Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

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Record number 491299
Title Phytophthora infestans RXLR effector AVR1 interacts with exocyst component Sec5 to manipulate plant immunity
Author(s) Du, Y.; Mpina, M.H.; Birch, P.R.J.; Bouwmeester, K.; Govers, F.
Source Plant Physiology 169 (2015)3. - ISSN 0032-0889 - p. 1975 - 1990.
Department(s) Laboratory of Phytopathology
Publication type Refereed Article in a scientific journal
Publication year 2015
Abstract Phytophthora infestans secretes numerous RXLR effectors that modulate host defence and thereby pave the way for successful invasion. Here we show that the RXLR effector AVR1 is a virulence factor that promotes colonization and suppresses callose deposition, a hallmark of basal defense. To identify host targets of AVR1 we performed yeast-2-hybrid screens and selected Sec5 as a candidate. Sec5 is a subunit of the exocyst, a protein complex that is involved in vesicle trafficking. AVR1-like (A-L), a close homolog of AVR1, also acts as a virulence factor but unlike AVR1, A-L does not suppress CRN2-induced cell death nor interacts with Sec5. Compared to AVR1, A-L is shorter and lacks the C-terminal tail, the T-region that is crucial for CRN2-induced cell death suppression and Sec5 interaction. In planta analyses revealed that AVR1 and Sec5 are in close proximity and co-immunoprecipitation confirmed the interaction. Sec5 is required for secretion of the pathogenesis-related protein PR-1 and callose deposition and also plays a role in CRN2-induced cell death. Our findings show that P. infestans manipulates an exocyst subunit and thereby potentially disturbs vesicle trafficking, a cellular process that is important for basal defence. This is a novel strategy that oomycete pathogens exploit to modulate host defence
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