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METTL14-Mediated Inhibition of Apoptosis via the MAPK and PI3K/AKT Pathways Promotes Chlamydia trachomatis

Wenbo Lei1, Yewei Yang1, Yating Wen1

  • 1Institute of Pathogenic Biology, Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, Department of Clinical Laboratory Medicine, Institution of Microbiology and Infectious Diseases, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang 421001, China.

Microorganisms
|May 27, 2026
PubMed

Insights

Chlamydia trachomatis infection relies on host METTL14 enzyme activity. This enzyme manipulates host signaling pathways, promoting bacterial reproduction and inhibiting apoptosis, offering potential therapeutic targets.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Host-Pathogen Interactions

Background:

  • * *Chlamydia trachomatis* manipulates host cell signaling for intracellular growth.
  • * N6-methyladenosine (m6A) RNA modification regulates pathogen and host processes.
  • * The role of m6A in *C. trachomatis* intracellular development is unclear.

Purpose of the Study:

  • * To investigate the impact of m6A modification on *C. trachomatis* intracellular reproduction.
  • * To identify host factors involved in m6A-mediated regulation of chlamydial growth.
  • * To elucidate the mechanisms by which *C. trachomatis* utilizes host pathways.

Main Methods:

  • * Analysis of host cell mRNA m6A methylation profiles post-*C. trachomatis* infection.
  • * Gene silencing of the host methyltransferase-like (METTL) enzyme METTL14.
  • * Investigation of MAPK and PI3K/AKT signaling pathway activation.
  • * Assessment of *C. trachomatis* reproduction efficiency and host cell apoptosis.

Main Results:

  • * *C. trachomatis* infection significantly alters host mRNA m6A modification patterns.
  • * Host METTL14 is essential for efficient intracellular reproduction of *C. trachomatis*.
  • * METTL14 activation by *C. trachomatis* promotes MAPK and PI3K/AKT signaling.
  • * METTL14-mediated signaling inhibits host cell apoptosis, facilitating bacterial growth.

Conclusions:

  • * METTL14 is a critical host factor enabling *C. trachomatis* intracellular reproduction.
  • * *C. trachomatis* hijacks METTL14 to modulate host signaling pathways, evade apoptosis, and promote its growth.
  • * Targeting METTL14 presents a potential therapeutic strategy against *Chlamydia trachomatis* infections.
Keywords:
Chlamydia trachomatisMAPKMETTL14PI3K/AKTapoptosism6A modification

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