M. tuberculosis phoP mutant lacking mcr7

ABSTRACT: The PhoPR two-component system is essential for virulence in Mycobacterium tuberculosis where it controls expression of approximately 2% of the genes, including those for the ESX-1 secretion apparatus, a major virulence determinant. Mutations in phoP lead to compromised production of pathogen-specific cell wall components and attenuation both ex vivo and in vivo. The PhoP regulon comprises several transcriptional regulators as well as genes for polyketide synthases and PE/PPE proteins. The most prominent site of PhoP regulation was located in the intergenic region between rv2395 and PE_PGRS41, where the mcr7 gene codes for a small non-coding RNA (ncRNA). Our prediction suggested that Mcr7 might regulate tatC at the post-transcriptional level by occlusion of the RBS and the consequent translational arrest. Consequently, we studied the secretome from exponentially grown cultures of strain H37Rv, its phoP mutant and a phoP complemented mutant by in-depth proteomics. The results are consistent with a regulatory model involving PhoP, Mcr7 and tatC mRNA since the absence of Mcr7 in the phoP mutant would result in more efficient TatC translation and therefore increased secretion.

OTHER RELATED OMICS DATASETS IN: PRJNA236021 PRJNA236023 PRJNA236024

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mycobacterium Tuberculosis H37rv

TISSUE(S): Cell Suspension Culture

SUBMITTER: Andrej Benjak  

LAB HEAD: Stewart Thomas Cole

PROVIDER: PXD000698 | Pride | 2018-08-29

REPOSITORIES: Pride