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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\n            \u003Cjats:italic>Arabidopsis thaliana\u003C\u002Fjats:italic>\n            requires three lysin-motif (LysM) domain proteins. LYM1 and LYM3 are plasma membrane proteins that physically interact with PGNs and mediate\n            \u003Cjats:italic>Arabidopsis\u003C\u002Fjats:italic>\n            sensitivity to structurally different PGNs from Gram-negative and Gram-positive bacteria.\n            \u003Cjats:italic>lym1\u003C\u002Fjats:italic>\n            and\n            \u003Cjats:italic>lym3\u003C\u002Fjats:italic>\n            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,\n            \u003Cjats:italic>lym1\u003C\u002Fjats:italic>\n            ,\n            \u003Cjats:italic>lym3\u003C\u002Fjats:italic>\n            , and\n            \u003Cjats:italic>lym3 lym1\u003C\u002Fjats:italic>\n            mutant genotypes exhibit supersusceptibility to infection with virulent\n            \u003Cjats:italic>Pseudomonas syringae\u003C\u002Fjats:italic>\n            pathovar\n            \u003Cjats:italic>tomato\u003C\u002Fjats:italic>\n            DC3000. Defects in basal immunity in\n            \u003Cjats:italic>lym3 lym1\u003C\u002Fjats:italic>\n            double mutants resemble those observed in\n            \u003Cjats:italic>lym1\u003C\u002Fjats:italic>\n            and\n            \u003Cjats:italic>lym3\u003C\u002Fjats:italic>\n            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\n            \u003Cjats:italic>Arabidopsis\u003C\u002Fjats:italic>\n            , phenocopies defects observed in\n            \u003Cjats:italic>lym1\u003C\u002Fjats:italic>\n            and\n            \u003Cjats:italic>lym3\u003C\u002Fjats:italic>\n            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. 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