RT Journal Article
SR Electronic
T1 Autophagy-mediated CTR1 turnover orchestrates the reciprocal interaction between autophagy and ethylene signaling
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2024.07.31.606019
DO 10.1101/2024.07.31.606019
A1 Park, Hye Lin
A1 Zhang, Weiwei
A1 Chien, Yuan-Chi
A1 Park, Chanung
A1 Yoon, Gyeong Mee
YR 2024
UL http://biorxiv.org/content/early/2024/08/01/2024.07.31.606019.abstract
AB The phytohormone ethylene and autophagy are crucial for plant adaptation to various environmental stresses, yet the integration of these signaling networks into stress responses is not fully understood. Here, we report that ethylene signaling and autophagy reciprocally regulate each other through Constitutive Triple Response 1 (CTR1), a negative regulator of ethylene signaling. Autophagy facilitates the turnover of the CTR1 protein, which interacts with the key autophagy-related protein ATG8 as autophagic cargo. Impaired autophagy attenuates ethylene responses. Conversely, ethylene-insensitive mutants exhibit enhanced autophagic flux, while a constitutive ethylene response mutant is hypersensitive to carbon starvation stress, which induces autophagy. This suggests that ethylene suppresses autophagy during carbon limitation. We further elucidated that ethylene receptors with a receiver domain play a primary role in modulating autophagy, while receptor kinase activity is not essential. Our findings uncover that the autophagic control of CTR1 degradation allows reciprocal cross-regulation between autophagy and ethylene transduction cascades, optimizing stress responses and resilience.Competing Interest StatementThe authors have declared no competing interest.