Abstract
Plants can activate defence to pathogen attack by two layers of innate immunity: basal immunity triggered by pathogen-associated molecular pattern (PAMP) triggered immunity (PTI) and effector-triggered immunity (ETI) linked with programmed cell death. Flg22 and Harpin are evolutionary distinct bacterial PAMPs. We have previously shown that Harpin triggers hypersensitive cell death mimicking ETI in Vitis rupestris, but not in the Vitis vinifera cultivar ‘Pinot Noir’. In contrast, the bacterial PAMP flg22 activating PTI does not trigger cell death. To get insight into the defence signalling triggered by flg22 and Harpin, we compared cellular responses upon flg22 and Harpin treatment in the two Vitis cell lines. We found that extracellular alkalinisation was blocked by inhibition of calcium influx, and modulated by pharmacological manipulation of the cytoskeleton and mitogen-activated protein kinase activity with quantitative differences between cell lines and type of PAMPs. In addition, an oxidative burst was detected that was much stronger and faster in response to Harpin as compared to flg22. In V. rupestris, both flg22 and Harpin induced transcripts of defence-related genes including stilbene synthase, microtubule disintegration and actin bundling in a similar way, whereas they differed in V. vinifera cv. ‘Pinot Noir’. In contrast to Harpin, flg22 failed to trigger significant levels of the stilbene trans-resveratrol, and did not induce hypersensitive cell death even in the highly responsive V. rupestris. We discuss these data in a model, where flg22- and Harpin-triggered defence shares a part of early signal components, but differs in perception, oxidative burst, and integration into a qualitatively different stilbene output, such that for flg22 a basal PTI is elicited in both cell lines, while Harpin induces cell death mimicking an ETI-like pattern of defence.
Highlights
Plants employ two distinct layers of immunity to encounter pathogen invasion [1]
We investigated the dependence of apoplastic alkalinisation on calcium influx, mitogen-activated protein kinase (MAPK) cascades, and cytoskeleton, oxidative burst, expression of defence genes, biosynthesis of stilbenes, and cytoskeletal reorganisation, and arrive at a model, where early defence responses triggered by flg22 and Harpin partially overlap, but differ in perception and oxidative burst, which are integrated into a qualitatively different final output with respect to stilbene patterns and cell death
One of the earliest responses detected is a modification of plasma membrane permeability, in particular, Ca2+, H+ and K+, and anion fluxes that can be conveniently followed as changes of extracellular pH [7],[42]
Summary
The first, evolutionarily ancient, layer involves the perception of conserved pathogen structures termed pathogen-associated molecular patterns (PAMPs) at the plasma membrane through conserved and ubiquitous receptors generally defined as pattern recognition receptors (PRRs) Binding to these receptors initiates an active defence response, so-called PAMPtriggered immunity (PTI), in both host and non-host plants. In a second round of host-pathogen warfare, several microbial pathogens have already developed the ability to secrete effector proteins into the cytoplasm using type-III secretion systems (T3SS) in bacteria. These effectors suppress PTI and result in the effectortriggered susceptibility (ETS) [2],[3]. On the side of the host, new plant resistance (R) proteins are developed to recognise the effectors to reconsolidate ETI [1],[6]
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