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Updated: Jan 26, 2026

Methyl-binding DNA capture Sequencing for Patient Tissues
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PRMT7 methylates and suppresses GLI2 binding to SUFU thereby promoting its activation

Tuan Anh Vuong1, Hyeon-Ju Jeong1, Hye-Jin Lee1

  • 1Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea.

Cell Death and Differentiation
|April 20, 2019
PubMed

Insights

Protein arginine methyltransferase 7 (PRMT7) prevents cellular senescence by activating Sonic hedgehog (Shh) signaling. PRMT7 methylates GLI2, enhancing Shh pathway activity and inhibiting senescence, offering new insights into aging and disease.

Area of Science:

  • Cellular and Molecular Biology
  • Epigenetics
  • Developmental Biology

Background:

  • Cellular senescence is linked to aging and age-related diseases.
  • Sonic hedgehog (Shh) signaling inhibits cellular senescence, but mechanisms are unclear.

Purpose of the Study:

  • To elucidate the mechanism by which Shh signaling is activated to prevent cellular senescence.
  • To investigate the role of Protein arginine methyltransferase 7 (PRMT7) in Shh signaling and senescence.

Main Methods:

  • Utilized mouse embryonic fibroblasts (MEFs) with and without PRMT7.
  • Assessed cellular senescence markers (p16, p21) and Shh signaling activity.
  • Investigated PRMT7 interaction with GLI2 using methylation assays and reporter gene activity.

Main Results:

  • PRMT7 deficiency led to premature senescence and increased cell cycle inhibitors.
  • PRMT7 promotes Shh signaling via GLI2 methylation.
  • PRMT7-mediated methylation of GLI2 at R225/R227 disrupts SUFU binding, promoting GLI2 nuclear accumulation.

Conclusions:

  • PRMT7 activates Shh signaling by methylating GLI2, which interferes with SUFU binding.
  • This mechanism inhibits cellular senescence, suggesting PRMT7 as a potential target for aging and related diseases.

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