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Posted by ATheoryofJustice86 on 23 May 2012 at 20:11 GMT

This is a very interesting study. I wonder, though, if the authors are overly conflating CIN and evolution. The gain or loss of an endogenous yeast chromosome will undoubtedly influence cellular growth rates. For this reason, most studies on CIN in yeast use marker plasmids to determine chromosome segregation rates. The authors find some highly aneuploid strains that they describe as stable - yet could it be instead that these karyotypes represent local fitness peaks? That is, the parental karyotype is more fit than any karyotype formed by easy gain/loss events, so no chromosomal variations are detected because they are always out-competed by cells harboring the parental karyotype? Alternately, "high CIN" lines could be those in which a sick parental strain is out-competed by many descendants with different karyotypes, regardless of the rate at which chromosomes are actually gained or lost.

No competing interests declared.

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normanpavelka replied to ATheoryofJustice86 on 04 Jun 2012 at 09:47 GMT

It is true that most studies on CIN in yeast use marker plasmids or artificial chromosomes to determine chromosome missegregation rates to avoid any potential complication due to the impact on fitness, but the main problem with these agents is that they are not segregated as accurately as native chromosomes due to their small size and structural differences. Furthermore, these assays usually can only detect plasmid loss but not gain events. The method used in this study, by contrast, allows detection of both gain and loss of any of the 16 endogenous chromosomes. The authors were aware of the potential confounding effect of fitness, and this was dealt with by limiting the proliferation of aneuploid spores no further than 30 cell generations (divisions). Much of the data presented in the study was actually collected between generations 20 and 25. Under these restrictions, there would have to be a huge fitness difference between the original aneuploid cell and one of its karyotypically deviant progeny in order for one to totally compete away the other. As long as a deviant karyotype is present in at least 10% of the population, the method would be able to pick it up because the growing population was spread to allow growth of single-cell colonies, which eliminated intra-population competition. As a testimony that this method works, several examples were shown of strains with low fitness that also had low CIN rates as well as strains with high fitness that also had high CIN rates. Overall, the analysis presented in Figure 3A shows a lack of correlation between fitness and CIN level.

Competing interests declared: Co-author on the paper