Biology

Regulation of multiple abiotic stress tolerance by LexA in the cyanobacterium Anabaena sp. strain PCC7120.

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Regulation of multiple abiotic stress tolerance by LexA in the cyanobacterium Anabaena sp. strain PCC7120.

Biochim Biophys Acta. 2018 Jul 25;:

Authors: Kumar A, Kirti A, Rajaram H

Abstract
The paradigm of involvement of LexA in regulation of only SOS-response in bacteria through the down-regulation of DNA repair genes was challenged in the unicellular cyanobacterium, Synechocystis PCC6803, wherein it was originally shown not to be associated with DNA repair and later also involved in management of carbon-starvation through up-regulation of C-metabolism genes. In the filamentous cyanobacterium, Anabaena sp. strain PCC7120, global stress management role for LexA and a consensus LexA-binding box (AnLexA-box) has been established using a LexA-overexpressing recombinant strain, AnlexA+. High levels of LexA rendered Anabaena cells sensitive to different DNA damage and oxidative stress-inducing agents, through the transcriptional down-regulation of the genes involved in DNA repair and alleviation of oxidative stress. LexA overexpression enhanced the ability of Anabaena to tolerate C-depletion, induced by inhibiting photosynthesis, by up-regulating genes involved in C-fixation and down-regulating those involved in C-breakdown, while maintaining the overall photosynthetic efficiency. A consensus LexA-binding box, AnLexA-box [AGT-N4-11-ACT] was identified upstream of both up- and down-regulated genes using a subset of Anabaena genes identified on the basis of proteomic analysis of AnlexA+ strain along with a few DNA repair genes. A short genome search revealed the presence of AnLexA box in at least 40 more genes, with functional roles in fatty acid biosynthesis, toxin-antitoxin systems in addition to DNA repair, oxidative stress, metal tolerance and C-metabolism. Thus, Anabaena LexA modulates the tolerance to multitude of stresses through transcriptional up/down-regulation of their functional genes directly by binding to the AnLexA Box present in their promoter region.

PMID: 30055321 [PubMed – as supplied by publisher]

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