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Cell Host Microbe. 2015 Jun 10;17(6):752-62. doi: 10.1016/j.chom.2015.05.007.

Pseudomonas syringae pv. tomato DC3000 Type III Secretion Effector Polymutants Reveal an Interplay between HopAD1 and AvrPtoB.

Author information

1
School of Integrative Plant Science, Section of Plant Pathology and Plant-Microbe Biology, Cornell University, Ithaca, NY 14853, USA.
2
Boyce Thompson Institute for Plant Research, Ithaca, NY 14853, USA.
3
United States Department of Agriculture-Agricultural Research Service, Ithaca, NY 14853, USA.
4
School of Integrative Plant Science, Section of Plant Pathology and Plant-Microbe Biology, Cornell University, Ithaca, NY 14853, USA; United States Department of Agriculture-Agricultural Research Service, Ithaca, NY 14853, USA.
5
School of Integrative Plant Science, Section of Plant Pathology and Plant-Microbe Biology, Cornell University, Ithaca, NY 14853, USA; Boyce Thompson Institute for Plant Research, Ithaca, NY 14853, USA. Electronic address: gbm7@cornell.edu.
6
School of Integrative Plant Science, Section of Plant Pathology and Plant-Microbe Biology, Cornell University, Ithaca, NY 14853, USA. Electronic address: arc2@cornell.edu.

Abstract

The bacterial pathogen Pseudomonas syringae pv. tomato DC3000 suppresses the two-tiered plant innate immune system by injecting a complex repertoire of type III secretion effector (T3E) proteins. Beyond redundancy and interplay, individual T3Es may interact with multiple immunity-associated proteins, rendering their analysis challenging. We constructed a Pst DC3000 polymutant lacking all 36 T3Es and restored individual T3Es or their mutants to explore the interplay among T3Es. The weakly expressed T3E HopAD1 was sufficient to elicit immunity-associated cell death in Nicotiana benthamiana. HopAD1-induced cell death was suppressed partially by native AvrPtoB and completely by AvrPtoBM3, which has mutations disrupting its E3 ubiquitin ligase domain and two known domains for interacting with immunity-associated kinases. AvrPtoBM3 also gained the ability to interact with the immunity-kinase MKK2, which is required for HopAD1-dependent cell death. Thus, AvrPtoB has alternative, competing mechanisms for suppressing effector-triggered plant immunity. This approach allows the deconvolution of individual T3E activities.

PMID:
26067603
PMCID:
PMC4471848
DOI:
10.1016/j.chom.2015.05.007
[Indexed for MEDLINE]
Free PMC Article

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