Selective Autophagy of BES1 Mediated by DSK2 Balances Plant Growth and Survival

Publication date: 10 April 2017
Source:Developmental Cell, Volume 41, Issue 1
Author(s): Trevor M. Nolan, Benjamin Brennan, Mengran Yang, Jiani Chen, Mingcai Zhang, Zhaohu Li, Xuelu Wang, Diane C. Bassham, Justin Walley, Yanhai Yin
Plants encounter a variety of stresses and must fine-tune their growth and stress-response programs to best suit their environment. BES1 functions as a master regulator in the brassinosteroid (BR) pathway that promotes plant growth. Here, we show that BES1 interacts with the ubiquitin receptor protein DSK2 and is targeted to the autophagy pathway during stress via the interaction of DSK2 with ATG8, a ubiquitin-like protein directing autophagosome formation and cargo recruitment. Additionally, DSK2 is phosphorylated by the GSK3-like kinase BIN2, a negative regulator in the BR pathway. BIN2 phosphorylation of DSK2 flanking its ATG8 interacting motifs (AIMs) promotes DSK2-ATG8 interaction, thereby targeting BES1 for degradation. Accordingly, loss-of-function dsk2 mutants accumulate BES1, have altered global gene expression profiles, and have compromised stress responses. Our results thus reveal that plants coordinate growth and stress responses by integrating BR and autophagy pathways and identify the molecular basis of this crosstalk.

Graphical abstract

Teaser

Plants must carefully balance growth and survival. Nolan et al. show that brassinosteroid-regulated and growth-promoting transcription factor BES1 is degraded during drought and starvation stress via DSK2, a phosphorylation-regulated selective autophagy receptor, thus revealing a mechanism that allows plants to shut down growth during unfavorable conditions.


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