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An evolutionary transcriptomics approach links CD36 to membrane remodeling in replicative senescence.

Marie Saitou1, Darleny Y Lizardo, Recep Ozgur Taskent

  • 1Department of Biological Sciences, University at Buffalo, The State University of New York, Buffalo, NY 14260, USA. omergokcumen@gmail.com.

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Cellular senescence, a key aging process, involves changes in gene expression, particularly in lipid metabolism. This study highlights CD36 as a crucial gene in senescence, impacting cell phenotypes and lipid accumulation.

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Area of Science:

  • Cellular and Molecular Biology
  • Genetics and Genomics
  • Aging Research

Background:

  • Cellular senescence, the permanent halt in cell division, plays roles in aging, cancer prevention, and development.
  • Understanding the evolutionary and biological underpinnings of senescence is crucial.

Purpose of the Study:

  • To investigate genes associated with replicative senescence using comparative RNA sequencing.
  • To explore the evolutionary conservation and functional roles of senescence-associated genes.
  • To identify specific genes and pathways involved in the senescence phenotype.

Main Methods:

  • Comparative RNA sequencing of human fibroblast cell lines at different time points.
  • Functional enrichment analysis of differentially expressed genes.
  • Analysis of gene conservation and genetic variation data.
  • CD36 gene overexpression studies.
  • Targeted lipidomics analysis.

Main Results:

  • Identified 841 and 900 core senescence-associated genes that were upregulated and downregulated, respectively.
  • Downregulated genes were enriched in cell cycle processes, while upregulated genes were linked to lipid metabolism.
  • Upregulated genes showed lower evolutionary conservation compared to downregulated genes.
  • CD36, a lipid metabolism gene, was identified as an outlier, and its overexpression induced a senescence-like phenotype.
  • Phosphatidylcholines accumulate during replicative senescence, potentially linked to CD36-mediated membrane remodeling.

Conclusions:

  • Cellular senescence involves significant alterations in gene expression, particularly in lipid metabolism.
  • CD36 plays a key role in inducing senescence phenotypes and may contribute to membrane changes.
  • The study provides insights into the evolution and biology of senescence, identifying CD36 as a potential therapeutic target.