A G-type lectin receptor-like kinase in Nicotiana benthamiana enhances resistance to the fungal pathogen Sclerotinia sclerotiorum by complexing with CERK1/LYK4

Fungal pathogens are among the main destructive microorganisms for crops and ecosystems worldwide, causing substantial agricultural and economic losses. Plant cell surface-localized lysin motif (LysM)-containing receptor-like kinases (RLKs) or receptor-like proteins (RLPs) enhance plant resistance to fungal pathogens via sensing chitin, which is a conserved component of the fungal cell wall. Other types of RLKs also regulate chitin signaling via distinct mechanisms in plants. In this study, we identified a G-type lectin RLK, NbERK1, which positively regulated chitin signaling and resistance to the fungal pathogen Sclerotinia sclerotiorum in the model plant Nicotiana benthamiana. In addition, the LysM-RLK NbCERK1/NbLYK4 was shown to mediate plant resistance to S. sclerotiorum positively. Further, the association of chitin-induced NbCERK1-NbLYK4 was found to be essential for chitin perception and signaling. Importantly, NbERK1 was associated with NbCERK1/NbLYK4 and positively regulated chitin-induced NbCERK1-NbLYK4 association. Moreover, chitin could induce the dissociation of NbERK1 from the NbCERK1-NbLYK4 complex. Also, the kinase activity of NbERK1 was likely essential for this dissociation and plant resistance-enhancing activity of NbERK1. Together, these results suggest that NbERK1 is a novel component of the chitin receptor complex and enhances plant resistance to fungal pathogens via regulating chitin signaling.

Automated summary

In this study, a G-type lectin RLK named NbERK1 was found to enhance plant resistance to the fungal pathogen Sclerotinia sclerotiorum through regulating chitin signaling. The LysM-RLK NbCERK1/NbLYK4 was also shown to positively mediate plant resistance to S. sclerotiorum. These findings highlight the importance of NbERK1 in chitin perception and signaling for plant resistance to fungal pathogens.