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

Abstract

Chilling stress restricts the geographical distribution of rice and severely affects its growth and development, ultimately reducing both yield and quality. The plant hormone ethylene is involved in 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 tolerance-promoting effects of abscisic acid (ABA). Treatment with ethylene or its biosynthetic precursor, 1-aminocyclopropane-1-carboxylic acid (ACC), resulted in a reduced survival rate after chilling and delayed stomatal closure in response to chilling. There are two Raf-like protein kinases related ethylene signalling, CONSTITUTIVE TRIPLE RESPONSE1 (CTR1) and CTR2, that have overlapping functions in ethylene signalling, and their loss-of-function mutants exhibit constitutive ethylene responses. The ctr1 ctr2 double-mutant displayed lower survival rates and slower stomatal closure under chilling stress compared with the wild type. In contrast, ABA treatment significantly enhanced the survival rate of the wild type under chilling stress and promoted stomatal closure in response to chilling. Furthermore, ethylene inhibited the effects of ABA on chilling tolerance and stomatal closure. The ctr1 ctr2 double-mutant failed to respond to external ABA treatment in terms of stomatal closure and increased survival rate under chilling stress. Overall, our findings suggest that ethylene negatively regulates chilling tolerance in rice by inhibiting ABA-induced stomatal closure through the action of CTR1 and CTR2.