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Amna Mhamdi, The Protein Phosphatase PP2A-B′γ Takes Control over Salicylic Acid to Suppress Defense and Premature Senescence, Plant Physiology, Volume 182, Issue 2, February 2020, Pages 681–682, https://doi.org/10.1104/pp.19.01466
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Long thought to be unselective and often referred to as housekeeping enzymes, type 2A protein phosphatases (PP2As) have emerging specific regulatory functions in cell signaling (Luan, 2003; Durian et al., 2016; Máthé et al., 2019). PP2As interact with several pathways to activate signal transduction and adaptive responses while preventing unnecessary investment of energy.
PP2A is a heterotrimer, with the core enzyme consisting of a scaffold A subunit, a catalytic C subunit, and a regulatory and variable B subunit with at least 17 isoforms in Arabidopsis (Arabidopsis thaliana). PP2A-B′γ acts as a negative regulator of pathogenesis responses and controls daylength-dependent responses to intracellular oxidative stress (Trotta et al., 2011; Li et al., 2014; Segonzac et al., 2014). However, how this phosphatase affects plant metabolism and defense remains to be established, simply because only a few targets of PP2A-B′γ have been identified.
In this issue of Plant Physiology, Durian et al. (2020) define the mechanisms by which PP2A-B′γ prevents defense responses and delays senescence (Fig. 1). First, the authors provide evidence for an interaction between PP2A-B′γ and CALCIUM-DEPENDENT PROTEIN KINASE1 (CPK1), a kinase that positively regulates defense against the necrotrophic fungal pathogen Botrytis cinerea (Coca and San Segundo, 2010). Under control conditions, pp2a-b′γ mutants displayed increased in-gel kinase activity of CPK1. Treatment with B. cinerea increased CPK1 abundance, and this was particularly strong in the pp2a-b′γ background (Durian et al., 2020). Even though CPK1 was previously implicated in salicylic acid (SA)-related gene expression in response to Fusarium oxysporum, in this study, analysis of cpk1 mutants revealed that CPK1 is not required for the accumulation of PATHOGENESIS RELATED1 (PR1) proteins after B. cinerea infection.
