Abstract
The phytohormone abscisic acid (ABA) is critical to plant development and stress responses. Abiotic stress triggers an ABA signal transduction cascade, which is comprised of the core components PYL/RCAR ABA receptors, PP2C-type protein phosphatases, and protein kinases. Small GTPases of the ROP/RAC family act as negative regulators of ABA signal transduction. However, the mechanisms by which ABA controls the behavior of ROP/RACs have remained unclear. Here, we show that an Arabidopsis guanine nucleotide exchange factor protein RopGEF1 is rapidly sequestered to intracellular particles in response to ABA. GFP-RopGEF1 is sequestered via the endosome-prevacuolar compartment pathway and is degraded. RopGEF1 directly interacts with several clade A PP2C protein phosphatases, including ABI1. Interestingly, RopGEF1 undergoes constitutive degradation in pp2c quadruple abi1/abi2/hab1/pp2ca mutant plants, revealing that active PP2C protein phosphatases protect and stabilize RopGEF1 from ABA-mediated degradation. Interestingly, ABA-mediated degradation of RopGEF1 also plays an important role in ABA-mediated inhibition of lateral root growth. The presented findings point to a PP2C-RopGEF-ROP/RAC control loop model that is proposed to aid in shutting off ABA signal transduction, to counteract leaky ABA signal transduction caused by “monomeric” PYL/RCAR ABA receptors in the absence of stress, and facilitate signaling in response to ABA.
Highlights
Abscisic acid (ABA) is a phytohormone that protects plants against abiotic stress and is involved in seedling development
To study the effects of abscisic acid (ABA) signal transduction on RopGEF1 protein, we first investigated the subcellular localization of GEF1 in the absence and presence of exogenous ABA
The results indicated that GFP-GEF1/abi1abi2hab1pp2ca seedlings were less sensitive to ABA-mediated inhibition of primary root growth than the pp2c quadruple mutant (Fig 6E and 6F)
Summary
Abscisic acid (ABA) is a phytohormone that protects plants against abiotic stress and is involved in seedling development. ABA can be perceived by a group of soluble “PYL/RCAR” ABA receptor proteins, which upon ABA binding lead to formation of ABA-PYL/RCAR-PP2C complexes that in turn inhibit PP2C protein phosphatase activity [4,5]. This releases PP2C-mediated inhibition of the downstream SnRK2 protein kinases [6,7]. Monomeric PYL/RCARs bind to PP2Cs and may downregulate PP2C activity even in the absence of the ABA ligand [9,10] This constitutive receptor activity would cause “leaky” ABA signal transduction [10]. The linkage of some factors with core ABA signal transduction components needs to be further addressed
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