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Mol Plant Microbe Interact. 2009 Nov;22(11):1341-55. doi: 10.1094/MPMI-22-11-1341.

Pseudomonas syringae pv. tomato DC3000 type III effector HopAA1-1 functions redundantly with chlorosis-promoting factor PSPTO4723 to produce bacterial speck lesions in host tomato.

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Department of Plant Pathology and Plant-Microbe Biology, Cornell University, Ithaca, NY 14853, USA.


The ability of Pseudomonas syringae pv. tomato DC3000 to cause bacterial speck disease in tomato is dependent on the injection, via the type III secretion system, of approximately 28 Avr/Hop effector proteins. HopAA1-1 is encoded in the conserved effector locus (CEL) of the P. syringae Hrp pathogenicity island. Transiently expressed HopAA1-1 acts inside Saccharomyces cerevisiae and plant cells to elicit cell death. hopAA1 homologs were cloned and sequenced from the CEL of seven P. syringae strains representing diverse pathovars. Analysis of the sequences revealed that HopAA1-1 carries a potential GTPase-activating protein (GAP) domain, GALRA, which is polymorphic (FEN instead of LRA) in HopAA1-2, a paralogous DC3000 effector. Deleting hopAA1-1 from DC3000 reduces the formation of necrotic speck lesions in dip-inoculated tomato leaves if effector-gene cluster IX or just PSPTO4723 within this region has been deleted. A HopAA1-1 mutant in which the putative catalytic arginine in the GAP-like domain has been replaced with alanine retains its ability to kill yeast and promote the formation of speck lesions by the DeltahopAA1-1DeltaIX mutant, but a HopAA1-1 mutant carrying the FEN polymorphism loses both of these abilities. Unexpectedly, PSPTO4723 does not appear to encode an effector and its deletion also reduces disease-associated chlorosis.

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