The Botrytis cinerea Crh1 transglycosylase is a cytoplasmic effector triggering plant cell death and defense response
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Altres documents de l'autoria: Bi, Kai; Scalschi, Loredana; Jaiswal, Namrata; Mengiste, Tesfaye; Fried, Renana; Sanz, A. Belen; Arroyo, Javier; Zhu, Wenjun; Masrati, Gal; Sharon, Amir
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The Botrytis cinerea Crh1 transglycosylase is a cytoplasmic effector triggering plant cell death and defense responseAutoria
Data de publicació
2021-04-12Editor
Springer NatureISSN
2041-1723Cita bibliogràfica
Bi, K., Scalschi, L., Jaiswal, N. et al. The Botrytis cinerea Crh1 transglycosylase is a cytoplasmic effector triggering plant cell death and defense response. Nat Commun 12, 2166 (2021). https://doi.org/10.1038/s41467-021-22436-1Tipus de document
info:eu-repo/semantics/articleVersió
info:eu-repo/semantics/publishedVersionParaules clau / Matèries
Resum
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 ... [+]
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. [-]
Publicat a
Nature Communications, volume 12 (2021)Entitat finançadora
Ministerio de Economía y Competitividad, MINECO, Spain
Codi del projecte o subvenció
BIO2016-79289-P | PID2019-105223GB-I00
Drets d'accés
info:eu-repo/semantics/openAccess
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