CBC Complex Regulates Hyphal Growth, Sclerotial Quantity, and Pathogenicity in the Necrotrophic Fungus <i>Botrytis cinerea</i>

The cap-binding protein complex (CBC), comprising Cbp20 and Cbp80, is crucial for gene expression, yet its role in the notorious crop pathogen <i>Botrytis cinerea</i> remains unclear. Immunoprecipitation coupled with LC-MS/MS demonstrated that BcCbp20 interacts with BcCbp80. Yeast two-hy...

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Main Authors: Yinshan Zhang, Xueting Chen, Guihua Li, Qingming Qin, Mingzhe Zhang, Jianchun Qin
Format: Article
Language:English
Published: MDPI AG 2025-06-01
Series:Journal of Fungi
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Online Access:https://www.mdpi.com/2309-608X/11/6/429
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Summary:The cap-binding protein complex (CBC), comprising Cbp20 and Cbp80, is crucial for gene expression, yet its role in the notorious crop pathogen <i>Botrytis cinerea</i> remains unclear. Immunoprecipitation coupled with LC-MS/MS demonstrated that BcCbp20 interacts with BcCbp80. Yeast two-hybrid, GST pull-down, and Split-luciferase complementation assays confirmed that the conserved RNA recognition motif (RRM, 54–127 aa) of BcCbp20 and the N-terminal MIF4G domain (1–370 aa, 1–577 aa) of BcCbp80 constitute the core interaction regions. Genetic transformation experiments revealed that <i>BcCBP80</i> exerts a more dominant role than <i>BcCBP20</i> in regulating hyphal morphology, growth rate, conidiophore development, and conidial yield. Furthermore, <i>BcCBP20</i> and <i>BcCBP80</i> differentially regulate sclerotium formation to maintain sclerotial quantity. Based on pathogenicity assays, <i>BcCBP80</i> associated with infection cushion development, with this phenotypic alteration possibly being among the factors correlated with altered pathogenicity. However, the increased sensitivity of Δ<i>Bccbp20</i> to various stress factors may be the primary reason for the diminished pathogenicity. Taken together, these results indicate that <i>BcCBP20</i> and <i>BcCBP80</i> play important roles in multiple aspects of <i>B. cinerea</i> growth, development, stress response, and pathogenicity.
ISSN:2309-608X