The genetics of a putative social trait in natural populations of yeast

The sharing of secreted invertase by yeast cells is a well established laboratory model for cooperation, but the only evidence that such cooperation occurs in nature is that the SUC loci, which encode invertase, vary in number and functionality. Genotypes that do not produce invertase can act as “cheats” in laboratory experiments, growing on the glucose that is released when invertase producers, or “cooperators”, digest sucrose. However, genetic variation for invertase production might instead be explained by adaptation of different populations to different local availabilities of sucrose, the substrate for invertase. Here we find that, 110 wild yeast strains isolated from natural habitats, all contained a single SUC locus and produced invertase; none were “cheats”. The only genetic variants we found were three strains isolated instead from sucrose-rich nectar, which produced higher levels of invertase from three additional SUC loci at their sub-telomeres. We argue that the pattern of SUC gene variation is better explained by local adaptation than by social conflict

Breaking a species barrier by enabling hybrid recombination

Hybrid sterility maintains reproductive isolation between species by preventing them from exchanging genetic material1. Anti-recombination can contribute to hybrid sterility when different species' chromosome sequences are too diverged to cross over efficiently during hybrid meiosis, resulting in chromosome mis-segregation and aneuploidy. The genome sequences of the yeasts Saccharomyces cerevisiae and Saccharomyces paradoxus have diverged by about 12% and their hybrids are sexually sterile: nearly all of their gametes are aneuploid and inviable. Previous methods to increase hybrid yeast fertility have targeted the anti-recombination machinery by enhancing meiotic crossing over. However, these methods also have counteracting detrimental effects on gamete viability due to increased mutagenesis2 and ectopic recombination3. Therefore, the role of anti-recombination has not been fully revealed, and it is often dismissed as a minor player in speciation1. By repressing two genes, SGS1 and MSH2, specifically during meiosis whilst maintaining their mitotic expression, we were able to increase hybrid fertility 70-fold, to the level of non-hybrid crosses, confirming that anti-recombination is the principal cause of hybrid sterility. Breaking this species barrier allows us to generate, for the first time, viable euploid gametes containing recombinant hybrid genomes from these two highly diverged parent species

Carbon disulfide. Just toxic or also bioregulatory and/or therapeutic?

The overview presented here has the goal of examining whether carbon disulfide (CS2) may play a role as an endogenously generated bioregulator and/or has therapeutic value. The neuro- and reproductive system toxicity of CS2 has been documented from its long-term use in the viscose rayon industry. CS2 is also used in the production of dithiocarbamates (DTCs), which are potent fungicides and pesticides, thus raising concern that CS2 may be an environmental toxin. However, DTCs also have recognized medicinal use in the treatment of heavy metal poisonings as well as having potency for reducing inflammation. Three known small molecule bioregulators (SMBs) nitric oxide, carbon monoxide, and hydrogen sulfide were initially viewed as environmental toxins. Yet each is now recognized as having intricate, though not fully elucidated, biological functions at concentration regimes far lower than the toxic doses. The literature also implies that the mammalian chemical biology of CS2 has broader implications from inflammatory states to the gut microbiome. On these bases, we suggest that the very nature of CS2 poisoning may be related to interrupting or overwhelming relevant regulatory or signaling process(es), much like other SMBs