mTORC1-chaperonin CCT signaling regulates m 6 A RNA methylation to suppress autophagy
Abstract
N6-methyladenosine (m 6 A) is the most prevalent modification in eukaryotic messenger RNA (mRNA) and affects RNA metabolism including splicing, stability, and translation. The m 6 A methyltransferase complex (MTC) is responsible for generating the m 6 A modifications in mRNA; however, the regulation of m 6 A modification is still unclear. We have identified Mechanistic Target of Rapamycin Complex 1 (mTORC1) as a key regulator of MTC and demonstrate that mTORC1 can stabilize MTC via activation of the chaperonin CCT complex and upregulate m 6 A modification to promote the degradation of ATG transcripts. Thus, our study unveils an mTORC1-signaling cascade that regulates m 6 A RNA methylation and autophagy.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Mar 01, 2021
- Source ID
- 10.1073/pnas.2021945118
Entities
People
- Ah-Ram Kim
- Cathleen Li
- Chiwei Xu
- Gina Lee
- Hong-wen Tang
- John Blenis
- John M Asara
- Jui-hsia Weng
- Jun Xu
- Lei Gu
- Min En Cheng
- Norbert Perrimon
- Richard Binari
- Sungyun Cho
- Wen Xing Lee
- Yanhui Hu
- Zhangfei Shen
Organizations
- Beth Israel Deaconess Medical Center
- Boston Children's Hospital
- Duke–NUS Medical School
- Harvard Medical School
- Howard Hughes Medical Institute
- Human Frontier Science Program
- Max Planck Institute for Heart and Lung Research
- National Institutes of Health
- National Science and Technology Council
- The Starr Foundation
- United States Department of Defense
- University of California, Irvine School of Medicine