The Brassica rapa line RLR22 was resistant to eight diverse turnip mosaic virus (TuMV) isolates. A B. rapa genetic map based on 213 marker loci segregating in 120 first back-cross (B 1 ) individuals was established and aligned with the B. rapa genome reference map using some of the RFLP probes. B 1 individuals were self-pollinated to produce B 1 S 1 families. The existence of two loci controlling resistance to TuMV isolate CDN 1 was established from contrasting patterns of segregation for resistance and susceptibility in the B 1 S 1 families. The first gene, recessive TuMV resistance 01 (retr01), had a recessive allele for resistance, was located on the upper portion of chromosome R4 and was epistatic to the second gene. The second gene, Conditional TuMV resistance 01 (ConTR01), possessed a dominant allele for resistance and was located on the upper portion of chromosome R8. These genes also controlled resistance to TuMV isolate CZE 1 and might be sufficient to explain the broad-spectrum resistance of RLR22. The dominant resistance gene, ConTR01, was coincident with one of the three eukaryotic initiation factor 4E (eIF4E) loci of B. rapa and possibly one of the loci of eIF(iso)4E. The recessive resistance gene retr01 was apparently coincident with one of the three loci of eIF(iso)4E in the A genome of Brassica napus and therefore, by inference, in the B. rapa genome. This suggested a mode of action for the resistance that is based on denying the viral RNA access to the translation initiation complex of the plant host. The gene retr01 is the first reported example of a recessive resistance gene mapped in a Brassica species. INTRODUCTIONTurnip mosaic virus (TuMV; genus Potyvirus) infects a wide range of cultivated plant species (Edwardson & Christie, 1991) and causes significant economic losses in Brassica crops (Shattuck, 1992). TuMV is a positive-strand RNA virus with a genome comprising 9830-9835 nt (Nicolas & Laliberté, 1992;Ohshima et al., 1996; Jenner et al., 2000) and is the subject of advanced molecular characterization (Revers et al., 1999; Jenner et al., 2000;. Plant genes for resistance to TuMV have been mapped in lettuce (Tu, Robbins et al., 1994), Brassica napus (TuRB01, Walsh et al., 1999; TuRB03, Hughes et al., 2003; TuRB04 and TuRB05, J. A. Walsh & D. J. Lydiate, unpublished) and Brassica rapa (TuRB01b, Rusholme et al., 2007). All are dominant resistance genes (R genes) that control resistance to narrow spectra of TuMV isolates. In the case of TuRB01, TuRB01b and TuRB04, the cytoplasmic inclusion protein has been identified as the viral avirulence determinant (Jenner et al., 2000Walsh et al., 2002). For TuRB03 and TuRB05, the viral avirulence determinant is the P3 protein .Plants possess a range of defence responses against viral pathogens. The best-characterized defence responses lead to a hypersensitive reaction with localized cell death and are often associated with activation of systemic acquired resistance and restriction of the virus to the initial site of infection (Staskawicz et al., ...
Russian apple R12740-7A is the designation for an accession grown from seed collected in Russia, which was found to be highly resistant to apple scab. The resistance has historically been attributed to a naturally pyramided complex involving three major genes: one race-nonspecific gene, Vr, conditioning resistance to all known races, plus two race-specific genes. The race-nonspecific gene was identified as an independently segregating gene by Dayton and Williams (1968) and is referred to in this paper as Vr-DW. The first researchers to study the scab resistance gene complex in Russian apple never described the phenotype conditioned by the race-nonspecific gene. Later, Aldwinckle et al. (1976) associated the name Vr with a scab resistance gene conditioning distinctive stellate necrotic reactions, which we refer to as Vr-A in order to distinguish it from Vr-DW. We show that the segregation ratios in progenies from the scab differential hosts 2 and 4 that are derived from Russian apple, crossed with susceptible cultivars were consistent with a single gene conditioning resistance in each host. The genes have been named Vh2 and Vh4, respectively. Resistant segregants from host 2 showed stellate necrotic reactions, while those from host 4 showed hypersensitive reactions. Both the phenotypes and the genetic maps for the genes in the respective hosts were very similar to those of the genes previously named Vr-A and Vx, respectively, in an F1 family of Russian apple. We showed that race 2 of V. inaequalis isolated from host 2 was able to infect resistant descendants of the non-differential accession PRI 442-23 as well as host 2. The descendants of PRI 442-23 were expected to carry the race-nonspecific Vr-DW gene, but in fact carry Vr-A. We conclude that the Vh2
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