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Published online 28 September 2008 | Nature | doi:10.1038/news.2008.1134
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How the jellyfish got its sting
From a bacterium, surprisingly.
Jellyfish may owe thanks to a humble bacterium for their ability to sting prey. Scientists have found that one of the genes necessary for them to sting is similar to a gene in bacteria, suggesting the ancestors of jellyfish picked up the gene from microbes.
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It is always more parsimonious to have acquired the same gene a couple of times, than to have lost it many times - and genes that have converged on a product function have no obvious similarity to one another, and nor do their products, outside of an active site. So I'm with the horizontal transfer idea.... And I am sure many more instances will be found: we all literally swim in a sea of DNA from other organisms; it would be most surprising if this did not result, over billenia, in acquisition of useful traits.
Interesting research. However, there is nothing new under the sun! As regards horizontal gene transfer, one must remember mitochondria in humans. At this point, I underline the relation between a functional mitochondrial cytopathy, i.e., Congenital Acidosic Enzyme-Metabolic Histangiopathy, and the most important biophysical semeiotic constitution, as the diabetic one: for instance, See www.nature.com Febbraio 17, 2008 http://blogs.nature.com/news/thegreatbeyond/2008/02/confusion_after_diabetes_study.html#comments
Hi, How the jellyfish got its sting: Complementary to this question the jellyfish population is increasing at an alarming rate. The sting has coursed a number of fatalities. A development of concern. Regards Dr. Terence Hale
I was misquoted above- I did not suggest that the gene originated multiple times, but that homoplasy frequently leads gene trees to be incongruent with species trees even when there is no horizontal transfer. This is especially common in highly conserved genes since a relatively small fraction of the sites vary. Another concern I had is that there was no evidence that the hypothesized horizontal gene transfer (HGT) was coincident with the origin of nematocysts, though this article and the manuscript imply a causative role of HGT in the origin of nematocysts. If the incongruence in the trees were due to HGT then the trees suggest that the transfer events preceded the most recent common ancestor of all or most metazoans. So while function of this gene in nematocysts is interesting -- and the authors do present good new expression data to this effect -- the hypothesized acquisition of the gene is not at all unique to Cnidaria and is shared widely with other animals. Perhaps nematocysts would not have arisen had this gene not been already present in the genome from a much earlier date, but there isn?t a correlation between transfer and nematocyst origin that would directly support this. So I am unclear why the nematocyst story was singled out from the potential function of this gene in all other animals, which got it in the same way from the same common ancestor
Thank you for your interest in our paper and for all your comments. I would like to answer to Casey Dunn's concerns. Of course homoplasy problems have always to be considered, and being aware of this we tried to be as careful as possible. But we think that in our case we had enough informative positions in the alignment block we chose for the phylogeny, moreover we tested different phylogenetic reconstruction methods and combined our analysis with a statistical test (AU test). Concerning the second point mentioned. Our results clearly suggest an acquisition of the gene by a common metazoan ancestor. (Moreover the phylogenetic analyses as well as the analysis of stop codons in introns helped us polarize this transfer from bacteria to metazoans.) So we don't claim that the transfert coincided with the apparition of nematocytes. But we suggest that the gene pgsAA, or the produced PGA, was co-opted in a cnidarian ancestor for this function in emerging nematocytes, and that this was a key evolutive event. Indeed it allowed the apparition of nematocytes their present form, by giving them an essential element: a powerful discharge system, allowing them to capture prey, defend themselves... And as nematocytes are a key feature of present cnidarians, we think that this, in the eye of natural selection, was a decisive acquisition that allowed early cnidarians to successfully colonize diverse ecological niches. So we don't claim that this gene "magically" allowed the apparition of nematocytes from nothing, it is absolutly clear that the transfer was not enough to give a nematocyte. Many other acquisitions were also necessary to generate this highly complex and specialized cell type through evolution (as the apparition of minicollagens, toxins...), but we claim that the acquisition of the PGA fast discharge system, thanks to a very specially acquired (from a bacterium) and very originally exploited gene, was a key event in cnidarian evolution. The function of this gene in other eukaryotes is unknown and the presence and maintenance of the gene in their genomes is really intriguing, as well as the number of independant acquisitions of the gene. Other metazoans also got the gene but from independant transfers, so the story of the gene acquired in cnidarians is today shared only by cnidarians and sponges.