Desensitization of ABA-Signaling: The Swing From Activation to Degradation

Abstract

Abscisic acid (ABA) is a key plant stress-signaling hormone that accumulates upon osmotic stresses such as drought and high salinity. Several proteins have been identified that constitute the ABA-signaling pathway. Among them ABA receptors (PYR/PYL/RCAR), co-receptor PP2Cs (protein phosphatases), SnRK2 kinases (SNF1-related protein kinases) and ABI5/ABFs (transcription factors) are the major components. Upon ABA signal, PYR/PYL receptors interact with and recruit PP2Cs, releasing SnRK2s kinases from sequestration with PP2Cs. This allows SnKR2s to promote the activation of downstream transcription factors of ABA pathway. However, apart from activation, ubiquitination and degradation of core proteins in the ABA pathway by the ubiquitin proteasome system is less explored. In this review we will focus on the recent findings about feedback regulation of ABA signaling core proteins through degradation, which is emerging as a critical step that modulates and eventually ceases the signal relay. Additionally, we also discuss the importance of the recently identified effector protein HOS15, which negatively regulate ABA-signaling through degradation of OST1.

Keywords: ABA core proteins; ABA-signaling; HOS15; OST1; protein degradation and stability.

FIGURE 1

HOS15 negatively regulates ABA signaling through OST1 degradation. Resting state: Under normal condition ABI1/2 and HOS15 interact with OST1. ABI1/2 inhibits OST1 activity by de-phosphorylation and HOS15 degrades OST1 to keep it in a resting state. Activation phase: In response to ABA, PYR1 binds to ABA thus interacting with and inhibiting ABI1, releasing OST1 from sequestration with ABI1/2. HOS15 and OST1 interaction is diminished by ABA, which leads to OST1 activation. OST1 is first auto-phosphorylated and then trans-phosphorylates target TFs. De-activation: After removal of ABA from the system (4 h later), ABI1/2 again interacts (reverse reaction) with and dephosphorylates OST1, recruiting HOS15 to OST1 for degradation. Note that HOS15 also degrades OST1 within hours of sustained ABA treatment by a mechanism that involves ABI1/2 upregulation and dephosphorylation of OST1, leading to ABA de-sensitization (Ali et al., 2019).

FIGURE 2

ABA signaling core proteins and their correspondent E3 ligases. In response to ABA, PYR/PYLs bind ABA, which promotes their interaction with PP2Cs and the release of SnRK2s from sequestration by PP2Cs. Activated SnRK2 kinases phosphorylate target transcription factors that induce the expression of ABA responsive genes. On the right side, E3 ligases are shown which have been shown to promote the degradation of ABA signaling core proteins.