Bacteria mount a physiologic stress response to survive hostile or stringent conditions. The genes that comprise the stress response can be defined in two ways: a transcriptional network composed of genes with expression changes during stress, and a phenotypic network of genes whose deletion lowers the bacteria’s fitness during stress. On first thought, one would expect these two networks to be the same, or at least have significant overlap. The genes important for surviving stress should be up- regulated, and genes not essential for tolerating the stress should be down-regulated. However, data from multiple microbes and conditions show that the transcriptional and phenotypic stress responses are nearly disjoint; genes with expression changes during stress can be deleted without changing fitness, and phenotypically important genes are rarely differentially expressed. During nutrient depletion, genes with expression changes are often adjacent to phenotypically important genes. By contrast, the response to antibiotic stress is largely incoherent, with expression changes located far from important genes. Overall, it appears that a microbe’s stress response can be either coordinated or chaotic depending on the type of stress.
About the Speaker:
Dr. Paul Jensen is an Assistant Professor of Bioengineering at the University of Illinois at Urbana-Champaign. Paul trained at the University of Minnesota, the University of Virginia, and Boston College before joining the faculty at Illinois in 2016. His lab uses high-throughput genomics, automation, and machine learning to decipher bacteria stress responses. Paul co-founded Cerillo, LLC, to commercialize low-cost microbial screening devices.
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