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Experiments on yeast cells that are hosts to a killer virus confirm that natural selection can sometimes reduce fitness.

Grape must is the precursor to wine, and consists of grape juice and its resident microbial community. We used Illumina MiSeq® to track changes in must fungal community composition over time in winery vats and laboratory microcosms. We also measured glucose consumption and biomass in microcosms derived directly from must, and glucose consumption in artificially assembled microcosms. Functional impacts of individual must yeasts in artificially assembled communities were calculated using a ''keystone index,'' developed for “Species richness influences wine ecosystem function through a dominant species” [1]. Community composition data and functional measurements are included in this article. DNA sequences were deposited in GenBank (GenBank: SRP073276). Discussion of must succession and ecosystem functioning in must are provided in [1].

Genome-wide sequence divergence between populations can cause hybrid sterility through the action of the anti-recombination system, which rejects crossover repair of double strand breaks between nonidentical sequences. Because crossovers are necessary to ensure proper segregation of homologous chromosomes during meiosis, the reduced recombination rate in hybrids can result in high levels of nondisjunction and therefore low gamete viability. Hybrid sterility in interspecific crosses of Saccharomyces yeasts is known to be associated with such segregation errors, but estimates of the importance of nondisjunction to postzygotic reproductive isolation have been hampered by difficulties in accurately measuring nondisjunction frequencies. Here, we use spore-autonomous fluorescent protein expression to quantify nondisjunction in both interspecific and intraspecific yeast hybrids. We show that segregation is near random in interspecific hybrids. The observed rates of nondisjunction can explain most of the sterility observed in interspecific hybrids through the failure of gametes to inherit at least one copy of each chromosome. Partially impairing the anti-recombination system by preventing expression of the RecQ helicase SGS1 during meiosis cuts nondisjunction frequencies in half. We further show that chromosome loss through nondisjunction can explain nearly all of the sterility observed in hybrids formed between two populations of a single species. The rate of meiotic nondisjunction of each homologous pair was negatively correlated with chromosome size in these intraspecific hybrids. Our results demonstrate that sequence divergence is not only associated with the sterility of hybrids formed between distantly related species but may also be a direct cause of reproductive isolation in incipient species.

Models of mRNA translation usually presume that transcripts are linear; upon reaching the end of a transcript each terminating ribosome returns to the cytoplasmic pool before initiating anew on a different transcript. A consequence of linear models is that faster translation of a given mRNA is unlikely to generate more of the encoded protein, particularly at low ribosome availability. Recent evidence indicates that eukaryotic mRNAs are circularized, potentially allowing terminating ribosomes to preferentially reinitiate on the same transcript. Here we model the effect of ribosome reinitiation on translation and show that, at high levels of reinitiation, protein synthesis rates are dominated by the time required to translate a given transcript. Our model provides a simple mechanistic explanation for many previously enigmatic features of eukaryotic translation, including the negative correlation of both ribosome densities and protein abundance on transcript length, the importance of codon usage in determining protein synthesis rates, and the negative correlation between transcript length and both codon adaptation and 5' mRNA folding energies. In contrast to linear models where translation is largely limited by initiation rates, our model reveals that all three stages of translation-initiation, elongation, and termination/reinitiation-determine protein synthesis rates even at low ribosome availability.

Is a group best off if everyone co-operates? Theory often considers this to be so (e.g. the "conspiracy of doves"), this understanding underpinning social and economic policy. We observe, however, that after competition between "cheat" and "co-operator" strains of yeast, population fitness is maximized under co-existence. To address whether this might just be a peculiarity of our experimental system or a result with broader applicability, we assemble, benchmark, dissect, and test a systems model. This reveals the conditions necessary to recover the unexpected result. These are 3-fold: (a) that resources are used inefficiently when they are abundant, (b) that the amount of co-operation needed cannot be accurately assessed, and (c) the population is structured, such that co-operators receive more of the resource than the cheats. Relaxing any of the assumptions can lead to population fitness being maximized when cheats are absent, which we experimentally demonstrate. These three conditions will often be relevant, and hence in order to understand the trajectory of social interactions, understanding the dynamics of the efficiency of resource utilization and accuracy of information will be necessary.

Diploid hybrids of Saccharomyces cerevisiae and its closest relative, Saccharomyces paradoxus, are viable, but the sexual gametes they produce are not. One of several possible causes of this gamete inviability is incompatibility between genes from different species--such incompatible genes are usually called "speciation genes." In diploid F1 hybrids, which contain a complete haploid genome from each species, the presence of compatible alleles can mask the effects of (recessive) incompatible speciation genes. But in the haploid gametes produced by F1 hybrids, recessive speciation genes may be exposed, killing the gametes and thus preventing F1 hybrids from reproducing sexually. Here I present the results of an experiment to detect incompatibilities that kill hybrid gametes. I transferred nine of the 16 S. paradoxus chromosomes individually into S. cerevisiae gametes and tested the ability of each to replace its S. cerevisiae homeolog. All nine chromosomes were compatible, producing nine viable haploid strains, each with 15 S. cerevisiae chromosomes and one S. paradoxus chromosome. Thus, none of these chromosomes contain speciation genes that were capable of killing the hybrid gametes that received them. This is a surprising result that suggests that such speciation genes do not play a major role in yeast speciation.

