Ideal plant architecture and drought tolerance are important determinants of yield potential in rice (Oryza sativa). Here, we found that OsNAC016, a rice stress-responsive NAC transcription factor, functions as a… Click to show full abstract
Ideal plant architecture and drought tolerance are important determinants of yield potential in rice (Oryza sativa). Here, we found that OsNAC016, a rice stress-responsive NAC transcription factor, functions as a regulator in the crosslink between BR-mediated plant architecture and ABA-regulated drought responses. The loss-of-function mutant osnac016 exhibited erect leaves and shortened internodes, but OsNAC016-overexpressing plants had opposite phenotypes. Further investigation revealed that OsNAC016 regulated the expression of the brassinosteroid biosynthesis gene D2 by binding to its promoter. Moreover, OsNAC016 interacted with and was phosphorylated by GSK3/SHAGGY-LIKE KINASE2 (GSK2), a negative regulator in the BR pathway. Meanwhile, the mutant osnac016 had improved drought stress tolerance, supported by a decreased water loss rate and enhanced stomatal closure in response to exogenous ABA, but OsNAC016-overexpressing plants showed attenuated drought tolerance and reduced ABA sensitivity. Further, OSMOTIC STRESS/ABA-ACTIVATED PROTEIN KINASE8 (SAPK8) phosphorylated OsNAC016 and reduced its stability. The ubiquitin/26S proteasome system is an important degradation pathway of OsNAC016 via the interaction with PLANT U-BOX PROTEIN43 (OsPUB43) that mediates the ubiquitination of OsNAC016. Notably, RNA-sequencing analysis revealed global roles of OsNAC016 in promoting BR-mediated gene expression and repressing ABA-dependent drought-responsive gene expression, which was confirmed by ChIP-qPCR analysis. Our findings establish that OsNAC016 is positively involved in BR-regulated rice architecture, negatively modulates ABA-mediated drought tolerance, and is regulated by GSK2, SAPK8, and OsPUB43 through post-translational modification. Our data provide insights into how plants balance growth and survival by coordinately regulating the growth-promoting signaling pathway and response under abiotic stresses.
               
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