomonas, and that these traits require new proteins:
Where do all these new proteins come from? Either they come from cooption of old proteins, or by making new ones.
Or, and much more parsimoniously, they were inherited by both Chlamydomonas reinhardtii and Volvox carteri from a common ancestor. Yes, the genes had to originate some time, but remember, Dr. Gauger’s post is about the evolution of multicellularity. Even if we didn’t know mechanisms for the origins of novel genes, Dr. Gauger has utterly failed to demonstrate that the evolution of multicellularity has any such requirement.
I’ve already been over how hard those processes are to accomplish multiple times. Where does their regulation come from? That involves yet more proteins to serve as genetic switches, which also must be coopted or made from spare sequence lying around. It’s an infinite regress of steps to be filled, and answering one question about mechanism leads to many more.
[Emphasis mine] And this is the larger point: the more we learn, the less (according to Dr. Gauger) we know. Until we know the entire sequence of events, a timeline that includes every mutation and its selective effect or fixation by neutral processes, the evolution of multicellularity by natural processes is implausible. Intelligent design creationism, in spite of their protests to the contrary, has not moved far from “god of the gaps” arguments.