Broad-spectrum resistance to turnip mosaic virus in Brassica rapa (Chinese cabbage)

TuMV is a member of the Potyvirus genus, infects a wide range of cultivated plant species and causes significant economic losses in Brassica crops (Shattuck, 1992). It is a positive strand RNA virus (genome comprises 9830- 9835 nucleotides) and is the subject of advanced molecular characterisation in terms of its interaction with brassicas (Walsh & Jenner, 2002). Plant genes for resistance to TuMV have been mapped in lettuce (Tu, Robbins et al., 1994), B. napus (TuRB01, Walsh et al., 1999; TuRB03, Hughes et al., 2003; TuRB04 and TuRB05, Walsh & Lydiate, unpublished) and B. rapa (TuRB01b, Rusholme et al., unpublished). All these brassica genes are dominant R genes that control resistance to narrow spectra of TuMV isolates; the viral avirulence determinants for these genes have been identified (Jenner et al., 2000; Walsh et al., 2002; Jenner et al., 2002; Jenner et al., 2003). The B. rapa line RLR22 is resistant to a diverse range of TuMV isolates from different regions of the world, different pathotypes, different serotypes and different genetic groups (Walsh et al., 2002; Rusholme et al., 2007). A B. rapa genetic map based on 213 marker loci segregating in 120 first backcross (B1) individuals was established. B1 individuals were self-pollinated to produce B1S1 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 B1S1 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 the recessive resistance gene retr01 was apparently co-incident with one of the three loci of eIF(iso)4E in the Agenome of B. 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. retr01 is the first example of a recessive resistance gene mapped in a brassica

Repression of Seed Maturation Genes by a Trihelix Transcriptional Repressor in Arabidopsis Seedlings[W]

The seed maturation program is repressed during germination and seedling development so that embryonic genes are not expressed in vegetative organs. Here, we describe a regulator that represses the expression of embryonic seed maturation genes in vegetative tissues. ASIL1 (for Arabidopsis 6b-interacting protein 1-like 1) was isolated by its interaction with the Arabidopsis thaliana 2S3 promoter. ASIL1 possesses domains conserved in the plant-specific trihelix family of DNA binding proteins and belongs to a subfamily of 6b-interacting protein 1-like factors. The seedlings of asil1 mutants exhibited a global shift in gene expression to a profile resembling late embryogenesis. LEAFY COTYLEDON1 and 2 were markedly derepressed during early germination, as was a large subset of seed maturation genes, such as those encoding seed storage proteins and oleosins, in seedlings of asil1 mutants. Consistent with this, asil1 seedlings accumulated 2S albumin and oil with a fatty acid composition similar to that of seed-derived lipid. Moreover, ASIL1 specifically recognized a GT element that overlaps the G-box and is in close proximity to the RY repeats of the 2S promoters. We suggest that ASIL1 targets GT-box–containing embryonic genes by competing with the binding of transcriptional activators to this promoter region

Segmental Structure of the Brassica napus Genome Based on Comparative Analysis With Arabidopsis thaliana

Over 1000 genetically linked RFLP loci in Brassica napus were mapped to homologous positions in the Arabidopsis genome on the basis of sequence similarity. Blocks of genetically linked loci in B. napus frequently corresponded to physically linked markers in Arabidopsis. This comparative analysis allowed the identification of a minimum of 21 conserved genomic units within the Arabidopsis genome, which can be duplicated and rearranged to generate the present-day B. napus genome. The conserved regions extended over lengths as great as 50 cM in the B. napus genetic map, equivalent to ∼9 Mb of contiguous sequence in the Arabidopsis genome. There was also evidence for conservation of chromosome landmarks, particularly centromeric regions, between the two species. The observed segmental structure of the Brassica genome strongly suggests that the extant Brassica diploid species evolved from a hexaploid ancestor. The comparative map assists in exploiting the Arabidopsis genomic sequence for marker and candidate gene identification within the larger, intractable genomes of the Brassica polyploids

Genetic Resistance to Turnip mosaic virus (TuMV) in Brassicas

Turnip mosaic virus (TuMV) is a member of the Potyvirus genus, infects a wide range of cultivated plant species and causes significant economic losses in Brassica crops (Shattuck, 1992). It is a positive strand RNA virus (genome comprises 9830-9835 nucleotides) and is the subject of advanced molecular characterisation in terms of its interaction with brassicas (Walsh & Jenner, 2002). Plant genes for resistance to TuMV have been mapped in lettuce (Tu, Robbins et al., 1994), B. napus(TuRB01, Walsh et al., 1999; TuRB03, Hughes et al., 2003; TuRB04 and TuRB05, Walsh & Lydiate, unpublished) and B. rapa (TuRB01b, Rusholme et al., unpublished). All these brassica genes are dominant R genes that control resistance to narrow spectra of TuMV isolates; the viral avirulence determinants for these genes have been identified (Jenner et al., 2000; Walsh et al., 2002; Jenner et al., 2002; Jenner et al., 2003)