Premium
Identification of Pseudomonas syringae type III effectors that can suppress programmed cell death in plants and yeast
Author(s) -
Jamir Yashitola,
Guo Ming,
Oh HyeSook,
PetnickiOcwieja Tanja,
Chen Shaorong,
Tang Xiaoyang,
Dickman Martin B.,
Collmer Alan,
R. Alfano James
Publication year - 2004
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 - 10.1046/j.1365-313x.2003.01982.x
Subject(s) - pseudomonas syringae , effector , biology , hypersensitive response , type three secretion system , mutant , secretion , arabidopsis , virulence , programmed cell death , microbiology and biotechnology , suppressor , gene , genetics , apoptosis , biochemistry
Summary The Pseudomonas syringae pv. tomato DC3000 type III secretion system (TTSS) is required for bacterial pathogenicity on plants and elicitation of the hypersensitive response (HR), a programmed cell death (PCD) that occurs on resistant plants. Cosmid pHIR11 enables non‐pathogens to elicit an HR dependent upon the TTSS and the effector HopPsyA. We used pHIR11 to determine that effectors HopPtoE, avirulence AvrPphE Pto , AvrPpiB1 Pto , AvrPtoB, and HopPtoF could suppress a HopPsyA‐dependent HR on tobacco and Arabidopsi s. Mixed inoculum and Agrobacterium ‐mediated transient expression experiments confirmed that suppressor action occurred within plant cells. These suppressors, with the exception of AvrPpiB1 Pto , inhibited the expression of the tobacco pathogenesis‐related (PR) gene PR1a. DC3000 suppressor mutants elicited an enhanced HR consistent with these mutants lacking an HR suppressor. Additionally, HopPtoG was identified as a suppressor on the basis of an enhanced HR produced by a hopPtoG mutant. Remarkably, these proteins functioned to inhibit the ability of the pro‐apoptotic protein, Bax to induce PCD in plants and yeast, indicating that these effectors function as anti‐PCD proteins in a trans ‐kingdom manner. The high proportion of effectors that suppress PCD suggests that suppressing plant immunity is one of the primary roles for DC3000 effectors and a central requirement for P. syringae pathogenesis.