A mutation in anti-sigma factor MAB_3542c may be responsible for tigecycline resistance in Mycobacterium abscessus

J Med Microbiol. 2018 Dec;67(12):1676-1681. doi: 10.1099/jmm.0.000857. Epub 2018 Oct 23.

Abstract

In this study, we characterized 7C, a spontaneous mutant selected from tigecycline-susceptible Mycobacterium abscessus ATCC 19977. Whole-genome sequencing (WGS) was used to identify possible resistance determinants in this mutant. Compared to the wild-type, 7C demonstrated resistance to tigecycline as well as cross-resistance to imipenem, and had a slightly retarded growth rate. WGS and subsequent biological verifications showed that these phenotypes were caused by a point mutation in MAB_3542c, which encodes an RshA-like protein. In Mycobacterium tuberculosis, RshA is an anti-sigma factor that negatively regulates the heat/oxidative stress response mechanisms. The MAB_3542c mutation may represent a novel determinant of tigecycline resistance. We hypothesize that this mutation may dysregulate the stress-response pathways which have been shown to be linked to antibiotic resistance in previous studies.

Keywords: MAB_3542c; Mycobacterium abscessus; RshA; anti-sigma factor; tigecycline resistance.

MeSH terms

  • Anti-Bacterial Agents / pharmacology*
  • Bacterial Proteins / genetics
  • Bacterial Proteins / metabolism*
  • Drug Resistance, Bacterial*
  • Gene Expression Regulation, Bacterial
  • Genome, Bacterial
  • Microbial Sensitivity Tests
  • Mutation
  • Mycobacterium abscessus / drug effects*
  • Mycobacterium abscessus / genetics*
  • Tigecycline / pharmacology*

Substances

  • Anti-Bacterial Agents
  • Bacterial Proteins
  • Tigecycline