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• W1977446413 abstract "The activities of promoters can be temporally and conditionally regulated by mechanisms other than classical DNA-binding repressors and activators. One example is the inherently weak σ(70)-dependent Pr promoter that ultimately controls catabolism of phenolic compounds. The activity of Pr is up-regulated through the joint action of ppGpp and DksA that enhance the performance of RNA polymerase at this promoter. Here, we report a mutagenesis analysis that revealed substantial differences between Pr and other ppGpp/DksA co-stimulated promoters. In vitro transcription and RNA polymerase binding assays show that it is the T at the -11 position of the extremely suboptimal -10 element of Pr that underlies both poor binding of σ(70)-RNAP and a slow rate of open complex formation--the process that is accelerated by ppGpp and DksA. Our findings support the idea that collaborative action of ppGpp and DksA lowers the rate-limiting transition energy required for conversion between intermediates on the road to open complex formation." @default.
• W1977446413 created "2016-06-24" @default.
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• W1977446413 date "2011-03-29" @default.
• W1977446413 modified "2023-10-01" @default.
• W1977446413 title "A hyper-mutant of the unusual σ70-Pr promoter bypasses synergistic ppGpp/DksA co-stimulation" @default.
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• W1977446413 doi "https://doi.org/10.1093/nar/gkr167" @default.
• W1977446413 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3152329" @default.
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