A Conserved EAR Motif Is Required for Avirulence and Stability of the Ralstonia solanacearum Effector PopP2 In Planta

(extract) Overall, this study reveals high conservation of the PopP2 effector in Korean R. solanacearum strains isolated from commercially cultivated tomato and pepper genotypes. Importantly, our data also indicate that the PopP2 conserved repressor motif could contribute to the effector accumulation in plant cells

The Arabidopsis Resistance-Like Gene SNC1 Is Activated by Mutations in SRFR1 and Contributes to Resistance to the Bacterial Effector AvrRps4

The SUPPRESSOR OF rps4-RLD1 (SRFR1) gene was identified based on enhanced AvrRps4-triggered resistance in the naturally susceptible Arabidopsis accession RLD. No other phenotypic effects were recorded, and the extent of SRFR1 involvement in regulating effector-triggered immunity was unknown. Here we show that mutations in SRFR1 in the accession Columbia-0 (Col-0) lead to severe stunting and constitutive expression of the defense gene PR1. These phenotypes were temperature-dependent. A cross between srfr1-1 (RLD background) and srfr1-4 (Col-0) showed that stunting was caused by a recessive locus in Col-0. Mapping and targeted crosses identified the Col-0-specific resistance gene SNC1 as the locus that causes stunting. SRFR1 was proposed to function as a transcriptional repressor, and SNC1 is indeed overexpressed in srfr1-4. Interestingly, co-regulated genes in the SNC1 cluster are also upregulated in the srfr1-4 snc1-11 double mutant, indicating that the overexpression of SNC1 is not a secondary effect of constitutive defense activation. In addition, a Col-0 RPS4 mutant showed full susceptibility to bacteria expressing avrRps4 at 24°C but not at 22°C, while RLD susceptibility was not temperature-dependent. The rps4-2 snc1-11 double mutant showed increased, but not full, susceptibility at 22°C, indicating that additional cross-talk between resistance pathways may exist. Intriguingly, when transiently expressed in Nicotiana benthamiana, SRFR1, RPS4 and SNC1 are in a common protein complex in a cytoplasmic microsomal compartment. Our results highlight SRFR1 as a convergence point in at least a subset of TIR-NBS-LRR protein-mediated immunity in Arabidopsis. Based on the cross-talk evident from our results, they also suggest that reports of constitutive resistance phenotypes in Col-0 need to consider the possible involvement of SNC1

Effect of achene morphology and mass on germination and seedling growth of Boltonia decurrens (Asteraceae), a threatened floodplain species

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Examination of host genetic determinants of the hypersensitive response in Nicotiana edwardsonii to CaMV and TMV

The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file.Title from title screen of research.pdf file viewed on (March 1, 2007)Vita.Thesis (Ph. D.) University of Missouri-Columbia 2006.[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT REQUEST OF AUTHOR.] The hypersensitive response (HR) is an indicator of genetic resistance when screening for disease resistance to viral pathogens. Genetic resistance has been described as having two characteristics: rapid cell death at the site of inoculation and localization of the pathogen to that site. I examined a resistant Nicotiana hybrid, which does not respond with HR-mediated cell death, yet maintains resistance to Cauliflower mosaic virus (CaMV) strain W260. Another host gene, CCD1, blocks both HR-mediated and systemic cell death induced specifically by P6 of CaMV strain W260. Interfering double stranded RNA (RNAi) technology has proven to be a very effective way to silence a single gene in plants. With the design and construction of gene silencing hairpins homologous with known conserved sequences of identified R genes, it is possible to silence large families of R genes. Examination of the HR in these silenced plants can identify putative resistance genes. With these silencing hairpins, I showed that the endogenous N gene can be silenced with both constructs. Additionally, resistance to another virus, Tomato bushy stunt virus (TBSV), breaks down in the silenced plants. This is evidence that not only the N gene can be silenced, but also that resistance genes that differ from the N gene by as much as 10% can also be silenced when homologous sequences are used.Includes bibliographical reference

The plant gene CCD1 selectively blocks cell death during the hypersensitive response to cauliflower mosaic virus infection

