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Exploring the Arginine Methylome by Nuclear Magnetic Resonance Spectroscopy
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The protein arginine methyltransferase PRMT9 attenuates MAVS activation through arginine methylation

Xuemei Bai1, Chao Sui1, Feng Liu1

  • 1Key Laboratory of Infection and Immunity of Shandong Province & Department of Immunology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, PR China.

Nature Communications
|August 26, 2022
PubMed

Insights

Protein arginine methyltransferase 9 (PRMT9) prevents spontaneous MAVS aggregation, a key step in innate immunity. This methylation modification by PRMT9 maintains immune homeostasis by keeping MAVS inactive until viral infection.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cellular Signaling

Background:

  • The adaptor protein MAVS aggregates to initiate the innate antiviral immune response.
  • Spontaneous MAVS aggregation can trigger autoimmune diseases, necessitating regulatory mechanisms.
  • The precise molecular control preventing MAVS aggregation in resting cells remained unclear.

Purpose of the Study:

  • To elucidate the mechanism preventing MAVS spontaneous aggregation in resting cells.
  • To identify the specific protein modifications regulating MAVS activity.
  • To understand how MAVS aggregation is controlled for immune homeostasis.

Main Methods:

  • Investigated the interaction between PRMT9 and MAVS.
  • Analyzed the catalytic activity of PRMT9 on MAVS, focusing on arginine methylation.
  • Examined MAVS aggregation and activation status in resting and virus-infected cells.

Main Results:

  • Protein arginine methyltransferase 9 (PRMT9) directly targets MAVS.
  • PRMT9 catalyzes arginine methylation of MAVS at Arg41 and Arg43, inhibiting its aggregation.
  • Upon viral infection, PRMT9 dissociates from mitochondria, allowing MAVS aggregation and immune activation.

Conclusions:

  • Arginine methylation of MAVS by PRMT9 is a critical post-translational modification for preventing autoimmune responses.
  • This regulatory mechanism ensures MAVS remains inactive in physiological conditions, maintaining innate immune homeostasis.
  • Understanding PRMT9-MAVS interaction offers insights into controlling inflammatory and autoimmune diseases.

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