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Unformatted text preview: RIN13 Is a Positive Regulator of the Plant Disease Resistance Protein RPM1 W Antonious Al-Daoude, 1 Marta de Torres Zabala, Jong-Hyun Ko, and Murray Grant 2 Department of Agricultural Science, Imperial College, London, TN25 5AH United Kingdom The RPM1 protein confers resistance to Pseudomonas syringae pv tomato DC3000 expressing either of the Type III effector proteins AvrRpm1 or AvrB. Here, we describe the isolation and functional characterization of RPM1 Interacting Protein 13 (RIN13), a resistance protein interactor shown to positively enhance resistance function. Ectopic expression of RIN13 ( RIN13s ) enhanced bacterial restriction mechanisms but paradoxically abolished the normally rapid hypersensitive response (HR) controlled by RPM1. In contrast with wild-type plants, leaves expressing RIN13s did not undergo electrolyte leakage or accumulate H 2 O 2 after bacterial delivery of AvrRpm1. Overexpression of RIN13 also altered the transcription profile observed during a normal HR. By contrast, RIN13 knockout plants had the same ion leakage signatures and HR timing of wild-type plants in response to DC3000( avrRpm1 ) but failed to suppress bacterial growth. The modified phenotypes seen in the RIN13s/as plants were specific to recognition of AvrRpm1 or AvrB, and wild-type responses were observed after challenge with other incompatible pathogens or the virulent DC3000 isolate. Our results suggest that cell death is not necessary to confer resistance, and engineering enhanced resistance without activation of programmed cell death is a real possibility. INTRODUCTION Generally, plant basal defenses function successfully to prevent pathogen infection, and disease is relatively rare. When bacterial phytopathogens enter the apoplast of plants via wounds, sto- mata, or hydathodes, they rapidly induce a set of pathogen genes encoding a specialized structure, the Type III secretion apparatus. The type III secretion system (TTSS) acts as a conduit via which a constellation of proteinaceous products known as TTSS effectors are delivered into the host cell. The subsequent outcome of the infection is dependent upon the genetic consti- tution of both the host and pathogen (Espinosa et al., 2003). The successful suppression of host defenses by TTSS effectors results in disease. Alternatively, resistance pathways may be ac- tivated after the direct or indirect interaction of a specific Type III effector (the avirulence gene product) with its cognate plant disease resistance ( R ) gene product (Jin et al., 2003). Usually such gene-for-gene recognition (Flor, 1971) results in a visible hypersensitive response (HR) that effectively restricts pathogen growth. The R proteins are key to integrating and transducing signals leading to the HR and play a central role in plant innate immune responses (reviewed in Bonas and Lahaye, 2002). Remarkably, the majority of R proteins fall into a single highly conserved class distinguished by two common structural features, the most...
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- Spring '10
- cell death, RIN13s, hypersensitive cell death