During heat shock and cold shock, plasmid DNA supercoiling changes transiently both in mesophilic bacteria and in hyperthermophilic archaea, despite a different overall topology (negative supercoiling versus relaxation to positive supercoiling). Transient changes in DNA supercoiling might be essential to generate the stress response, but they could also be a consequence of the physical effects of temperature on cellular components. Indeed, both appear intertwined. Comparison of the mechanisms acting in the two biological systems suggests that the dependence on temperature of the activity of different DNA topoisomerases, as well as of protein binding, are key factors for the control of DNA topology during stress, which may in turn be relevant for the expression of stress-induced genes.
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