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. 2019 May 1;10:923. doi: 10.3389/fmicb.2019.00923

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Copyright © 2019 Ogura, Sato and Abe.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Requirement of acetyl-CoA produced by PDHc for GI of sigX-lacZ. (A) Expression of sigX-lacZ in the mutants. Means of the β-Gal activities from three independent experiments and the standard deviations are shown. The x axis represents the growth time in hours relative to the end of vegetative growth (T0). All strains are the derivatives of wild-type OAM709 and the relevant genotype is indicated below the panel. (B) Model of GI of sigX/sigM and acetyl-CoA metabolism. Glucose addition stimulates the acetylation of CshA (Ogura and Asai, 2016). CshA has been shown to associate with RNAP. RNAP with acetylated CshA may stimulate the replacement of σ^X/M for σ^A in the RNAP holoenzyme. σ^A -associated RNAP holoenzyme with acetylated CshA stimulate the transcription of ylxR (Ogura and Kanesaki, 2018). YlxR regulates many genes and changes the cellular metabolic state, which may lead to induction of the SigX/M regulons. Ac, acetyl moiety; PdhABCD, pyruvate dehydrogenase (PDH); Pta, phosphotransacetylase; AcsA, acetyl-CoA syntheatse; AckA, acetate kinase. “P” in the circle indicates phosphate residue.