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Nat Commun. 2017 Feb 24;8:14573. doi: 10.1038/ncomms14573.

RD26 mediates crosstalk between drought and brassinosteroid signalling pathways.

Author information

1
Department of Genetics, Development and Cell Biology, Iowa State University, Ames, Iowa 50011, USA.
2
Department of Agronomy, Iowa State University, Ames, Iowa 50011, USA.
3
Data2Bio LLC, Ames, Iowa 50011-3650, USA.
4
Department of Molecular Biology, Massachusetts General Hospital and Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA.
5
Institute of Genetics, Chinese Academy of Sciences, Beijing 100101, China.
6
State Key Laboratory of Plant Physiology and Biochemistry, Department of Agronomy, College of Agronomy and Biotechnology, China Agricultural University, Beijing 100193, China.
7
School of Biology, Georgia Institute of Technology, Atlanta, Georgia 30332, USA.
8
School of Computational Science and Engineering, Georgia Institute of Technology, Atlanta, Georgia 30332, USA.

Abstract

Brassinosteroids (BRs) regulate plant growth and stress responses via the BES1/BZR1 family of transcription factors, which regulate the expression of thousands of downstream genes. BRs are involved in the response to drought, however the mechanistic understanding of interactions between BR signalling and drought response remains to be established. Here we show that transcription factor RD26 mediates crosstalk between drought and BR signalling. When overexpressed, BES1 target gene RD26 can inhibit BR-regulated growth. Global gene expression studies suggest that RD26 can act antagonistically to BR to regulate the expression of a subset of BES1-regulated genes, thereby inhibiting BR function. We show that RD26 can interact with BES1 protein and antagonize BES1 transcriptional activity on BR-regulated genes and that BR signalling can also repress expression of RD26 and its homologues and inhibit drought responses. Our results thus reveal a mechanism coordinating plant growth and drought tolerance.

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