ABI3 regulates ABI1 function to control cell length in primary root elongation zone.

Abstract

Post-embryonic primary root growth is effectively an interplay of several hormone signalling pathways. Here, we show that the ABA-responsive transcription factor ABI3 controls primary root growth through the regulation of JA signalling molecule JAZ1 along with ABA-responsive factor ABI1. In the absence of ABI3, the primary root elongation zone is shortened with significantly reduced cell length. Expression analyses and ChIP-based assays indicate that ABI3 negatively regulates JAZ1 expression by occupying its upstream regulatory sequence and enriching repressive histone modification mark H3K27 trimethylation, thereby occluding RNAPII occupancy. Previous studies have shown that JAZ1 interacts with ABI1, the protein phosphatase 2C, that works during ABA signalling. Our results indicate that in the absence of ABI3, when JAZ1 expression levels are high, the ABI1 protein shows increased stability, compared to when JAZ1 is absent, or ABI3 is overexpressed. Consequently, in the abi3-6 mutant, due to the higher stability of ABI1, reduced phosphorylation of plasma membrane H+-ATPase (AHA2) occurs. HPTS staining further indicated that abi3-6 root cell apoplasts show reduced protonation, compared to wild-type and ABI3 overexpressing seedlings. Such impeded proton extrusion negatively affects cell length in the primary root elongation zone. ABI3 therefore controls cell elongation in the primary root by affecting the ABI1-dependent protonation of root cell apoplasts. In summary, ABI3 controls the expression of JAZ1 and in turn modulates the function of ABI1 to regulate cell length in the elongation zone during primary root growth.