A colleague's lab has been working on the molecular biology of the 'Gene Transfer Agent' (GTA) of the bacterium Rhodobacter capsulatus. He and I have very different ideas about the evolutionary function of GTA, and we plan to sit down together and work through our disagreements, maybe coming up with a synthesis as a review article. I haven't been paying close attention to GTA, and in this post I'm going to take the first step by summarizing what I think I remember about it (before I go back and read any papers).
The phenomenon: Cultures of R. capsulatus have been known for many years to produce small phage-like particles, each consisting of a protein coat surrounding a 3-4kb fragment of R. capsulatus DNA. These particles can be separated from the source culture and are able to introduce their DNA into other R. capsulatus cells, where it can recombine with the chromosome and change the recipient cell's genotype. The variety of genes that can be transferred suggests that the DNA fragments may be random segments of the source cell's DNA.
I read about GTA when I was in grad school in the 1980s and first becoming interested in the evolution of processes causing gene transfer. I was already coming to the heretical conclusion that bacterial gene transfer by conjugation and transduction occurs as accidental side effects of infectious processes, not because such transfer is beneficial to the cell. At that time only Barry Marrs' lab had worked on GTA. My supervisor, the phage biologist Allan Campbell, thought that GTA was probably produced by a defective prophage. I was working on a cryptic prophage at the time, and this made sense to me. GTA would then be a form of transduction, a side effect of activity of genes whose normal function is to package phage DNA so it can infect new host cells.
The genes: More recently my colleague's lab has identified the R. capsulatus genes responsible for production of GTA and has partially characterized their regulation. As I recall, these genes are in a couple of clusters that do resemble defective prophage but that also have some properties of normal genes. In particular, aspects of the regulation suggest selection for a cellular function. My colleague has also done some analysis of the distribution of the GTA-producing genes, and as I recall this was not consistent with a single acquisition of a defective prophage. He thus interprets his findings as evidence that the ability to transfer genes by GTA is beneficial to R. capsulatus, i.e. that GTA has evolved as a form of bacterial sex.
Questions that I think have not yet been answered, or whose answers I forget: Does the individual cell that produces GTA die, as phage-infected cells normally do? Do only a small fraction of cells in a R. capsulatus culture produce GTA? How many genes are specific to GTA production (have no other function in the cell)? Have phage-derived genes acquired cellular functions independent of GTA production? Does GTA production directly reduce fitness? Can the ability to produce GTA be transferred by GTA? How strong is the phylogenetic evidence?
Next steps: Perhaps we should start our collaboration by working our way through the GTA literature, starting with Barry Marrs' 1974 PNAS paper. This would have the advantage of giving us both the same foundation of facts and factoids (things that look like facts but later turn out to be wrong) to base our discussions on. At the same time we ought to read one or more papers that clarify the evolutionary issues. My "Do bacteria have sex" paper is an obvious choice but shouldn't be the only one.
I'll ask my colleague to read this post, and we can then set up a time for our first meeting and decide what we should read in preparation for it.
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