The Botrytis cinerea Crh1 transglycosylase is a cytoplasmic effector triggering plant cell death and defense response

Abstract

Crh proteins catalyze crosslinking of chitin and glucan polymers in fungal cell walls. Here, we show that the BcCrh1 protein from the phytopathogenic fungus Botrytis cinerea acts as a cytoplasmic effector and elicitor of plant defense. BcCrh1 is localized in vacuoles and the endoplasmic reticulum during saprophytic growth. However, upon plant infection, the protein accumulates in infection cushions; it is then secreted to the apoplast and translocated into plant cells, where it induces cell death and defense responses. Two regions of 53 and 35 amino acids are sufficient for protein uptake and cell death induction, respectively. BcCrh1 mutant variants that are unable to dimerize lack transglycosylation activity, but are still able to induce plant cell death. Furthermore, Arabidopsis lines expressing the bccrh1 gene exhibit reduced sensitivity to B. cinerea, suggesting a potential use of the BcCrh1 protein in plant immunization against this necrotrophic pathogen.

Multiple knockout mutants reveal a high redundancy of phytotoxic compounds contributing to necrotrophic pathogenesis of Botrytis cinerea

“…Therefore, the remaining phytotoxic activity in the 12x mutants is due to further, as yet uncharacterized CDIPs. These include Crh1, a newly described CDIP that has been shown to be translocated via infection cushions into host cells [ 31 ], and several apoplastic CDIPs that have been recently described in fungi related to B . cinerea , Ciborinia camelliae [ 66 ], Monilinia fructigena [ 67 ] and Sclerotinia sclerotiorum [ 43 ], for which homologues exist in B .…”

“…Recently, a novel B . cinerea CDIP, called Crh1, was discovered that is translocated into plant cells, but it does not seem to contribute to infection [ 31 ].…”

Role of Dicer-Dependent RNA Interference in Regulating Mycoparasitic Interactions

“…Moreover, among the upregulated genes there was also a homolog (BCIN_14g03930) of the S. sclerotiorum transcription factor SsNsd1 , necessary for pathogenicity and appressorium formation ( 97 ). Furthermore, upon contact with the Δ dcl2 mutant, B. cinerea upregulated several genes encoding proteins involved in chitin and cell wall synthesis, such as Bccrh1, BcchsIV, BcchsV, BcchsVI, and BcchsVII ( 98 – 101 ). The upregulation of BcCHSVI and BcCHSVII is of particular interest because these proteins have a role in plant infection ( 101 ).…”

Multiple knockout mutants reveal a high redundancy of phytotoxic compounds that determine necrotrophic pathogenesis of Botrytis cinerea

“…Therefore, the remaining phytotoxic activity in the 12x mutants is due to further, as yet uncharacterized CDIPs. These include Crh1, a newly described CDIP that has been shown to be translocated via infection cushions into host cells (Bi et al 2021).…”

“…A PAMP-like behavior of CDIPs was indicated by the observation that their activity was dependent on the presence of the PRR coreceptors BAK1 and/or SOBIR1 in the treated plants (Franco-Orozco et al 2017;Frías et al 2011;Yang et al 2018;Zhu et al 2017), and PRRs for Nep1/Nep2, Xyn11A and PG1/PG2 have already been identified (Albert et al 2015;Ron and Avni, 2004;Zhang et al 2014). Recently, a novel B. cinerea CDIP was discovered that is translocated into plant cells, but it does not seem to contribute to infection (Bi et al 2021).…”