Mutation as a Stress Response and the Regulation of Evolvability

By R. Galhardo, P. Hastings, S. Rosenberg. Critical reviews in biochemistry and molecular biology, 2007

630 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/d38d68f9e21d39643d7557e40bc9b2d8695902b6

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Citations in the corpus

Life is Physics: Evolution as a Collective Phenomenon Far From Equilibrium (2010, background): “Although early experiments are generally recognized as not being properly analyzed (197), a plethora of mechanisms have now been reported to give rise to an adaptive response to stress, including regulation of mutation rates (nonrandom in time) and localized variation along the genome (nonrandom in ”
Bistability, epigenetics, and bet-hedging in bacteria. (2008, background): “The mechanisms involved in hypermutation include double-strand break (DSB) repair, SOS response, and a general stress response, of which the first two have a causal relationship (33).”
A chromatin-mediated reversible drug tolerant state in cancer cell subpopulations (2010, background): “Significantly, accumulating evidence supports a role for stress-induced mutagenesis as an adaptive mechanism both in bacteria and in cancer cells (Galhardo et al., 2007), raising the possibility that an increased mutagenesis rate within drug-tolerant cells leads to a greater opportunity for drug…”
Cellular Decision-Making and Biological Noise: From Microbes to Mammals (2011, background): “subtilis cell fate decision that has attracted much attention recently is the transition to competence, when cells take up extracellular DNA and use it as food or perhaps to integrate it into the genome as a mechanism of increased evolvability under stress (Galhardo et al., 2007).”
Stress Physiology of Lactic Acid Bacteria (2016, background): “Interestingly, stress-induced mutations can also occur; cells exposed to certain stresses can enter a hypermutable state, thereby increasing the diversity of a clonal population, which may lead to new genotypes allowing survival under conditions otherwise detrimental to the wild type (48).”
Genetic drift, selection and the evolution of the mutation rate (2016, background): “A3(2) and Escherichia coli B/r: an integrative theoretical approach.”
The role of specialized DNA polymerases in mutagenesis in Pseudomonas putida (2009, background): “Though, instead of double-strand break formation due to conjugal functions in case of Lac reversion mutations, ciprofloxacin induces double-strand breaks by inhibition of topoisomerase-DNA complex after the cleavage and before the ligation of DNA strands (Galhardo et al., 2007).”
Mechanisms of change in gene copy number (2009, background): “The idea of mutation as a stress response has been developed to explain how mutagenesis affects the evolution of bacterial populations (reviewed in Ref”