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Distinct Pseudomonas type‐ III effectors use a cleavable transit peptide to target chloroplasts
Author(s) -
Li Guangyong,
Froehlich John E.,
Elowsky Christian,
Msanne Joseph,
Ostosh Andrew C.,
Zhang Chi,
Awada Tala,
Alfano James R.
Publication year - 2014
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/tpj.12396
Subject(s) - effector , pseudomonas syringae , arabidopsis , biology , virulence , transit peptide , microbiology and biotechnology , type three secretion system , chloroplast , mutant , genetics , pathogen , gene , plastid
Summary The pathogen Pseudomonas syringae requires a type‐ III protein secretion system and the effector proteins it injects into plant cells for pathogenesis. The primary role for P. syringae type‐ III effectors is the suppression of plant immunity. The P. syringae pv. tomato DC 3000 HopK1 type‐ III effector was known to suppress the hypersensitive response ( HR ), a programmed cell death response associated with effector‐triggered immunity. Here we show that DC 3000 hopK1 mutants are reduced in their ability to grow in Arabidopsis, and produce reduced disease symptoms. Arabidopsis transgenically expressing HopK1 are reduced in PAMP ‐triggered immune responses compared with wild‐type plants. An N‐terminal region of HopK1 shares similarity with the corresponding region in the well‐studied type‐ III effector AvrRps4; however, their C‐terminal regions are dissimilar, indicating that they have different effector activities. HopK1 is processed in planta at the same processing site found in AvrRps4. The processed forms of HopK1 and AvrRps4 are chloroplast localized, indicating that the shared N‐terminal regions of these type‐ III effectors represent a chloroplast transit peptide. The HopK1 contribution to virulence and the ability of HopK1 and AvrRps4 to suppress immunity required their respective transit peptides, but the AvrRps4‐induced HR did not. Our results suggest that a primary virulence target of these type‐ III effectors resides in chloroplasts, and that the recognition of AvrRps4 by the plant immune system occurs elsewhere. Moreover, our results reveal that distinct type‐ III effectors use a cleavable transit peptide to localize to chloroplasts, and that targets within this organelle are important for immunity.