Cdc13 (cyclin B) is degraded by autophagy under sulfur depletion in fission yeast

• Published in: Autophagy reports 2022-12, Vol.1 (1), p.51-64
• Main Authors: Ohtsuka, Hokuto, Hatta, Yoshiko, Hayashi, Kana, Shimasaki, Takafumi, Otsubo, Yoko, Ito, Yurika, Tsutsui, Yu, Hattori, Nobutake, Yamashita, Akira, Murakami, Hiroshi, Aiba, Hirofumi
• Format: Article
• Language: English
• Subjects: autophagy; cyclin; ecl1-family gene; fission yeast; torc1
• ISSN: 2769-4127; 2769-4127
• DOI: 10.1080/27694127.2022.2047442

Cyclins are degraded by the anaphase-promoting complex/cyclosome (APC/C)-mediated proteasome in normal mitosis. We showed that Cdc13 (cyclin B) is also degraded by macroautophagy/autophagy in sulfur-deficient fission yeast. Sulfur depletion causes G2 cell cycle arrest and reduces cell size; however, the associated mechanisms are unknown. We found that autophagy is required for the degradation of Cdc13, which is associated with cell cycle arrest and reduced cell size, by examining cell morphology under sulfur depletion. The analysis of the Cdc13-GFP fusion protein supported the conclusion that Cdc13 is degraded by autophagy. Moreover, we showed that sulfur depletion results in the inactivation of target of rapamycin complex 1 (TORC1) activity via Ecl1-family proteins. Our data indicate that the cyclin is degraded by two different systems: APC/C-mediated proteasome and autophagy. The latter is induced under nutrient-depleted situations. This switch in degradation systems will contribute to appropriate cell cycle arrest when resources are depleted. Abbreviations: APC, anaphase-promoting complex; CDK, cyclin-dependent kinase; DB, destruction box; EMM, Edinburgh minimal medium; GFP, green fluorescent protein; PCR, polymerase chain reaction; TOR, target of rapamycin; UPS, ubiquitin-proteasome system