The P6 protein of Cauliflower mosaic virus (CaMV) W260 elicits a hypersensitive response (HR) on inoculated leaves of Nicotiana edwardsonii. This defense response, common to many plant pathogens, has two key characteristics, cell death within the initially infected tissues and restriction of the pathogen to this area. We present evidence that a plant gene designated CCD1, originally identified in N. bigelovii, can selectively block the cell death pathway during HR, whereas the resistance pathway against W260 remains intact. Suppression of cell death was evident not only macroscopically but also microscopically. The suppression of HR-mediated cell death was specific to CaMV, as Tobacco mosaic virus was able to elicit HR in the plants that contained CCD1. CCD1 also blocks the development of a systemic cell death symptom induced specifically by the P6 protein of W260 in N. clevelandii. Introgression of CCD1 from N. bigelovii into N. clevelandii blocked the development of systemic cell death in response to W260 infection but could not prevent systemic cell death induced by Tomato bushy stunt virus. Thus, CCD1 blocks both local and systemic cell death induced by P6 of W260 but does not act as a general suppressor of cell death induced by other plant viruses. Furthermore, experiments with CCD1 provide further evidence that cell death could be uncoupled from resistance in the HR of Nicotiana edwardsonii to CaMV W260

Isolation and characterization of the N family of resistance genes [abstract]

Abstract only availableFaculty Mentor: James Schoelz, Plant PathologyThe N gene is a virus resistance gene found in the genome of Nicotiana glutinosa, which confers resistance to tobacco mosaic virus (TMV), among many other plant diseases. It is characteristic of a family of plant receptors that contain an N-terminal nucleotide-binding site (NBS) and a C-terminal leucine-rich repeat (LRR) which recognize and defend against attack by plant pathogens. Recently, a gene silencing assay has found that a second N. glutinosa resistance gene is responsible for targeting tombusviruses, such as tomato bushy stunt virus (TBSV), and is also closely related to the N gene. In order to identify and clone the TBSV resistance gene, NBS-LRR genes that are closely related to the N gene are being characterized. A previous PCR-based assay coupled with nucleotide sequencing indicated that the N-family of resistance genes consists of approximately 15 members. Currently, N homologs are being physically isolated from a N. glutinosa bacterial artificial chromosome (BAC) library. The N. glutinosa BAC library was probed with a portion of Exon1 of the N gene and to date, 13 BAC clones have been isolated. Portions of the N gene present on each of the BAC clones are being sequenced in an effort to further characterize the members of the N family of resistance genes

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Hypersensitive response (HR)-conferred resistance to viral infection restricts the virus spread and is accompanied by the induction of cell death, manifested as the formation of necrotic lesions. While it is known that salicylic acid is the key component in the orchestration of the events restricting viral spread in HR, the exact function of the cell death in resistance is still unknown. We show that potato virus Y (PVY) can be detected outside the cell death zone in Ny-1-mediated HR in potato plants (cv. Rywal), observed as individual infected cells or small clusters of infected cells outside the cell death zone. By exploiting the features of temperature dependent Ny-1-mediated resistance, we confirmed that the cells at the border of the cell death zone are alive and harbor viable PVY that is able to reinitiate infection. To get additional insights into this phenomenon we further studied the dynamics of both cell death zone expansion and occurrence of viral infected cell islands outside it. We compared the response of Rywal plants to their transgenic counterparts, impaired in SA accumulation (NahG-Rywal), where the lesions occur but the spread of the virus is not restricted. We show that the virus is detected outside the cell death zone in all lesion developmental stages of HR lesions. We also measured the dynamics of lesions expansion in both genotypes. We show that while rapid lesion expansion is observed in SA-depleted plants, virus spread is even faster. On the other hand the majority of analyzed lesions slowly expand also in HR-conferred resistance opening the possibility that the infected cells are eventually engulfed by cell death zone. Taken altogether, we suggest that the HR cell death is separated from the resistance mechanisms which lead to PVY restriction in Ny-1 genetic background. We propose that HR should be regarded as a process where the dynamics of events is crucial for effectiveness of viral arrest albeit the exact mechanism conferring this resistance remains unknown