ABA signal in rice under stress conditions

Abstract

Ever since its discovery, abscisic acid (ABA) has been intensively studied due to its versatile functions in plant developmental and physiological processes. Many signaling details of ABA have been well elucidated and reviewed. The identification of ABA receptors is a great breakthrough in the field of ABA study, whereas the discovery of ABA transporter has changed our concept that ABA is delivered solely by passive transport. The intensity of ABA signaling pathway is well known to be controlled by multi-regulators. Nonetheless, the interaction and coordination among ABA biosynthesis, catabolism, conjugation and transportation are seldom discussed. Here, we summarize the biological functions of ABA in response to different stresses, especially the roles of ABA in plant defense to pathogen attack, and discuss the possible relationships of these determinants in controlling the specificity and intensity of ABA signaling pathway in the rice.

Keywords: ABA biosynthesis; ABA metabolism; ABA receptor; ABA signaling; ABA transporter; abiotic and biotic stresses; abscisic acid (ABA); rice (Oryza sativa).

Figure 1

A simplified model for abscisic acid generation, transport and perception in plants. ABA biosynthesis is induced by environmental cues in the vascular tissues. ABA can also be released at ER from ABA-GE that stored in the vacuole or transported from the vacuolar system by an unknown ABA-GE transporter (? stand for unknown a mechanism). Both sourced ABAs are transported to intercellular space by the ABA transporters, AtABCG25 which majorly located in vascular tissue and exports ABA outward the cells. The newly synthesized ABA is then transported to the cells of acting site for ABA-responses by passive and/or active transport. The ABA importers and exporters can efficiently and directly deliver ABA to the acting site. However, part of the ABA is catabolic inactivated, which also plays a pivotal in regulating the intensity of ABA signal. PYR/PYL/RCAR receptors percept ABA signal intracellularly then combine with the negative regulators of ABA signal, PP2Cs/ABI1, to form a ternary complex. Thus, the negative regulator is inactivated whereas the downstream targets of PP2Cs, SnRK2s, are allowed to be activated by phosphorylation. The activation of SnRK2s will thus initiate an ABA response. In cell without ABA signal, the SnRK2s is inactivated by PP2Cs.