Red Queen Dynamics of Daphnia and P. ramosa
1 comment April 30th, 2008
“Developmental cheating in the social bacterium Myxococcus xanthus” Notes
Developmentally defective genotype has 5 fates when mixed with developmentally proficient WT:
1. (Null Hypothesis, H1) Defector sporulates with same efficiency as in pure culture by itself.
2. Defector sporulation is worse than when by itself in pure culture.
3. Partial rescue (extracellular complementation), defector sporulates better in mixed culture than in pure culture by itself.
4. (Null Hypothesis, H2) Complete rescue to WT sporulation from crossfeeding complementation.
5. Evolutionary cheating: defector produces more spores in presence of WT than WT levels (defector obtains disproportionate reproductive success)
ExperimentsFirst
-6 populations of M. xanthus DK1622 were evolved for 1,000 generations under asocial conditions; one sporulation defective isolate from each pop was chosen
-each is mixed with WT
-5 of 6 isolates had higher spore production when mixed than in pure culture alone (partial complementation)
-those 5 were 10-fold rescued over pure culture
-the 1 of 6 not partially complemented had worse sporulation when mixed than in pure culture (fate #2)
-of the 5 partially complemented, 3 were cheaters (rescued to at least WT sporulation)
-2 of the cheaters were better than WT when rescued (when rare)
-One of the cheaters was almost completely defective at sporulation in pure culture, but as a minority was 50x greater at sporulating than WT
Second
-The two evolved cheaters better than WT were mixed at 9 dif frequencies with WT
*As initial frequency increased, mixed culture sporulation output dropped below WT output (if in pure culture)
MEANING: cheaters harm group performance
Third
-3 mutant genotypes of defined single mutations in signal production
-Question: Can the cheating phenotype arise from one mutation? Or does it require multiple mutations?
-Answer: The phenotype can arise from one mutation, but that doesn’t mean that the evolved defectors have defects in the genes targeted.
Add comment April 20th, 2008
Prisoner’s dilemma in an RNA virus
I’ll admit that when I read a paper with a lot of numbers (as in the game matrices), my eyes kind of glaze over. It takes some extra effort to figure out where the matrix numbers come from, and even though we discussed this in class, I’m still not extremely comfortable with the derivations: extrapolated numbers from a hypothetical portion of a line seem a little fishy.
Hesitations aside, in figure 1b (Nature, 1999), showing observed fitness values for a game in which opponents use conflicting strategies of cooperation and defection, the authors state that the realized payoff matrix for evolved high MOI phiH2 relative to phi6 ancestor shows evolution of an ESS of prisoner’s dilemma. The lowest payoff is to the ancestor during co-infection; the ESS is to defect even though a higher pay-off occurs when phage cooperate. This is said to be paradoxical, but in a way I think it makes sense if we give the cheater phage selfish characteristics: its fitness is lower when cooperating (0.65) with ancestor than with the ‘cheat:cheat’ scenario (0.83), so the logical ‘choice’ is to go the cheat:cheat way.
If the ‘cheaters’ were DI particles, the population would surely collapse without cooperators present. Would the population survive if it were just evolved cheaters, though? I think so, otherwise the cheat:cheat scenario would probably be zero…
Add comment April 20th, 2008
As in the first time we spoke about this paper, I am interested in the genetics behind the adaptive changes undergone by P. fluorescens in only 7 days. This makes me think of irreversible phase variation in Photorhabdus that we just heard about in Holli’s seminar this week in the Micro Dept Seminar Series, in which cells go from primary to secondary phase. This also is very relevant and interesting to Steffen’s evolved populations and morphotypes he’s seen come out of the mix.
Add comment March 26th, 2008
As I was reading Tim Cooper’s paper of recombination speeding adaptation, I wondered which experimental group best represented a population we might most often find in nature. So I guess the question I have really is: are there usually high mutation rate populations who also are recombination proficient? As I went on in this paper, I think my question was answered: “competition between different lineages of the same species may be common in… clinical settings where adaptation to novel hosts can select for strains with high mutation rates.” So, adaptation by infecting bacteria to a host can happen quickly through beneficial alleles being fixed quickly due to recombination and high mutation rate. This is scary! Giving this example of clinical isolates helped me to understand the relevance of these findings supporting the FM model.
