Concepedia

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<i>Arabidopsis</i> lysin-motif proteins LYM1 LYM3 CERK1 mediate bacterial peptidoglycan sensing and immunity to bacterial infection

501

Citations

32

References

2011

Year

TLDR

Recognition of microbial patterns by host pattern recognition receptors is a key step in immune activation, and peptidoglycans—major bacterial cell‑wall components—stimulate immunity in metazoans and plants. We propose that Arabidopsis LysM proteins LYM1, LYM3, and CERK1 constitute a lineage‑specific peptidoglycan recognition system that evolved via convergent evolution, distinct from metazoan receptors. We demonstrate that Arabidopsis LYM1, LYM3, and CERK1 are required for peptidoglycan perception and immunity, with mutants lacking PGN‑induced transcriptional responses and showing heightened susceptibility to *Pseudomonas syringae*, indicating that plants possess a lineage‑specific PGN recognition system shared with metazoans.

Abstract

Recognition of microbial patterns by host pattern recognition receptors is a key step in immune activation in multicellular eukaryotes. Peptidoglycans (PGNs) are major components of bacterial cell walls that possess immunity-stimulating activities in metazoans and plants. Here we show that PGN sensing and immunity to bacterial infection in Arabidopsis thaliana requires three lysin-motif (LysM) domain proteins. LYM1 and LYM3 are plasma membrane proteins that physically interact with PGNs and mediate Arabidopsis sensitivity to structurally different PGNs from Gram-negative and Gram-positive bacteria. lymp1 and lym3 mutants lack PGN-induced changes in transcriptome activity patterns, but respond to fungus-derived chitin, a pattern structurally related to PGNs, in a wild-type manner. Notably, lym1 , lym3 , and lym3 lym1 mutant genotypes exhibit supersusceptibility to infection with virulent Pseudomonas syringae pathovar tomato DC3000. Defects in basal immunity in lym3 lym1 double mutants resemble those observed in lym1 and lym3 single mutants, suggesting that both proteins are part of the same recognition system. We further show that deletion of CERK1, a LysM receptor kinase that had previously been implicated in chitin perception and immunity to fungal infection in Arabidopsis , phenocopies defects observed in lym1 and lym3 mutants, such as peptidoglycan insensitivity and enhanced susceptibility to bacterial infection. Altogether, our findings suggest that plants share with metazoans the ability to recognize bacterial PGNs. However, as Arabidopsis LysM domain proteins LYM1, LYM3, and CERK1 form a PGN recognition system that is unrelated to metazoan PGN receptors, we propose that lineage-specific PGN perception systems have arisen through convergent evolution.

References

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