TYLCV-Is is a major tomato pathogen, causing extensive crop losses in Israel and the U.S. We have identified a TYLCV-Is protein, V2, which acts as a suppressor of RNA silencing. Intriguingly, the counter-defense function of V2 may not be limited to silencing suppression. Our recent data suggest that V2 interacts with the tomato CYP1 protease. CYP1 belongs to the family of papain-like cysteine proteases which participate in programmed cell death (PCD) involved in plant defense against pathogens. Based on these data we proposed a model for dual action of V2 in suppressing the host antiviral defense: V2 targets SGS3 for degradation and V2 inhibits CYP1 activity. To study this we proposed to tackle three specific objectives. I. Characterize the role of V2 in SGS3 proteasomal degradation ubiquitination, II. Study the effects of V2 on CYP1 maturation, enzymatic activity, and accumulation and, III. Analyze the effects of the CYP1-V2 interaction on TYLCV-Is infection. Here we describe results from our study that support our hypothesis: the involvement of the host's innate immune system—in this case, PCD—in plant defense against TYLCV-Is. Also, we use TYLCV-Is to discover the molecular pathway(s) by which this plant virus counters this defense. Towards the end of our study we discovered an interesting involvement of the C2 protein encoded by TYLCV-Is in inducing Hypersensitive Response in N. benthamianaplants which is not the case when the whole viral genome is introduced. This might lead to a better understanding of the multiple processes involved in the way TYLCV is overcoming the defense mechanisms of the host plant cell. In a parallel research supporting the main goal described, we also investigated Agrobacteriumtumefaciens-encoded F-box protein VirF. It has been proposed that VirF targets a host protein for the UPS-mediated degradation, very much the way TYLCV V2 does. In our study, we identified one such interactor, an Arabidopsistrihelix-domain transcription factor VFP3, and further show that its very close homolog VFP5 also interacted with VirF. Interestingly, interactions of VirF with either VFP3 or VFP5 did not activate the host UPS, suggesting that VirF might play other UPS-independent roles in bacterial infection. Another target for VirF is VFP4, a transcription factor that both VirF and its plant functional homolog VBF target to degradation by UPS. Using RNA-seqtranscriptome analysis we showed that VFP4 regulates numerous plant genes involved in disease response, including responses to viral and bacterial infections. Detailed analyses of some of these genes indicated their involvement in plant protection against Agrobacterium infection. Thus, Agrobacterium may facilitate its infection by utilizing the host cell UPS to destabilize transcriptional regulators of the host disease response machinery that limits the infection.
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