PUBLICATION

Mycobacterium PPE31 Contributes to Host Cell Death

Authors
Feng, S., Hong, Z., Zhang, G., Li, J., Tian, G.B., Zhou, H., Huang, X.
ID
ZDB-PUB-210501-49
Date
2021
Source
Frontiers in cellular and infection microbiology   11: 629836 (Journal)
Registered Authors
Keywords
JNK signaling, Mycobacterium tuberculosis, PPE31, cell death, virulence factors
MeSH Terms
  • Animals
  • Cell Death
  • Mycobacterium Infections, Nontuberculous*
  • Mycobacterium marinum*
  • Mycobacterium tuberculosis*
  • Virulence
  • Zebrafish
PubMed
33928042 Full text @ Front Cell Infect Microbiol
Abstract
Genome scale mutagenesis identifies many genes required for mycobacterial infectivity and survival, but their contributions and mechanisms of action within the host are poorly understood. Using CRISPR interference, we created a knockdown of ppe31Mm gene in Mycobacterium marinum (M. marinum), which reduced the resistance to acid medium. To further explore the function of PPE31, the ppe31 mutant strain was generated in M. marinum and Mycobacterium tuberculosis (M. tuberculosis), respectively. Macrophages infected with the ppe31Mm mutant strain caused a reduced inflammatory mediator expressions. In addition, macrophages infected with M. marinum Δppe31Mm had decreased host cell death dependent on JNK signaling. Consistent with these results, deletion of ppe31Mtb from M. tuberculosis increased the sensitivity to acid medium and reduced cell death in macrophages. Furthermore, we demonstrate that both ppe31 mutants from M. marinum and M. tuberculosis resulted in reduced survival in macrophages, and the survivability of M. marinum was deceased in zebrafish due to loss of ppe31Mm . Our findings confirm that PPE31 as a virulence associated factor that modulates innate immune responses to mycobacterial infection.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping