A recent paper I found interesting (and I am sure was interesting to Dr Logsdon) about Multiple losses of sex within a single genus of Microsporidia. In the paper Joseph Ironside describes multiple instances of loss of sex within the Nosema/Vairimorpha group testing the hypothesis that the ancestral lineage was asexual. The group of species are undergoing rapid evolution where changes in lifestyle/lifecycle can occur even among very closely related lineages. In order to do test a formal hypothesis about whether the ancestor was asexual or sexual this the author had to improve the resolution of the phylogenetic relationships of these species and deal with some technical problems due to mutational biases in the rDNA sequences. The result he found was that the ancestral lineage was sexual and that asexuality arose multiple times among these species. He also provides a caution:
“The rapid evolution of microsporidian life cycles indicated by this study also suggests that even closely related microsporidia cannot be assumed to have similar life cycles and the life cycle of each newly discovered species must therefore be completely described.”
Something one has to be careful about in comparative studies of these species.
Microsporidia are an interesting group as it has been debated as to whether they are a deep branching lineage of eukaryotes or a fast evolving lineage within the fungi. On reason it is hard to place these species is the very long branches that are often associated with obligate intracellular pathogens as a result of streamlining of their genome.
On the idea of streamlining – currently I am reading Leo Buss‘s The Evolution of Individuality as well as Mike Lynch’s new book on The Origins of Genome Architecture (also discussed by John recently). Lynch argues that the metabolic cost of DNA may not be what limits or reduces genome size. That effective population size may be driving many of the observed changes in genome sizes and other genome properties; or at least we need to consider the neutral process before invoking directional selection to explain differences. What is driving the streamlining then in these organisms – they can obtain nutrients from the host so they dispense with some biosynthetic pathways. But why also reduce all intragenic and essentially lose nearly all of their introns? Keeling and Slamovits discuss review ideas in more detail that normally weak evolutionary forces of may dominate in these lineages.
Another idea that resonated as I was reading Leo Buss’s book. One reason why these intracellular parasites might be undergoing genome reduction is described in a footnote in the text (pp 84-85). Buss suggests that perhaps reducing the number of molecules that must be constructed and thus can be recognized by the host immune system would also drive a streamlining of the organism (and though he doesn’t say it — reduction in the genome size). He states:
A survey of morphological complexity of parasites with complex life cycles, say, a mollusc is the first host and a vertebrate is the second, may shed light on this question.
So it would be interesting if we can at least use genome size as a crude proxy to this question and ask if genome reduction is as dramatic in parasites that must cycle through multiple hosts with very different types of immune systems?
I am still not sure I accept all the ideas, but I think it is important to consider what selective and neutral forces could be driving genome streamlining in these parasitic organisms.