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- Title
The Pseudomonas syringae type III-secreted protein HopPtoD2 possesses protein tyrosine phosphatase activity and suppresses programmed cell death in plants.
- Authors
Espinosa, Avelina; Guo, Ming; Tam, Vincent C.; Fu, Zheng Qing; Alfano, James R.
- Abstract
Summary The bacterial plant pathogen Pseudomonas syringae possesses a type III protein secretion system that delivers many virulence proteins into plant cells. A subset of these proteins (called Avr proteins) is recognized by the plant's innate immune system and triggers defences. One defence-associated response is the hypersensitive response (HR), a programmed cell death (PCD) of plant tissue. We have previously identified HopPtoD2 as a type III secreted protein from P. s. pv. tomato DC3000. Sequence analysis revealed that an N-terminal domain shared homology with AvrPphD and a C-terminal domain was similar to protein tyrosine phosphatases (PTPs). We demonstrated that purified HopPtoD2 possessed PTP activity and this activity required a conserved catalytic Cys residue (Cys378 ). Interestingly, HopPtoD2 was capable of suppressing the HR elicited by an avirulent P. syringae strain on Nicotiana benthamiana . HopPtoD2 derivatives that lacked Cys378 no longer suppressed the HR indicating that HR suppression required PTP activity. A constitutively active MAPK kinase, called NtMEK2DD , is capable of eliciting an HR-like cell death when transiently expressed in tobacco. When NtMEK2DD and HopPtoD2 were co-delivered into plant cells, the HR was suppressed indicating that HopPtoD2 acts downstream of NtMEK2DD . DC3000 hopPtoD2 mutants were slightly reduced in their ability to multiply in planta and displayed an enhanced ability to elicit an HR. The identification of HopPtoD2 as a PTP and a PCD suppressor suggests that the inactivation of MAPK pathways is a virulence strategy utilized by bacterial plant pathogens.
- Subjects
PSEUDOMONAS; PLANT cells &; tissues; PROTEIN-tyrosine phosphatase; CELL death
- Publication
Molecular Microbiology, 2003, Vol 49, Issue 2, p377
- ISSN
0950-382X
- Publication type
Article
- DOI
10.1046/j.1365-2958.2003.03588.x