Regulation of plant autophagy by YWHA/14-3-3 proteins.

Autophagy reports Pub Date : 2023-03-01 eCollection Date: 2023-01-01 DOI:10.1080/27694127.2023.2184015
Hua Qi, Yao Wang, Li-Juan Xie, Qing-Qi Lin, Rong-Liang Qiu
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Abstract

ATG1/ATG13, a core kinase complex regulator in the macroautophagy/autophagy machinery during autophagosome formation, is modulated in a sophisticated manner by posttranslational ubiquitination to determine proper autophagy levels in eukaryotic cells. However, the mechanisms that regulate the stability and activity of this complex remain elusive. We recently identified two negative regulators of autophagy, 14-3-3λ and 14-3-3k, that help redundantly regulate autophagy by directly associating with SINAT and ATG13s. The specific interaction between the molecular adaptors 14-3-3λ and 14-3-3κ and phosphorylated ATG13a is crucial for SINAT-mediated ubiquitination and degradation of ATG13a, and for maintenance of the ATG1-ATG13 complex. Consistent with the function of 14-3-3s in autophagy, the 14-3-3λ 14-3-3κ double mutant exhibits enhanced tolerance to nutrient deprivation with constitutive induction of autophagy. These findings demonstrate that 14-3-3λ and 14-3-3k coordinate with SINATs to regulate both the homeostasis of ATG13 phosphorylation and the induction of autophagy in plants.

YWHA/14-3-3蛋白对植物自噬的调控
ATG1/ATG13是自噬体形成过程中巨噬/自噬机制中的核心激酶复合物调节因子,通过翻译后泛素化以复杂的方式调节真核细胞中适当的自噬水平。然而,调节这种复合物的稳定性和活性的机制仍然难以捉摸。我们最近发现了两个自噬的负调控因子,14-3-3λ和14-3-3 3k,它们通过直接与SINAT和ATG13s相关来帮助冗余调节自噬。分子接头14-3-3λ和14-3-3κ与磷酸化的ATG13a之间的特异性相互作用对于sinat介导的ATG13a的泛素化和降解以及ATG1-ATG13复合物的维持至关重要。与14-3-3 -3s在自噬中的功能一致,14-3-3 -3λ 14-3-3 -3κ双突变体通过组成性诱导自噬,对营养剥夺的耐受性增强。这些发现表明,14-3-3λ和14-3-3 3k与SINATs协同调节ATG13磷酸化的稳态和植物自噬的诱导。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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