Abstract
Specific populations of plant microtubules cooperate with the plasma membrane to sense and process abiotic stress signals, such as cold stress. The current study derived from the question, to what extent this perception system is active in biotic stress signalling. The experimental system consisted of grapevine cell lines, where microtubules or actin filaments are visualised by GFP, such that their response became visible in vivo. We used the bacterial elicitors harpin (inducing cell-death related defence), or flg22 (inducing basal immunity) in combination with modulators of membrane fluidity, or microtubules. We show that DMSO, a membrane rigidifier, can cause microtubule bundling and trigger defence responses, including activation of phytoalexin transcripts. However, DMSO inhibited the gene expression in response to harpin, while promoting the gene expression in response to flg22. Treatment with DMSO also rendered microtubules more persistent to harpin. Paradoxically, Benzylalcohol (BA), a membrane fluidiser, acted in the same way as DMSO. Neither GdCl3, nor diphenylene iodonium were able to block the inhibitory effect of membrane rigidification on harpin-induced gene expression. Treatment with taxol stabilised microtubule against harpin but amplified the response of PAL transcripts. Therefore, the data support implications of a model that deploys specific responses to pathogen-derived signals.
Highlights
Plant basal immunity is generally activated through the perception of pathogen-associated molecular patterns (PAMPs) by plasma-membrane localised patternrecognition receptors (PRRs), and designated as PAMP-triggered immunity (PTI)[1,2,3]
After pre-treatment with 10 mM BA (Fig. 1E), microtubules were seen in partially depleted arrays of thinner and less ordered microtubules as compared to the solvent control, there was no significant difference in terms of integrity, if compared to untreated cells (Fig. 1H)
The finding that membrane-fluidity changes are a component of early defence responses[21] motivated our question, whether the microtubule-membrane fluidity circuit can deploy defence as well. We addressed this in grapevine cells expressing a GFP-tagged tubulin, such that we could follow the responses of microtubules to modulations of membrane fluidity
Summary
Plant basal immunity is generally activated through the perception of pathogen-associated molecular patterns (PAMPs) by plasma-membrane localised patternrecognition receptors (PRRs), and designated as PAMP-triggered immunity (PTI)[1,2,3]. Guan et al Horticulture Research (2021)8:260 input is a mixture of chemical (such as microbial molecules that bind as ligands to receptors) and physical clues (such as perturbations of wall or membrane integrity), which assigns the plasma membrane itself an important role in signalling the plasma membrane itself. This role has not attracted the same attention as ligand–receptor interactions and, has remained somewhat elusive. A classic example is the complex between the immune receptor FLAGELLIN SENSING 2 (FLS2) that, upon binding of its ligand, the bacterial PAMP flg[22], recruits the co-receptor BRI1-associated receptor kinase 1
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