Synthetic reconstruction of extreme high hydrostatic pressure resistance in Escherichia coli

Abstract

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Dynamics of high hydrostatic pressure resistance development in RpoS-deficient Escherichia coli

“…Indeed, loss-offunction mutations in cyaA (encoding the adenylate cyclase or cAMP synthetase) or crp (encoding the cAMP receptor protein), or gain-offunction mutations in tnaA (encoding the tryptophanase) were found to be acquired to overcome the HHP-hypersensitivity of an E. coli ΔrpoS mutant (Gayán, Cambré et al, 2017;Mortier et al, 2021;Vanlint, Pype et al, 2013). While it remains mechanistically unclear how attenuated cAMP/CRP activity exactly contributes to HHP resistance, specific mutations in tnaA were found to provoke aggregation of the TnaA protein and concomitant upregulation of heat shock proteins that, in agreement with earlier findings (Aertsen et al, 2004;Gayán, Van den Bergh, Michiels, Michiels, & Aertsen, 2020), exert a HHP protective effect (Mortier et al, 2021).…”

“…Mutations upregulating RpoS activity reflect a relevant evolutionary strategy in E. coli in both natural and laboratory settings to acquire increased stress resistance, with such mutations often found among the many genes modulating the extensive regulatory network of the general stress response (Battesti, Majdalani, & Gottesman, 2011;Donovan, Norton, Bower, & Mulvey, 2013;Gayán, Cambré, Michiels, & Aertsen, 2016;Gayán et al, 2020;Tenaillon et al, 2012;. This straightforward mutational upregulation of RpoS activity, however, obstructs the evolutionary emergence of informative RpoSindependent genetic routes towards resistance development that might expedite our understanding of cryptic pleiotropic stresses such as HHP stress.…”