Microbiome Assembly in Fermented Foods.

For thousands of years, humans have enjoyed the novel flavors, increased shelf-life, and nutritional benefits that microbes provide in fermented foods and beverages. Recent sequencing surveys of ferments have mapped patterns of microbial diversity across space, time, and production practices. But a mechanistic understanding of how fermented food microbiomes assemble has only recently begun to emerge. Using three foods as case studies (surface-ripened cheese, sourdough starters, and fermented vegetables), we use an ecological and evolutionary framework to identify how microbial communities assemble in ferments. By combining in situ sequencing surveys with in vitro models, we are beginning to understand how dispersal, selection, diversification, and drift generate the diversity of fermented food communities. Most food producers are unaware of the ecological processes occurring in their production environments, but the theory and models of ecology and evolution can provide new approaches for managing fermented food microbiomes, from farm to ferment.

Genomic signatures of UV resistance evolution in Escherichia coli depend on the growth phase during exposure.

Physiological states can determine the ability of organisms to handle stress. Does this mean that the same selection pressure will lead to different evolutionary outcomes, depending on the organisms' physiological state? If yes, what will be the genomic signatures of such adaptation(s)? We used experimental evolution in Escherichia coli followed by whole-genome whole-population sequencing to investigate these questions. The sensitivity of Escherichia coli to ultraviolet (UV) radiation depends on the growth phase during which it experiences the radiation. We evolved replicate E. coli populations under two different conditions of UV exposures, namely exposure during the lag and the exponential growth phases. Initially, the UV sensitivity of the ancestor was greater during the exponential phase than the lag phase. However, at the end of 100 cycles of exposure, UV resistance evolved to similar extents in both treatments. Genome analysis showed that mutations in genes involved in DNA repair, cell membrane structure and RNA polymerase were common in both treatments. However, different functional groups were found mutated in populations experiencing lag and exponential UV treatment. In the former, genes involved in transcriptional and translational regulations and cellular transport were mutated, whereas the latter treatment showed mutations in genes involved in signal transduction and cell adhesion. Interestingly, the treatments showed no phenotypic differences in a number of novel environments. Taken together, these results suggest that selection pressures at different physiological stages can lead to differences in the genomic signatures of adaptation, which need not necessarily translate into observable phenotypic differences.