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Phosphatidylcholine mediates the crosstalk between LET-607 and DAF-16 stress response pathways

Bin He1, Jie Xu1, Shanshan Pang1

  • 1School of Life Sciences, Chongqing University, Chongqing, China.

Plos Genetics
|May 20, 2021
PubMed

Insights

Suppressing the transcription factor LET-607/CREBH enhances stress resistance and extends lifespan in C. elegans by activating DAF-16. This involves sphingomyelin synthase SMS-5 and specific phosphatidylcholine levels.

Area of Science:

  • Cellular Biology
  • Genetics
  • Aging Research

Background:

  • Cellular homeostasis relies on coordinated stress response pathways.
  • Crosstalk between these pathways and its physiological impact are not well understood.

Purpose of the Study:

  • To investigate the crosstalk between stress response pathways in C. elegans.
  • To understand the role of transcription factor LET-607/CREBH in stress resistance and longevity.

Main Methods:

  • Utilized the model organism C. elegans.
  • Investigated the effects of suppressing LET-607/CREBH.
  • Analyzed DAF-16-dependent pathways.
  • Identified key molecular mediators like SMS-5 and phosphatidylcholine.

Main Results:

  • Suppression of LET-607/CREBH induces DAF-16-dependent stress responses.
  • LET-607/CREBH suppression enhances stress resistance and extends lifespan in a DAF-16-dependent manner.
  • Sphingomyelin synthase SMS-5 mediates communication between LET-607 and DAF-16 by regulating unsaturated phosphatidylcholine levels.

Conclusions:

  • Crosstalk between stress response pathways is significant for animal fitness.
  • LET-607/CREBH and specific phosphatidylcholine act as regulators of DAF-16 and longevity.

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