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Title: Tomato 14-3-3 protein 7 (TFT7) positively regulates immunity-associated programmed cell death by enhancing accumulation and signaling ability of MAPKKKalpha

item OH, CHANG-SIK - Boyce Thompson Institute
item Pedley, Kerry
item MARTIN, GREGORY - Boyce Thompson Institute

Submitted to: The Plant Cell
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/17/2009
Publication Date: 1/8/2010
Citation: Oh, C., Pedley, K.F., Martin, G.B. 2010. Tomato 14-3-3 protein 7 (TFT7) positively regulates immunity-associated programmed cell death by enhancing accumulation and signaling ability of MAPKKKalpha. The Plant Cell. 22(1):260-272.

Interpretive Summary: Pseudomonas syringae pv. tomato is the causal agent of bacterial speck disease of tomato. Resistance is mediated by proteins that recognize bacterial effector proteins during the early stages of infection. The recognition of the pathogen triggers a form of defense response called programmed cell death that ultimately limits the spread of the pathogen beyond the initial site of infection. In this paper, we describe studies to identify and characterize proteins that interact with each other during the infection process, and signal to the plant to initiate or enhance defense responses. We identified and characterized two specific proteins that interact in plant defense signaling pathways that are required for tomato resistance against bacterial speck disease. Knowledge of these specific interactions will be useful in understanding and developing novel strategies for plant resistance to bacterial pathogens.

Technical Abstract: Programmed cell death (PCD) is triggered when Pto, a serine-threonine protein kinase recognizes either the AvrPto or AvrPtoB effector from Pseudomonas syringae pv. tomato. This PCD requires MAPKKKalpha as a positive regulator in tomato and Nicotiana benthamiana. To examine how PCD-eliciting activity of tomato MAPKKKalpha (SlMAPKKKalpha) protein is regulated, we screened for SlMAPKKKalpha-interacting proteins in tomato and identified two 14-3-3 proteins, TFT7 and TFT10. Virus-induced gene silencing using the TFT7 gene in N. benthamiana compromised both Pto- and SlMAPKKKalpha-mediated PCD and co-expression of TFT7 with SlMAPKKKalpha enhanced SlMAPKKKalpha-mediated PCD. TFT7 was also required for PCD associated with several other disease resistance proteins and contributed to resistance against Pseudomonas syringae pv. tomato. Co-expression of TFT7 with SlMAPKKKalpha in vivo caused increased accumulation of the kinase and enhanced phosphorylation of two MAP kinases. TFT7 protein contains a phosphopeptide-binding motif that is present in human 14-3-3epsilon and substitutions in this motif abolished interaction with SlMAPKKKalpha in vivo and also the PCD-enhancing activity of TFT7. A 14-3-3 binding motif, including a putative phosphorylated Ser535, is present in the C-terminal region of SlMAPKKKalpha. An S535A substitution in SlMAPKKKalpha reduced TFT7 interaction with the kinase, TFT7 ability to increase accumulation of SlMAPKKKalpha, and TFT7-mediated enhancement of PCD. Our results indicate that TFT7 positively regulates multiple immunity-associated PCD pathways probably by affecting stability of client proteins such as MAPKKKalpha.