Rice-specific miR1850.1 targets NPR3 to regulate cold stress response.

Abstract

Cold stress in temperate rice-production regions is responsible for yield losses of up to 30%-40%, and improving cold tolerance is a practical strategy to safeguard rice production. Numerous genes and signaling networks for cold stress have been identified in rice. However, little is known about the roles of microRNAs in the cold-stress response. Here, we find that the rice-specific pri-miR1850 and its two mature products, miR1850.1 and miR1850.2, are downregulated by cold stress. Using gain- and loss-of-function genetic approaches in elite japonica cultivars, we show that pri-miR1850 and miR1850.1 negatively regulate cold tolerance at both the young-seedling and booting stages. miR1850.1 targets and suppresses the immune gene NPR3 by mediating transcript cleavage and translational repression. Upon cold treatment, NPR3 transcripts and proteins are upregulated owing to the alleviation of miR1850.1-mediated repression and the activation of NPR3 transcription. miR1850.1 functions genetically through NPR3 in the cold-stress response. The miR1850.1-NPR3 module also controls rice disease resistance and grain yields. Our findings reveal a cold-signaling network and provide targets for the engineering of cold-tolerant japonica varieties to endure fluctuating future climates.