SOBER1 phospholipase activity suppresses phosphatidic acid accumulation and plant immunity in response to bacterial effector AvrBsT

Abstract

Arabidopsis thaliana ecotype Pi-0 is resistant to Pseudomonas syringae pathovar tomato (Pst) strain DC3000 expressing the T3S effector protein AvrBsT. Resistance is due to a loss of function mutation (sober1-1) in a conserved ␣/␤ hydrolase, SOBER1 (Suppressor of AvrBsT Elicited Resistance1). Members of this superfamily possess phospholipase and carboxylesterase activity with diverse substrate specificity. The nature of SOBER1 enzymatic activity and substrate specificity was not known. SOBER1-dependent suppression of the hypersensitive response (HR) in Pi-0 suggested that it might hydrolyze a plant lipid or precursor required for HR induction. Here, we show that Pi-0 leaves infected with Pst DC3000 expressing AvrBsT accumulated higher levels of phosphatidic acid (PA) compared to leaves infected with Pst DC3000. Phospholipase D (PLD) activity was required for high PA levels and AvrBsT-dependent HR in Pi-0. Overexpression of SOBER1 in Pi-0 reduced PA levels and inhibited HR. These data implicated PA, phosphatidylcholine (PC) and lysophosphatidylcholine (LysoPC) as potential SOBER1 substrates. Recombinant His 6-SOBER1 hydrolyzed PC but not PA or LysoPC in vitro indicating that the enzyme has phospholipase A 2 (PLA2) activity. Chemical inhibition of PLA 2 activity in leaves expressing SOBER1 resulted in HR in response to Pst DC3000 AvrBsT. These data are consistent with the model that SOBER1 PLA 2 activity suppresses PLD-dependent production of PA in response to AvrBsT elicitation. This work highlights an important role for SOBER1 in the regulation of PA levels generated in plants in response to biotic stress. disease resistance ͉ hypersensitive response ͉ lipid profiling ͉ pathogen

Capping Protein Modulates Actin Remodeling in Response to Reactive Oxygen Species during Plant Innate Immunity

“…Nod factors have also been reported to induce PA production in vivo (den Hartog et al, 2001). Recognition of pathogen effectors leads to increased PA level in host cells (de Jong et al, 2004;Andersson et al, 2006;Kirik and Mudgett, 2009). Pharmacological studies suggest that actin remodeling upon perception of elf26 and chitin requires PLD-dependent PA signaling (Li et al, 2015b).…”

Quantitative Proteomics Reveals Dynamic Changes in the Plasma Membrane During Arabidopsis Immune Signaling

“…PLP2a/pPLA-II␣ has diverse lipid substrates in vitro and has been shown to accumulate during ETI and positively regulate cell death (41). In contrast, SOBER1 activity suppresses phosphatidic acid accumulation during ETI and represses HR in response to the effector AvrBsT (63). Thus, phospholipases with positive and negative roles in cell death accumulated at the PM during ETI, and lipid-derived signaling processes likely play a major role in the execution of ETI.…”

A Small Phospholipase A2-α from Castor Catalyzes the Removal of Hydroxy Fatty Acids from Phosphatidylcholine in Transgenic Arabidopsis Seeds

“…Their involvement in membrane trafficking, however, is emerging: reductions in sPLA 2 expression in Arabidopsis (Arabidopsis thaliana) plants led to Golgi disruption and the inhibition of PIN auxin efflux transporter traffic to the plasma membrane in roots (Lee et al, 2010) and also to membrane disruption in pollen (Kim et al, 2011). Two other proteins, SOBER1 (Kirik and Mudgett, 2009) and Lecithin Cholesterol Acyltransferase (LCAT)-like4 , unrelated to these three main families, also have been identified as PLA 2 s.…”