| Literature DB >> 35695778 |
Longyun Xiao1,2, Yiyuan Shi1, Rong Wang1, Yu Feng1, Lesheng Wang1, Hongsheng Zhang1, Xingyu Shi1, Guangqin Jing1, Ping Deng1, Tengzhao Song1, Wen Jing1,3, Wenhua Zhang1,3.
Abstract
Sodium (Na+) and potassium (K+) homeostasis is essential for plant survival in saline soils. A member of the High-Affinity K+ Transporter (HKT) family in rice (Oryza sativa), OsHKT1;1, is a vital regulator of Na+ exclusion from shoots and is bound by a MYB transcription factor (OsMYBc). Here, we generated transgenic rice lines in the oshkt1;1 mutant background for genetic complementation using genomic OsHKT1;1 containing a native (Com) or mutated (mCom) promoter that cannot be bound by OsMYBc. In contrast to wild-type (WT) or Com lines, the mCom lines were not able to recover the salt-sensitive phenotype of oshkt1;1. The OsMYBc-overexpressing plants were more tolerant to salt stress than WT plants. A yeast two-hybrid screen using the OsMYBc N-terminus as bait identified a rice MYBc stress-related RING finger protein (OsMSRFP). OsMSRFP is an active E3 ligase that ubiquitinated OsMYBc in vitro and mediated 26S proteasome-mediated degradation of OsMYBc under semi-in vitro and in vivo conditions. OsMSRFP attenuated OsMYBc-mediated OsHKT1;1 expression, and knockout of OsMSRFP led to rice salt tolerance. These findings uncover a regulatory mechanism of salt response that fine-tunes OsHKT1;1 transcription by ubiquitination of OsMYBc. © American Society of Plant Biologists 2022. All rights reserved. For permissions, please email: journals.permissions@oup.com.Entities:
Mesh:
Substances:
Year: 2022 PMID: 35695778 PMCID: PMC9434319 DOI: 10.1093/plphys/kiac283
Source DB: PubMed Journal: Plant Physiol ISSN: 0032-0889 Impact factor: 8.005