| Autor: |
Hao W; Department of Oncology, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, China.; Cancer Research Institute, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China., Dian M; Department of Thoracic Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.; Institute of Comparative Medicine & Laboratory Animal Center, Southern Medical University, Guangzhou, China., Wang J; Cancer Research Institute, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China., Sun Y; Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China., Xiao D; Cancer Research Institute, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.; Institute of Comparative Medicine & Laboratory Animal Center, Southern Medical University, Guangzhou, China. |
| Abstrakt: |
Mcroautophagy/autophagy plays an important role in maintaining homeostasis during nutrient starvation. However, whether epitranscriptomic events are involved in this process remains unclear. Our recent findings suggest that m 6 A reader YTHDF3 has an essential role in autophagy induction. Elevated m 6 A modifications installed by METTL3 enable YTHDF3 to promote autophagosome formation and lysosomal function upon nutrient deficiency. This is due to YTHDF3 binding to the m 6 A modifications at the coding DNA sequence (CDS) and 3' untranslated region (UTR) around the stop codon of Foxo3 mRNA, recruiting EIF3A and EIF4B to facilitate FOXO3 translation, thus boosting autophagy. In this punctum, we discuss our finding for how YTHDF3 responds to nutrient starvation to promote autophagy flux, providing insights into RNA post-transcriptional modifications linking nutrient cues to autophagic upcycling. |
