GSE130958
Receptor-like cytoplasmic kinase CDG1 negatively regulates Arabidopsis pattern-triggered immunity and is co-opted by the Pseudomonas syringae effector AvrRpm1
In this study, we conducted protoplast-based gain-of-function assay to screen 23 members of the RLCK VII family for those whose overexpression can affect flg22-induced MAPK activation. We identified CDG1, a previously characterized positive regulator in brassinosteroid (BR) signaling (Kim et al., 2011), as a new negative regulator of flg22-triggered MAPK activation. We further found that CDG1 could constitutively associate with FLS2 and CERK1, and its transgenic overexpression could significantly reduce the abundances of these two essential PRRs, leading to impaired immune responses to both flg22 and chitin as well as increased susceptibility to bacterial and fungal pathogens. Surprisingly, the CDG1-mediated degradation of FLS2 and CERK1 is independent of E3 ubiquitin ligases PUB12/PUB13, but requires the kinase activity of MEKK1, a MAPKKK positively regulating plant innate immunity (Asai et al., 2002). Moreover, we demonstrated that RIN4 and the P. syringae effector AvrRpm1 could also interact with CDG1, and obtained evidence that CDG1 may be one of the RLCK VII members responsible for the AvrRpm1-induced RIN4 phosphorylation. Our data thus reveal multifaceted moonlight function of CDG1 in Arabidopsis innate immunity in addition to its originally characterized role in BR signaling. Overall design: We noted that the growth defects of CDG1 OE plants were largely suppressed in the mekk1/pMEKK1::MEKK1K361M-FLAG/CDG1 OE (hereafter referred to as MEKK1K361M/CDG1 OE) plants. We want to know which genes transcriptional level variation leads the growth defects  of CDG1 OE .So we prepared the samples for RNAseq. We use 4 samples, WT is control. There are not repetitions.