| Literature DB >> 28399398 |
Trevor M Nolan1, Benjamin Brennan1, Mengran Yang2, Jiani Chen1, Mingcai Zhang3, Zhaohu Li3, Xuelu Wang2, Diane C Bassham1, Justin Walley4, Yanhai Yin5.
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.Entities:
Keywords: brassinosteroid; drought response; growth and stress responses; kinases; selective autophagy; signal transduction; transcription factors; ubiquitin receptor
Mesh:
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Year: 2017 PMID: 28399398 PMCID: PMC5720862 DOI: 10.1016/j.devcel.2017.03.013
Source DB: PubMed Journal: Dev Cell ISSN: 1534-5807 Impact factor: 12.270