Research
Dot1 triggers a conserved ribophagy signal to govern ribosome quality and longevity by methylating Rpl12
Molecular Cell · By Yuting Chen, Yuzhuo Shao, Yibin Pan, Xuechun Guo, Pengwei Zhao, Yi Zhang, Yuzhi Wang, Xiaodi Liu, Shuang Lei, Weijing Yao, Mingzhu Fan, Shan Feng, Fang Xu, Ying Xing, Wei Liu, Qiming Sun, Wei Zou, Yunpeng Huang & Cong Yi ·
The Brief
- Chen et al. report that Dot1-mediated methylation of the ribosomal protein Rpl12 acts as an autophagic signal that directs selective ribosome degradation (ribophagy).
- The mechanism links nutrient sensing to ribosome quality control.
- The authors describe the pathway as conserved and linked to cellular stress adaptation, tissue homeostasis and longevity.
Why it matters
It identifies a specific molecular tag that marks ribosomes for selective autophagic removal, connecting nutrient signalling to ribosome quality and to longevity, which is relevant to aging and stress biology research.
Who’s affected
- cell and molecular biologists
- aging and stress-response researchers
- #ribophagy
- #ribosome-quality-control
- #autophagy
- #protein-methylation
- #longevity
Chen et al. show Dot1-mediated Rpl12 methylation as a conserved autophagic “eat-me” signal that directs selective ribosome degradation. By coupling nutrient sensing to ribosome quality control, this mechanism promotes cellular adaptation to stress, maintains tissue homeostasis…
Timeline
Study published in Molecular Cell
cell.com
Dot1 triggers a conserved ribophagy signal to govern ribosome quality and longevity by methylating Rpl12