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Elevated WTAP promotes hyperinflammation by increasing m6A modification in inflammatory disease models.

Yong Ge1,2, Rong Chen1,2, Tao Ling1,2

  • 1Guangdong Province Key Laboratory of Pharmaceutical Functional Genes, MOE Key Laboratory of Gene Function and Regulation, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-Sen University, Guangzhou, China.

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|July 15, 2024
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High N6-methyladenosine (m6A) levels in inflammation are linked to Wilms tumor 1-associated protein (WTAP). Targeting WTAP

Keywords:
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Area of Science:

  • Molecular Biology
  • Immunology
  • Epigenetics

Background:

  • N6-methyladenosine (m6A) modification dysregulation is implicated in inflammatory diseases.
  • The precise mechanisms linking m6A to inflammation require further elucidation.

Purpose of the Study:

  • To investigate the role of Wilms tumor 1-associated protein (WTAP) in m6A modification during hyperinflammatory states.
  • To explore the therapeutic potential of targeting WTAP-mediated m6A deposition in inflammatory diseases.

Main Methods:

  • Investigated the transcriptional regulation of WTAP by p65 in hyperinflammatory conditions.
  • Analyzed the impact of WTAP overexpression on m6A levels and inflammatory responses.
  • Utilized myeloid-specific WTAP deficiency models to assess its role in sepsis and inflammatory bowel disease (IBD).

Main Results:

  • WTAP is transcriptionally regulated by p65, leading to increased m6A levels in hyperinflammation.
  • Upregulated WTAP promotes m6A deposition on inflammatory transcripts via phase separation and aggregation of the m6A writer complex.
  • Myeloid WTAP deficiency ameliorates LPS-induced sepsis and DSS-induced IBD severity.

Conclusions:

  • WTAP-driven m6A modification exacerbates proinflammatory responses.
  • Targeting WTAP phase separation to reduce global m6A levels presents a promising therapeutic strategy for hyperinflammation.
  • WTAP's role in inflammation highlights a general risk-increasing mechanism in inflammatory diseases.