Add comment March 26th, 2008
Please see my blog about the Travisano paper for my best of blog “relative effects of adaptation…”
Add comment March 1st, 2008
I agree with Abe’s post about ‘replaying the tape,’ in that the evolution experiment in the Travisano et al paper can’t begin to replay the tape, probably not even a short track, of the evolution of life. In their experiment, over 2000 generations, then another 1000 generations of E. coli, they saw the effects of adaptation and chance on fitness of evolved populations, and the effect of history on the trait of cell size, since no fitness effect was observed. In the paper, they say that for “less important traits,” (cell size) the effects of history were more visible than chance or adaptation. But, it would seem that the persistence of a certain cell size must have some advantages, and would therefore be the effect of chance and adaptation. As far as making generalizations about macro-organisms though, we can only really speculate that the same relativities of chance, history and adaptation apply. I would hazard a guess that as Abe said, the last paragraph of the Travisano paper might be backwards. Chance and adaptation, after deep time, should be the dominant effectors of evolution, losing the footprint of history after thousands of generations. It does follow that if you’ve adapted to growth on a certain carbon source, you would lose the ability to grow on other carbon sources as well (as long as the physiology of how such carbon sources are utilized is different). But the example of trees that we talked about in class doesn’t really make sense, that bark color is an unimportant trait whose evolution is effected by history, where the ancestor started out. Maybe this example is not the best one, since none of us are plant biologists, but I think a lot of what we see is ‘convergent evolution.’ Obviously tree bark has some function, protection, at least, but I don’t think that the color of bark is unimportant (who knows!). The fact that most tree bark is brown probably is due to adaptation to the environment, chance mutations that allow that adaptation, and convergent evolution of different trees who also adapted in a similar way. Maybe this is just a lot of babble and I don’t know what I’m talking about, but all of the organisms we see now, have evolved over many more than 3000 generations. I think the Travisano experiment was sound and showed that evolution occurs, but the most important thing I take away from the paper is that bacteria evolve in an environment in a predictable manner, which is important in my research with Burkholderia and how these bacteria will evolve to the CF lung.
1 comment March 1st, 2008
Clarification From the Glossary:Horizontal gene transfer (HGT), also Lateral gene transfer (LGT), is any process in which an organism transfers genetic material to another cell that is not its offspring. By contrast, vertical transfer occurs when an organism receives genetic material from its ancestor, e.g. its parent or a species from which it evolved.
I think that in class we all agreed that we need a theory-based method of bacterial taxonomy. In the Cohan and Perry review, they propose a taxonomic system based on ecological and physiological characteristics. Dave, Abe, and I talked about delineating species of bacteria by measuring rates of genetic recombination and HGT, along with whole genome comparisons. It makes sense that ecotypes would have genes allowing them to persist in their ecological niche, giving them the same ecology, genetics, and function. I think a system incorporating ecology, physiology, and genetics (including whole genome comparisons and rates of recombination, interbreeding), would be the most comprehensive method of taxonomy.
Rates of recombination and HGT should be similar among ecotypes because they face the same environmental pressures, right?
Many of the concepts in this review are pretty new to me; I’m still trying to wrap my head around much of it.
2 comments February 11th, 2008
I think that the Whitaker paper on Sulfolobus supports the idea that everything is everywhere and the environment puts selective pressures on organisms which result in adaptation; but the environment is not the only factor. Horizontal gene transfer occurs in the environment between bacteria, making them genetically different than ancestors. But, you could argue that this is still the environment selecting because HGT allows the recipient to function in the environment the same way the donor has done.
Add comment January 31st, 2008
I’m interested in our course about microbial population biology because I think it will help me to think differently or better about my research. I’m especially interested in bacterial cell differentiation into niches in an environment such as a biofilm; I liked the example given in class where Pseudomonas fluorescens differentiated into three different colony morphologies in simple media with different aerobic areas. In a biofilm, this differentiation must also occur, where cells have taken over different aerobic niches.
Add comment January 23rd, 2008
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