Abstract

Plants and animals perceive diverse microbe-associated molecular patterns (MAMPs) via pattern recognition receptors and activate innate immune signalling. The actin cytoskeleton has been suggested as a target for innate immune signalling and a key transducer of cellular responses. However, the molecular mechanisms underlying actin remodelling and the precise functions of these rearrangements during innate immunity remain largely unknown. Here we demonstrate rapid actin remodelling in response to several distinct MAMP signalling pathways in plant epidermal cells. The regulation of actin dynamics is a convergence point for basal defence machinery, such as cell wall fortification and transcriptional reprogramming. Our quantitative analyses of actin dynamics and genetic studies reveal that MAMP-stimulated actin remodelling is due to the inhibition of capping protein (CP) by the signalling lipid, phosphatidic acid. In addition, CP promotes resistance against bacterial and fungal phytopathogens. These findings demonstrate that CP is a central target for the plant innate immune response.

Highlights

  • Plants and animals perceive diverse microbe-associated molecular patterns (MAMPs) via pattern recognition receptors and activate innate immune signalling

  • In an adf[4] mutant, the frequency of filament–filament annealing still increases to a level that is comparable with wild type (WT) following elf[26] treatment, suggesting that additional regulators are required to control the availability of actin filament ends during innate immune signalling[22]

  • We found that rearrangement of cortical actin arrays in hypocotyl cells occurs within minutes following treatment with the bacterial MAMP elf[26]

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Summary

Introduction

Plants and animals perceive diverse microbe-associated molecular patterns (MAMPs) via pattern recognition receptors and activate innate immune signalling. The recognition of different MAMPs by specific PRRs induces common signalling events involving activation of mitogen-associated and calcium-dependent protein kinases (MAPK and CDPK), bursts of cytosolic calcium and reactive oxygen species (ROS), as well as extensive transcriptional reprogramming[4,11,12] Cellular immune responses, such as rearrangement of cytoplasmic organelles and cell wall reinforcement by callose deposition, are activated to abrogate the pathogen infection[4,12,13,14]. Treatment with MAMPs was sufficient to stimulate an increase in filament abundance[18] Many defence responses, such as cytoplasmic rearrangements and targeted delivery of defence compounds to the infection site, are dependent on actin remodelling[15,19]. The ADF4 pathway may be limited in scope, since adf[4] mutants have a WT response for actin remodelling when challenged with the fungal MAMP, chitin[22]

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