Campus Units

Genetics, Development and Cell Biology, Plant Pathology and Microbiology

Document Type

Article

Publication Version

Accepted Manuscript

Publication Date

4-10-2017

Journal or Book Title

Developmental Cell

Volume

41

Issue

1

First Page

33

Last Page

46.e7

DOI

10.1016/j.devcel.2017.03.013

Abstract

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.

Comments

This is a manuscript of an article published as Nolan, Trevor M., Benjamin Brennan, Mengran Yang, Jiani Chen, Mingcai Zhang, Zhaohu Li, Xuelu Wang, Diane C. Bassham, Justin Walley, and Yanhai Yin. "Selective autophagy of BES1 mediated by DSK2 balances plant growth and survival." Developmental cell 41, no. 1 (2017): 33-46.e7. doi: 10.1016/j.devcel.2017.03.013. Posted with permission.

Creative Commons License

Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.

Copyright Owner

Elsevier Inc.

Language

en

File Format

application/pdf

Published Version

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