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. RNA-seq data for M. abscessus ATCC19977 in the presence and absence of rifampicin

本研究通过RNA测序（RNA sequencing）证实，将脓肿分枝杆菌（Mycobacterium abscessus, M. abscessus）暴露于亚致死剂量的利福平（RIF）时，其Mab_helR基因的表达量上调约25倍；Mab_helR的同基因缺失突变株对利福平（RIF）与利福布汀（RBT）表现出高敏感性，而Mab_helR的过表达可使结核分枝杆菌（Mycobacterium tuberculosis, M. tuberculosis）获得利福平耐受性，这表明Mab_helR是诱导型利福平及利福布汀耐药性的关键决定因子。本数据集涵盖利福平存在与缺失条件下脓肿分枝杆菌ATCC 19977的RNA测序（RNA-seq）数据。