Genetically distinct Mycobacterium tuberculosis ?sufR mutants display diverse phenotypes
Iron-sulphur (FeS) cluster biogenesis is a tightly regulated process in vivo. In Mycobacterium tuberculosis (Mtb), regulation of FeS cluster biogenesis is mediated in part by SufR, which functions as a transcriptional repressor of the sufR-sufB-sufD-sufC-csd-nifU-sufT (suf) operon. Three genetically distinct sufR deletion mutants (?SufRMTB, Mtb?SufR, ?Rv1460stop) were previously generated, each displaying distinct phenotypes. In this study, we explored the phenotype of the ?Rv1460stop mutant by reproducing conditions used for the phenotyping of the ?SufRMTB and Mtb?SufR mutants. Consistent with the previous study, unique growth properties were observed for the ?Rv1460stop mutant in complex and metal defined media, suggesting that underlying genetic differences rather than experimental differences are responsible for phenotypic inconsistencies. Whole genome sequencing confirmed that one of the ?Rv1460stop mutants harbours no additional polymorphisms relative to its wild-type progenitor, and this mutant therefore represents a useful tool for elucidating the role of SufR in the complex regulation of the suf operon.