Abstract
SummaryThe cell wall is the primary interface between plant cells and their immediate environment and must balance multiple functionalities, including the regulation of growth, the entry of beneficial microbes, and protection against pathogens. Here, we demonstrate how API, a SCAR2 protein component of the SCAR/WAVE complex, controls the root cell wall architecture important for pathogenic oomycete and symbiotic bacterial interactions in legumes. A mutation in API results in root resistance to the pathogen Phytophthora palmivora and colonization defects by symbiotic rhizobia. Although api mutant plants do not exhibit significant overall growth and development defects, their root cells display delayed actin and endomembrane trafficking dynamics and selectively secrete less of the cell wall polysaccharide xyloglucan. Changes associated with a loss of API establish a cell wall architecture with altered biochemical properties that hinder P. palmivora infection progress. Thus, developmental stage-dependent modifications of the cell wall, driven by SCAR/WAVE, are important in balancing cell wall developmental functions and microbial invasion.
Highlights
The cell wall protects plant cells from microbial invasion while maintaining properties enabling growth and development
We demonstrate that the Medicago api (C) transgenic roots (API) gene, as well as its L. japonicus and Arabidopsis orthologs, can control cell wall properties required for efficient Medicago root entry by the oomycete pathogen P. palmivora
Plants Mutated in the SCAR2 Gene API Are Compromised in Root Entry of a Pathogenic Oomycete When surveying mutants impaired in symbiosis [10] for their ability to resist pathogen infection, we found that seedling roots carrying the api mutation [37] displayed significantly reduced disease symptoms upon infection with P. palmivora zoospores
Summary
The cell wall protects plant cells from microbial invasion while maintaining properties enabling growth and development. Reinforcement of the cell wall through the deposition of carbohydrates results in the formation of papilla structures at attempted penetration sites [2] Despite these measures, adapted pathogens have evolved strategies to ensure their passage through the cell wall. P. palmivora grows mostly intercellularly and projects short specialized hyphae, termed haustoria, through the walls of individual living root cells, resulting in the invagination of their protoplast. This is followed by a necrotrophic stage, characterized by host tissue necrosis and the formation of sporangia, which release new zoospores for further infection [10].
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