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Fig 1.

Overview of known components of PGN perception in plants.

Upon entry of bacteria into the plant apoplast, their presence is most likely sensed either by PGN fragments spontaneously released into the apoplast or via unrelated bacterial MAMPs, such as flagellin or lipopolysaccharides. PGN fragments of yet unknown size bind to GPI-anchored LysM-proteins localized in the plasma membrane (AtLYM1/3 in Arabidopsis, OsLYP4/6 in rice). Upon PGN binding (1), OsLYP4/6 dissociate to form a complex with OsCERK1, which triggers the release of cytoplasmic OsRLCK176 (and possibly OsRLCK185) and subsequent downstream signalling (2). In Arabidopsis, AtLYM1, AtLYM3, and AtCERK1 mediate PGN perception (1); however, whether a PGN-dependent LysM protein complex is formed and whether receptor-like cytoplasmic kinases (RLCKs), such as avrPphB sensitive 1-like proteins (PBLs), are required is still unknown. Downstream signalling events lead to a transcriptional reprogramming of the cell, and defence proteins, such as the lysozyme-like activity LYS1, are produced. LYS1 is secreted into the plant apoplast to generate more immunogenic PGN fragments (3), which results in an amplification of PGN-triggered immune responses. In a successful infection, however, CERK1 is targeted by bacterial effectors such as AvrPtoB (in the ArabidopsisPseudomonas syringae interaction) and Xoo1488 (in the rice–Xanthomonas oryzae interaction) to suppress plant immunity (4).

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