Journal
AUTOPHAGY
Volume 17, Issue 7, Pages 1794-1795Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2021.1938915
Keywords
Autophagy; GATOR complex; Gcn2; RAG GTPase; TOR; TSC complex
Categories
Funding
- Japan Society for the Promotion of Science [20K06552, 19H03224]
- Takeda Science Foundation
- Grants-in-Aid for Scientific Research [19H03224, 20K06552] Funding Source: KAKEN
Ask authors/readers for more resources
The GATOR2 component Sea3 in fission yeast unexpectedly acts as part of GATOR1 to suppress TORC1. In fission yeast, GATOR1 is not required for amino acid starvation-induced TORC1 attenuation, which is mediated by the Gcn2 pathway. Absence of a nitrogen source suppresses TORC1 through GATOR1 and the Tsc1-Tsc2 complex.
Target of rapamycin complex 1 (TORC1) promotes cellular anabolism and suppresses macroautophagy/autophagy. In mammalian cells starved of amino acid, the GATOR1 complex, a negative regulator of TORC1, is released from its inhibitor GATOR2 and inactivates TORC1. We have recently identified the evolutionarily conserved GATOR2 components in fission yeast including Sea3, an ortholog of mammalian WDR59, but, unexpectedly, Sea3 acts as a part of GATOR1 to suppress TORC1. Moreover, fission yeast GATOR1 is not required for the amino-acid starvation-induced TORC1 attenuation, which is instead mediated by the Gcn2 pathway. Conversely, absence of a nitrogen source suppresses TORC1 in a manner dependent on GATOR1 as well as the Tsc1-Tsc2 complex, whose mammalian equivalent functions as a growth-factor sensitive TORC1 inhibitor. Thus, the evolutionarily conserved signaling modules are utilized differently between fission yeast and mammals to control TORC1 activity and autophagy.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available