Background: Since the ancient times the skin aging application of honeybee venom (BV) is practiced and persisted until nowadays. The present study evaluated the effect of the honeybee venom (BV) on keratinocyte migration in wound healing model in vitro. Objective: To access BV further as a cosmetic ingredient and a potential external application for topical uses, we performed studies to investigate the biologic effect of BV treatment on keratinocyte proliferation and migration in vitro. Material and Methods: BV cytotoxicity was assessed by using a 3-[4,5-dimethyl-2- thiazolyl]-2,5-diphenyl tetrazolium bromide (MTT) assay over 24 h. To assess BV genotoxicity, damage to human epidermal keratinocyte (HEK) was evaluated using the Comet assay. HEK migration was evaluated using a commercial wound healing kit. The skin pro-inflammatory cytokines interleukin (IL)-8 and tumor necrosis factor (TNF)-α were examined to evaluate the pro-inflammatory response to BV. Results: It was found that BV (<100 μg/ml) was not cytotoxic and stimulated more HEK proliferation and migration compared to negative control, and did not induce DNA damage. There were also decreases in IL-8 and TNF-α expression levels in HEK at all time points. Conclusion: These findings highlight the potential of topical application of BV for promoting cell regeneration and wound treatment. [ABSTRACT FROM AUTHOR]

The fundamental principle underlying sexual selection theory is that an allele conferring an advantage in the competition for mates will spread through a population. Remarkably, this has never been demonstrated empirically. We have developed an experimental system using yeast for testing genetic models of sexual selection. Yeast signal to potential partners by producing an attractive pheromone; stronger signallers are preferred as mates. We tested the effect of high and low levels of sexual selection on the evolution of a gene determining the strength of this signal. Under high sexual selection, an allele encoding a stronger signal was able to invade a population of weak signallers, and we observed a corresponding increase in the amount of pheromone produced. By contrast, the strong signalling allele failed to invade under low sexual selection. Our results demonstrate, for the first time, the spread of a sexually selected allele through a population, confirming the central assumption of sexual selection theory. Our yeast system is a powerful tool for investigating the genetics of sexual selection. [ABSTRACT FROM AUTHOR]

The SUC multigene family of the single-celled yeast Saccharomyces cerevisiae is polymorphic, with genes varying both in number and activity. All of the genes encode invertase, an enzyme that is secreted to digest sucrose outside of the cell. This communal endeavour creates the potential for individual cells to defect (cheat) by stealing the sugar digested by their neighbours without contributing the enzyme themselves. We measured the fitness of a defector, with a deleted suc2 gene, relative to an otherwise isogenic cooperator, with a functional SUC2 gene. We manipulated the level of social interaction within the community by varying the population density and found that the defector is less fit than the cooperator at low levels of sociality but more fit in dense communities. We propose that selection for antisocial cheating causes SUC polymorphism in nature. The infamous Prisoner's Dilemma game shows that social behaviour is generally unstable, and the success of both cooperation and defection can vary continuously in time and space. The variation in SUC genes reflects constant adaptation to an ever-changing biotic environment that is a consequence of the instability of cooperation. It is interesting that social interactions can have a direct effect on molecular evolution, even in an organism as simple as yeast. [ABSTRACT FROM AUTHOR]

Background: Since the ancient times the skin aging application of honeybee venom (BV) is practiced and persisted until nowadays. The present study evaluated the effect of the honeybee venom (BV) on keratinocyte migration in wound healing model in vitro., Objective: To access BV further as a cosmetic ingredient and a potential external application for topical uses, we performed studies to investigate the biologic effect of BV treatment on keratinocyte proliferation and migration in vitro., Material and Methods: BV cytotoxicity was assessed by using a 3-[4,5-dimethyl-2-thiazolyl]-2,5-diphenyl tetrazolium bromide (MTT) assay over 24 h. To assess BV genotoxicity, damage to human epidermal keratinocyte (HEK) was evaluated using the Comet assay. HEK migration was evaluated using a commercial wound healing kit. The skin pro-inflammatory cytokines interleukin (IL)-8 and tumor necrosis factor (TNF)-α were examined to evaluate the pro-inflammatory response to BV., Results: It was found that BV (<100 μg/ml) was not cytotoxic and stimulated more HEK proliferation and migration compared to negative control, and did not induce DNA damage. There were also decreases in IL-8 and TNF-α expression levels in HEK at all time points., Conclusion: These findings highlight the potential of topical application of BV for promoting cell regeneration and wound treatment.