MvaT binds to the P exsC promoter to repress the type III secretion system in Pseudomonas aeruginosa

Front Cell Infect Microbiol. 2023 Nov 6:13:1267748. doi: 10.3389/fcimb.2023.1267748. eCollection 2023.

Abstract

Pseudomonas aeruginosa is an opportunistic human pathogen capable of causing a variety of acute and chronic infections. Its type III secretion system (T3SS) plays a critical role in pathogenesis during acute infection. ExsA is a master regulator that activates the expression of all T3SS genes. Transcription of exsA is driven by two distinct promoters, its own promoter PexsA and its operon promoter PexsC. Here, in combination with a DNA pull-down assay and mass spectrometric analysis, we found that a histone-like nucleoid-structuring (H-NS) family protein MvaT can bind to the PexsC promoter. Using EMSA and reporter assays, we further found that MvaT directly binds to the PexsC promoter to repress the expression of T3SS genes. The repression of MvaT on PexsC is independent of ExsA, with MvaT binding to the -429 to -380 bp region relative to the transcription start site of the exsC gene. The presented work further reveals the complex regulatory network of the T3SS in P. aeruginosa.

Keywords: MvaT; P. aeruginosa; PexsA; PexsC; T3SS; transcriptional regulation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bacterial Proteins / metabolism
  • Gene Expression Regulation, Bacterial
  • Humans
  • Promoter Regions, Genetic
  • Pseudomonas aeruginosa / genetics
  • Pseudomonas aeruginosa / metabolism
  • Trans-Activators* / genetics
  • Type III Secretion Systems* / genetics
  • Type III Secretion Systems* / metabolism

Substances

  • Type III Secretion Systems
  • Trans-Activators
  • Bacterial Proteins

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by the National Key Research and Development Project of China (2021YFE0201300 and 2021YFE0101700), the Science and Technology Committee of Tianjin (22JCYBJC00790 and 22JCYBJC00560), the National Science Foundation of China (31970179, 31970680, 32170177, 82061148018, and 32170199), and the Fundamental Research Funds for the Central Universities, Nankai University (63231048 and 63231047). The funders had no role in the study design, data collection and interpretation, or the decision to submit the work for publication.