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Reduced Usage of GLS Intronic Polyadenylation Promotes Cellular Senescence.

Xueping Li1, Yuxin Li1, Dong Ding1

  • 1State Key Laboratory of Genetic Engineering, National Clinical Research Center for Aging and Medicine, Collaborative Innovation Center of Genetics and Development, Center for Evolutionary Biology, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Sciences, Huashan Hospital, Human Phenome Institute, Fudan University, Shanghai, 200438 China.

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Summary

Intronic polyadenylation of the Glutaminase gene creates Glutaminase C, a protein that regulates cellular senescence. This finding reveals a new role for intronic polyadenylation in aging and cancer.

Keywords:
Alternative Polyadenylation (APA)Cellular SenescenceGlutaminaseIntronic PolyadenylationMitochondria

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • Alternative polyadenylation (APA) fine-tunes gene expression and impacts biological processes.
  • Intronic polyadenylation is a prevalent but poorly understood APA mechanism.
  • The biological functions of intronic polyadenylation remain largely unexplored.

Purpose of the Study:

  • To investigate the biological function of intronic polyadenylation in the Glutaminase gene (GLS).
  • To explore the role of the GLS intronic polyadenylation isoform, Glutaminase C (GAC), in cellular senescence.

Main Methods:

  • Analysis of GLS intronic polyadenylation in human and mouse senescence models.
  • Localization studies of GAC protein.
  • Investigating the effects of GAC downregulation on cellular senescence, ROS levels, and ATP synthesis.
  • Identifying regulatory factors, such as CPSF6, involved in GAC expression.

Main Results:

  • Reduced usage of the GLS intronic polyadenylation site was observed in senescence models.
  • Downregulation of GAC induced cellular senescence, characterized by increased ROS and decreased ATP.
  • CPSF6 was identified as a factor binding to GAC to regulate its expression.
  • A CPSF6-GAC signaling axis was confirmed to regulate cellular senescence.

Conclusions:

  • Intronic polyadenylation of GLS generates GAC, which plays a regulatory role in cellular senescence.
  • This study demonstrates a novel function for intronic polyadenylation in regulating cellular senescence, extending understanding of its biological roles.