Emerging roles of protein kinase CK2 in abscisic acid signaling

Abstract

The phytohormone abscisic acid (ABA) regulates many aspects of plant growth and development as well as responses to multiple stresses. Post-translational modifications such as phosphorylation or ubiquitination have pivotal roles in the regulation of ABA signaling. In addition to the positive regulator sucrose non-fermenting-1 related protein kinase 2 (SnRK2), the relevance of the role of other protein kinases, such as CK2, has been recently highlighted. We have recently established that CK2 phosphorylates the maize ortholog of open stomata 1 OST1, ZmOST1, suggesting a role of CK2 phosphorylation in the control of ZmOST1 protein degradation (Vilela et al., 2015). CK2 is a pleiotropic enzyme involved in multiple developmental and stress-responsive pathways. This review summarizes recent advances that taken together suggest a prominent role of protein kinase CK2 in ABA signaling and related processes.

Keywords: ABA signaling; circadian clock; post-translational modifications; proteasome degradation; protein kinase CK2.

FIGURE 1

(A) Regulation of ABA signaling by the control of protein turnover. In the absence of ABA, major regulators of the hormone such as the PYR/PYL/RCAR receptors, the SnRK2 kinases, and several transcription factors (ABI3, ABI5, ABF1, ABF3) are degraded by the proteasome, and/or inactivated. In this way the output of the ABA signal is thoroughly dampened in the absence of the hormone. When ABA levels rise, these major regulators are protected from degradation through the inactivation or degradation of the negative regulators such as KEG. CK2 is known to mediate the stabilization and destabilization of proteins in other systems and is a likely candidate to also have a role as a housekeeping kinase controlling protein turnover in ABA signaling. (B) Integration of the plant circadian clock on ABA signaling. The core circadian clock consists of a negative feedback loop between the CCA1 and LHY on one hand and TOC1 on the other. ABA treatment induces TOC1 expression and, in another feedback loop, TOC1 attenuates ABA signaling and negatively regulates the expression of ABA signaling genes like ABAR, known to interact with the ABA central signaling complex. CCA1 an LHY act synergistic to ABA and antagonistic to TOC1 expression. CCA1 and LHY are phosphorylated by CK2 targeting them for degradation, promoting CCA1 dimerization, CCA1-DNA complex formation, and interaction with the promoters of downstream genes. ABAR is also a substrate of CK2 and, even though the effects of this activity are still unknown, they could include protein turnover and altered gene expression by retrograde signaling from the chloroplast.