Ethylene antagonizes ABA and inhibits stomatal closure and chilling tolerance in rice.

Abstract

Chilling stress restricts the geographical distribution of rice and severely impacts its growth and development, ultimately reducing both yield and quality. The plant hormone ethylene is involved in plant stress responses; however, its role in rice chilling tolerance has not been thoroughly explored. This study reveals that ethylene negatively regulates chilling tolerance in rice by antagonizing the chilling tolerance-promoting effects of abscisic acid (ABA). Treatment with ethylene or its biosynthetic precursor, 1-aminocyclopropane-1-carboxylic acid (ACC), results in a reduced survival rate after chilling and delayed stomatal closure in response to chilling. There are two ethylene signaling-related Raf-like protein kinases, OsCTR1 and OsCTR2, which have overlapping functions in ethylene signaling; their loss-of-function mutants exhibit constitutive ethylene responses. The ctr1 ctr2 double mutant displays lower survival rates and slower stomatal closure under chilling stress compared to the wild type. In contrast, ABA treatment significantly enhances the survival rate of the wild type under chilling stress and promotes stomatal closure in response to chilling. Furthermore, ethylene inhibits the effects of ABA on chilling tolerance and stomatal closure. The ctr1 ctr2 double mutant fails to respond to external ABA treatment regarding stomatal closure and increased survival rate under chilling stress. In conclusion, our findings suggest that ethylene negatively regulates chilling tolerance in rice by inhibiting ABA-induced stomatal closure through the action of OsCTR1 and OsCTR2.