A previously established multiscale population genetics model posits that fitness can be inferred from the physical properties of proteins under the physiological assumption that a loss of stability by any protein confers the lethal phenotype to an organism. Here, we develop this model further by positing that replication rate (fitness) of a bacterial or viral strain directly depends on the copy number of folded proteins, which determine its replication rate. Using this model, and both numerical and analytical approaches, we studied the adaptation process of bacteria and viruses at varied environmental temperatures. We found that a broad distribution of protein stabilities observed in the model and in experiment is the key determinant of thermal response for viruses and bacteria. Our results explain most of the earlier experimental observations: the striking asymmetry of thermal response curves; the absence of evolutionary tradeoff, which was expected but not found in experiments; correlation between denaturation temperature for several protein families and the optimal growth temperature of their carrier organisms; and proximity of bacterial or viral optimal growth temperatures to their evolutionary temperatures. Our theory quantitatively and with high accuracy described thermal response curves for 35 bacterial species using, for each species, only two adjustable parameters-the number of rate-determining genes and the energy barrier for metabolic reactions.
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