Good thoughts. If I had to place a bet, I would go with a mix-up of cell cultures. The lab who published the PKT5 works on cms, and conceivable may have had some cmsT maize cell cultures going. Once you get plant cells into culture, it’s impossible to tell a carrot culture from a maize culture by eye. If labels get mixed up during passaging of cultures (say, some ethanol erases the Sharpie notations), then …
EN actually leaves us a tangential clue that tells us how one would get the mutated cmsT region in PKT5 (talking about a paper by Pring et al.):
In fact, one of the major reasons we know that T-urf13 is responsible for cytoplasmic male sterility and disease susceptibility is the presence of revertant mutations that delete the T-urf13 gene in cell culture experiments where cms-T maize is grown on a medium containing BmT toxin, rendering the plants disease resistant and male fertile. What’s surprising, however, is that when those experiments were repeated without toxin selection, occasional revertant mutations were nonetheless obtained. These results suggest that the T-urf13 gene confers a selective disadvantage that is independent of sensitivity to the BmT toxin (Pring et al ., 1988).
Could you elaborate on that? The quote seems to be saying that revertant mutations (that delete t-urf13) can be be obtained in normal cell cell culture without any particular pressures (like the presence of a toxin). How does this produce a clue for how a similar very similar to t-urf13 would arise in PKT5?
I took him to imply that a revertant mutation is a rationalization built on the implicit assumption that the recombination first detected is not a result of mixing up cultures.
The idea is that, if the lab that reported on PKT5 was also growing cmsT maize cells in culture, and if they mixed these up with the male sterile carrot cell cultures, then the PKT5 clone they isolated would instead be from cmsT maize (in other words, it is the maize T-urf13 locus). The reason that the identify between PKT5 and T-urf13 is not 100% (which is what @evograd showed above) is that this locus accumulated mutations, even without the toxin. The mutations needn’t be complete deletions, but just some changes to abrogate production of T-urf13.
My guess is it was flagged due to the “anti-meme” policy. However, if it was flagged because somebody somehow perceived it as as insult against me, I’d like to state for the record that I thought it was funny.
Joshua is allergic to memes. It’s his call. (Sometimes there are copyright issues too, I suppose… Especially with the European Copyright Directive coming up soon.)
Definitely. Interesting to me how there’s recombination directly in the genes encoding the different transmembrane transporters, and that “parts” from different, though related transporters, can combine to yield a still-functioning transporter with a novel function.
Made me recall the T-urf13 membrane channel also resulting from recombination of different parts of the mitochondrial genome.