Mycobacterium abscessus HelR interacts with RNA Polymerase to confer intrinsic rifamycin resistance

Using RNA sequencing we show that exposure of M. abscessus to sublethal doses of RIF results in ~25-fold upregulation of Mab_helR; an isogenic deletion mutant of Mab_helR is hypersensitive to RIF and RBT, and over-expression of Mab_helR confers RIF tolerance in M. tuberculosis, implying that Mab_helR constitutes a significant determinant of inducible RIF and RBT resistance. Overall design: RNA-seq data for M. abscessus ATCC19977 in the presence and absence of rifampicin