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Yeast MED2 is involved in the endoplasmic reticulum stress response and modulation of the replicative lifespan

Wei Zhao1, Jia-Xin Liu1, Fang Guo1

  • 1Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, Institute of Aging Research, Guangdong Medical University, Dongguan, 523808, China; Institute of Biochemistry and Molecular Biology, Guangdong Medical University, Dongguan, 523808, China.

Mechanisms of Ageing and Development
|October 12, 2020
PubMed

Insights

The MED2 protein regulates endoplasmic reticulum (ER) stress and lifespan in yeast. Deleting MED2 shortens lifespan and increases ER stress sensitivity, while overexpressing it enhances resistance and longevity.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • The Mediator complex subunit MED2 (YDL005C) in Saccharomyces cerevisiae is known to regulate gene transcription.
  • Previous studies indicated MED2's altered localization under hypoxic stress, but its specific functions remained undescribed.

Purpose of the Study:

  • To investigate the role of MED2 in endoplasmic reticulum (ER) stress response and replicative lifespan (RLS) in yeast.
  • To elucidate the molecular mechanisms underlying MED2's function in cellular homeostasis.

Main Methods:

  • Yeast genetics: deletion and overexpression of MED2.
  • Phenotypic analysis: tunicamycin (TM) sensitivity assays, replicative lifespan determination.
  • Mitochondrial function assessment: ROS levels and membrane potential.
  • Molecular analysis: IRE1-HAC1 pathway activation and unfolded protein response (UPR) activity.

Main Results:

  • MED2 deletion resulted in tunicamycin sensitivity, shortened RLS, increased reactive oxygen species (ROS), and mitochondrial hyperpolarization.
  • MED2 overexpression conferred tunicamycin resistance and extended RLS, dependent on the IRE1-HAC1 pathway.
  • MED2 deficiency led to enhanced ER unfolded protein response (UPR) activity compared to wild-type cells.

Conclusions:

  • MED2 plays a crucial role in managing ER stress and extending replicative lifespan in Saccharomyces cerevisiae.
  • MED2 acts as a novel regulator of ER homeostasis and longevity, potentially through modulation of the UPR pathway.
Keywords:
Endoplasmic reticulumMED2Replicative lifespan

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