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A secreted effector protein (SNE1) from Phytophthora infestans is a broadly acting suppressor of programmed cell death
Author(s) -
Kelley Brendan S.,
Lee SangJik,
Damasceno Cynthia M. B.,
Chakravarthy Suma,
Kim ByungDong,
Martin Gregory B.,
Rose Jocelyn K. C.
Publication year - 2010
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2010.04160.x
Subject(s) - effector , oomycete , phytophthora infestans , biology , programmed cell death , microbiology and biotechnology , phytophthora , secretion , suppressor , type three secretion system , gene , apoptosis , genetics , virulence , botany , biochemistry
Summary Evasion or active suppression of host defenses are critical strategies employed by biotrophic phytopathogens and hemibiotrophs whose infection mechanism includes sequential biotrophic and necrotrophic stages. Although defense suppression by secreted effector proteins has been well studied in bacteria, equivalent systems in fungi and oomycetes are poorly understood. We report the characterization of SNE1 ( suppressor of necrosis 1 ), a gene encoding a secreted protein from the hemibiotrophic oomycete Phytophthora infestans that is specifically expressed at the transcriptional level during biotrophic growth within the host plant tomato ( Solanum lycopersicum ). Using transient expression assays, we show that SNE1 suppresses the action of secreted cell death‐inducing effectors from Phytophthora that are expressed during the necrotrophic growth phase, as well as programmed cell death mediated by a range of Avr–R protein interactions. We also report that SNE1 contains predicted NLS motifs and translocates to the plant nucleus in transient expression studies. A conceptual model is presented in which the sequential coordinated secretion of antagonistic effectors by P. infestans first suppresses, but then induces, host cell death, thereby providing a highly regulated means to control the transition from biotrophy to necrotrophy.