Botrytis cinerea, a widespread plant pathogen with a necrotrophic lifestyle, causes gray mold disease in many crops. Massive secretion of enzymes and toxins was long considered to be the main driver of infection, but recent studies have uncovered a rich toolbox for B. cinerea pathogenicity. The emerging picture is of a multilayered infection process governed by the exchange of factors that collectively contribute to disease development. No plant shows complete resistance against B. cinerea, but pattern-triggered plant immune responses have the potential to significantly reduce disease progression, opening new possibilities for producing B. cinerea-tolerant plants. We examine current B. cinerea infection models, highlight knowledge gaps, and suggest directions for future studies.

Cell death-inducing proteins (CDIPs) play important roles in the infection of Botrytis cinerea, a broad host-range necrotrophic phytopathogen. Here, we show that the secreted protein BcCDI1 (Cell Death Inducing 1) can cause necrosis in tobacco leaves and at the same time elicit plant defense. The transcription of Bccdi1 was induced at the infection stage. Deletion or overexpression of Bccdi1 resulted in no notable change in disease lesion on bean, tobacco, and Arabidopsis leaves, indicating that Bccdi1 has no effect on the final outcome of B. cinerea infection. Furthermore, the plant receptor-like kinases BAK1 and SOBIR1 are required to transduce the cell death-promoting signal induced by BcCDI1. These findings suggest that BcCDI1 is possibly recognized by plant receptors and then induces plant cell death.

Botrytis cinerea is a necrotrophic fungal plant pathogen that causes grey mould and rot diseases in many crops. Here, we show that the B. cinerea BcCrh4 transglycosylase is secreted during plant infection and induces plant cell death and pattern‐triggered immunity (PTI), fulfilling the characteristics of a cell death‐inducing protein (CDIP). The CDIP activity of BcCrh4 is independent of the transglycosylase enzymatic activity, it takes place in the apoplast and does not involve the receptor‐like kinases BAK1 and SOBIR1. During saprophytic growth, BcCrh4 is localized in the endoplasmic reticulum and in vacuoles, but during plant infection, it accumulates in infection cushions (ICs) and is then secreted to the apoplast. Two domains within the BcCrh4 protein determine the CDIP activities: a 20aa domain at the N′ end activates intense cell death and PTI, while a stretch of 52aa in the middle of the protein induces a weaker response and suppresses the activity of the 20aa N′ domain. Deletion of bccrh4 affected fungal development and IC formation in particular, resulting in reduced virulence. Collectively, our findings demonstrate that BcCrh4 is required for fungal development and pathogenicity, and hint at a dual mechanism that balances the virulence activity of this, and potentially other CDIPs.

Cell death‐inducing proteins (CDIPs) are critical mediators of infection in the necrotrophic pathogen Botrytis cinerea , enabling host colonisation across its broad plant host range. Here, we identified a novel plant CDIP from B. cinerea , BcGH61, that exhibits dual activity: triggering extensive plant cell death while simultaneously promoting host defence responses. Functional analysis demonstrates that its full cell death‐inducing capacity requires its apoplastic compartmentalisation, intact glycoside hydrolase activity, two conserved cysteine residues, and specific structural motifs spanning residues 193–240. Notably, this phytotoxic activity operates through a mechanism independent of the canonical immune coreceptors BAK1 and SOBIR1. During pathogenic invasion, bcgh61 demonstrates upregulated expression. While the bcgh61 gene deletion mutant displays no significant developmental defects, it exhibits severely attenuated virulence, establishing BcGH61 as an essential pathogenicity factor. Furthermore, we identified NbHrBP1, a Nicotiana benthamiana hypersensitive response‐binding protein, as a direct interactor of BcGH61 during infection, functioning in intracellular immune perception but not in cell death induction. Taken together, our results provide evidence that BcGH61 is a novel critical virulence factor for establishing infection in host plant by its phytotoxic activity and underscore the role of NbHrBP1‐based plant surveillance system in recognising fungal secreted proteins as a pivotal defence strategy against necrotrophic pathogens.

Cynanchum hemsleyanum (Oliv.) Liede & Khanum (2016) is a Chinese endemic vine belonging to Cynanchum (Apocynaceae), mainly distributed in Shaanxi, Sichuan, Yunnan, Guizhou, Guangxi, Hubei and Jiang...