4.7 Article

BES1/BZR1 Homolog 3 cooperates with E3 ligase AtRZF1 to regulate osmotic stress and brassinosteroid responses in Arabidopsis

Journal

JOURNAL OF EXPERIMENTAL BOTANY
Volume 72, Issue 2, Pages 636-653

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/jxb/eraa458

Keywords

AtRZF1; BEH3; brassinosteroid; osmotic stress; pca mutant; ROS

Categories

Funding

  1. Next-Generation BioGreen21 (SSAC) - Rural Development Administration, Republic of Korea [PJ013171]
  2. New Breeding Technology program - Rural Development Administration, Republic of Korea [PJ01477701]

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The study found that the Arabidopsis intergenic enhancer double mutant pca41 plays important roles in proline and brassinosteroid signaling pathways, potentially negatively regulating BEH3 proton responses via the BR signaling pathway. This suggests that AtRZF1 and BEH3 may play important roles in osmotic stress response through ubiquitination and BR signaling.
Proline (Pro) metabolism plays important roles in protein synthesis, redox balance, and abiotic stress response. However, it is not known if cross-talk occurs between proline and brassinosteroid (BR) signaling pathways. Here, an Arabidopsis intergenic enhancer double mutant, namely proline content alterative 41 (pca41), was generated by inserting a T-DNA tag in the Arabidopsis thaliana ring zinc finger 1 (atrzf1) mutant background. pca41 had a T-DNA inserted at the site of the gene encoding BES1/BZR1 Homolog 3 (BEH3). pca41 has a drought-insensitive phenotype that is stronger than atrzf1 under osmotic stress, including high Pro accumulation and decreased amounts of reactive oxygen species. Analysis of physiological, genetic, and molecular networks revealed that negative regulation of BEH3 during abiotic stress was linked to the BR signaling pathway. Our data also suggest that AtRZF1, an E3 ubiquitin ligase, might control osmotic stress, abscisic acid, and BR responses in a BEH3-dependent manner. Under darkness, pca41 displays a long hypocotyl phenotype, which is similar to atrzf1 and beh3, suggesting that BEH3 acts in the same pathway as AtRZF1. Overexpression of BEH3 results in an osmotic stress-sensitive phenotype, which is reversed by exogenous BR application. Taken together, our results indicate that AtRZF1 and BEH3 may play important roles in the osmotic stress response via ubiquitination and BR signaling.

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