Long‐term abscisic acid promotes golden2‐like1 degradation through constitutive photomorphogenic 1 in a light intensity‐dependent manner to suppress chloroplast development

Abiotic stress, a serious threat to plants, occurs for extended periods in nature. Abscisic acid (ABA) plays a critical role in abiotic stress responses in plants. Therefore, stress responses mediated by ABA have been studied extensively, especially in short‐term responses. However, long‐term stress responses mediated by ABA remain largely unknown. To elucidate the mechanism by which plants respond to prolonged abiotic stress, we used long‐term ABA treatment that activates the signalling against abiotic stress such as dehydration and investigated mechanisms underlying the responses. Long‐term ABA treatment activates constitutive photomorphogenic 1 (COP1). Active COP1 mediates the ubiquitination of golden2‐like1 (GLK1) for degradation, contributing to lowering expression of photosynthesis‐associated genes such as glutamyl‐tRNA reductase (HEMA1) and protochlorophyllide oxidoreductase A (PORA), resulting in the suppression of chloroplast development. Moreover, COP1 activation and GLK1 degradation upon long‐term ABA treatment depend on light intensity. Additionally, plants with COP1 mutation or exposed to higher light intensity were more sensitive to salt stress. Collectively, our results demonstrate that long‐term treatment of ABA leads to activation of COP1 in a light intensity‐dependent manner for GLK1 degradation to suppress chloroplast development, which we propose to constitute a mechanism of balancing normal growth and stress responses upon the long‐term abiotic stress. Here, we show that long‐term ABA promotes GLK1 degradation through COP1 to suppress chloroplast development dependent on light intensity, revealing that balancing normal growth and stress response in long‐term stress.