BcXYG1, a secreted xyloglucanase from Botrytis cinerea, triggers both cell death and plant immune responses

Wenjun Zhu, Mordechi Ronen, Yonatan Gur, Anna Minz-Dub, Gal Masrati, Nir Ben-Tal, Alon Savidor, Itai Sharon, Elad Eizner, Oliver Valerius, Gerhard H. Braus, Kyle Bowler, Maor Bar-Peled, Amir Sharon*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

74 Scopus citations


In search of Botrytis cinerea cell death-inducing proteins, we found a xyloglucanase (BcXYG1) that induced strong necrosis and a resistance response in dicot plants. Expression of the BcXYG1 gene was strongly induced during the first 12 h post inoculation, and analysis of disease dynamics using PathTrack showed that a B. cinerea strain overexpressing BcXYG1 produced early local necrosis, supporting a role of BcXYG1 as an early cell death-inducing factor. The xyloglucanase activity of BcXYG1 was not necessary for the induction of necrosis and plant resistance, as a mutant of BcXYG1 lacking the xyloglucanase enzymatic activity retained both functions. Residues in two exposed loops on the surface of BcXYG1 were found to be necessary for the induction of cell death but not to induce plant resistance. Further analyses showed that BcXYG1 is apoplastic and possibly interacts with the proteins of the plant cell membrane and also that the BcXYG1 cell death-promoting signal is mediated by the leucine-rich repeat receptor-like kinases BAK1 and SOBIR1. Our findings support the role of cell death-inducing proteins in establishing the infection of necrotrophic pathogens and highlight the recognition of fungal apoplastic proteins by the plant immune system as an important mechanism of resistance against this class of pathogens.

Original languageEnglish
Pages (from-to)438-456
Number of pages19
JournalPlant Physiology
Issue number1
StatePublished - Sep 2017


FundersFunder number
United States - Israel Binational Agricultural Research and Development FundIS4937-16, CA9122-09
Deutsche Forschungsgemeinschaft
National Natural Science Foundation of China31501587, 1775/12
Israel Science Foundation
Israeli Centers for Research Excellence


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