Auxin antagonism of ABA-induced stomatal closure in Arabidopsis requires the TIR1/AFB-AUX/IAA module and ROS suppression
Auxin inhibits ABA-induced stomatal closure, yet the underlying mechanism remains unclear. In this work we quantified 3-Indoleacetic acid (IAA) inhibition of ABA-triggered closure in Arabidopsis thaliana mutants and transgenic plants and observed that IAA inhibition of ABA-induced stomatal closure was lost or weakened in tir1-1 and axr3-1 mutants, affected in auxin perception. The same was found in aux1-7, yuc5/8/9 and pils5-2/2-5 mutants, and in YUCCA8 and PILS5 overexpressors, all altered in auxin synthesis or transport. Stomatal sensitivity to IAA was also reduced in phyB-9 and rbohd, toc1 and cca1/lhy mutants, in certain ecotypes, and in response to mild drought. H+-ATPase mutant aha2-5 showed reduced stomatal sensitivity to IAA at 22{degrees}C but not at 35{degrees}C, while high-temperature-induced stomatal opening was not affected in tir1-1. IAA also caused partial degradation of the DII-VENUS auxin reporter, and inhibited ABA-induced ROS production in guard cells. Our results show that IAA counteracts ABA signalling via the TIR1/AFB-AUX/IAA module and ROS suppression, with genetic factors and mild drought modulating the response.