Perception of microbe‐associated molecular patterns by host cell surface pattern recognition receptors (PRRs) triggers the intracellular activation of mitogen‐activated protein kinase (MAPK) cascades. However, it is not known how PRRs transmit immune signals to MAPK cascades in plants. Here, we identify a complete phospho‐signaling transduction pathway from PRR‐mediated pathogen recognition to MAPK activation in plants. We found that the receptor‐like cytoplasmic kinase PBL27 connects the chitin receptor complex CERK1‐LYK5 and a MAPK cascade. PBL27 interacts with both CERK1 and the MAPK kinase kinase MAPKKK5 at the plasma membrane. Knockout mutants of MAPKKK5 compromise chitin‐induced MAPK activation and disease resistance to Alternaria brassicicola. PBL27 phosphorylates MAPKKK5 in vitro, which is enhanced by phosphorylation of PBL27 by CERK1. The chitin perception induces disassociation between PBL27 and MAPKKK5 in vivo. Furthermore, genetic evidence suggests that phosphorylation of MAPKKK5 by PBL27 is essential for chitin‐induced MAPK activation in plants. These data indicate that PBL27 is the MAPKKK kinase that provides the missing link between the cell surface chitin receptor and the intracellular MAPK cascade in plants.

In this study, we evaluated the effectiveness of hyperparasitic fungi in controlling powdery mildew (PM). In a greenhouse, we spray-inoculated single colonies of the melon PM-causing fungus Podosphaera xanthii strain KMP-6N at three different fungal developmental stages (i.e., 5, 10, and 15 days old) with spores of the hyperparasitic fungus Ampelomyces sp. strain Xs-q. After spray inoculation, we collected and counted KMP-6N conidia produced as asexual progeny from PM colonies using an electrostatic rotational spore collector. Collector insulator films were replaced at 24 h intervals until KMP-6N ceased to release additional progeny conidia. Conidial releases from each of the single Xs-q-inoculated KMP-6N colonies gradually reduced, then stopped within ca. 4 and 8 days of the first treatment in 5- and 10-day-old KMP-6N colonies, and within ca. 20 days of the second spray treatment in 15-day-old KMP-6N colonies, respectively. The total numbers of asexual progeny conidia collected from single 5-, 10-, and 15-day-old colonies were ca. 156, 1167, and 44,866, respectively. After electrostatic spore collection, conidiophores in Xs-q-uninoculated KMP-6N colonies appeared normal, whereas almost all conidiophores in 5- and 10-day-old Xs-q-inoculated KMP-6N colonies were completely deformed or collapsed due to the infection of the hyperparasitic fungus. This is the first study to apply electrostatic and digital microscopic techniques to clarify the impact of fungal hyperparasitism on mycohost survival, and, in particular, to assess quantitatively and visually the suppression of conidial release from any PM colonies infected with Ampelomyces.

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