Black rot, caused by Xanthomonas campestris pv. campestris (Xcc) is possibly the most important disease of Brassica worldwide. To compare chromosomal positions of Xcc resistance loci in Brassica oleracea between the p...Black rot, caused by Xanthomonas campestris pv. campestris (Xcc) is possibly the most important disease of Brassica worldwide. To compare chromosomal positions of Xcc resistance loci in Brassica oleracea between the present and published studies and to develop marker assisted selection (MAS) to resistance against Xcc race 1, we constructed a B. oleracea map, including pW, pX and BoCL markers that were closely linked to previously reported Xcc resistance QTLs. We also analyzed Xcc resistance QTLs by improving our previously reported map derived from the cross of a susceptible double-haploid line (GC P09) with a resistant double-haploid line (Reiho P01). In the nine linkage groups obtained (C1-C9), the major QTL, XccBo(Reiho)2, was derived from Reiho with a maximum LOD score (7.7) in C8. The QTL (LOD 4.4) located in C9, XccBo(GC)1 was derived from the susceptible GC. The other QTL (LOD 4.4), XccBo(Reiho)1, was found in C5. Based on common markers, it was possible to compare our finding Xcc resistance QTLs with the B. oleraceaXcc loci reported by previous authors;XccBo(Reiho)1 and XccBo(GC)1 may be identical to the Xcc resistance QTLs reported previously or a different member contained in the same resistance gene cluster. Our map includes public SSR markers linked to Xcc resistance genes that will promote pyramiding Xcc resistance genes in B. oleracea. The present study will also contribute to a better understanding of genetic control of Xcc resistance.展开更多
Bacterial proliferation in hosts requires activation of a number of housekeeping pathways, including purine de novo biosynthesis. Although inactivation of purine biosynthesis genes can attenuate virulence, it is uncle...Bacterial proliferation in hosts requires activation of a number of housekeeping pathways, including purine de novo biosynthesis. Although inactivation of purine biosynthesis genes can attenuate virulence, it is unclear which biochemical or virulence factors are associated with the purine biosynthesis pathway in vivo. We report that inactivation of purC, a gene encoding phosphoribosylaminoimidazole-succinocarboxamide synthase, caused complete loss of virulence in Xanthomonas campestris pv. cam- pestris, the causal agent of black rot disease of cruciferous plants. The purC mutant was a purine auxotroph; it could not grow on minimal medium, whereas addition of purine derivatives, such as hypoxanthine or adenine plus guanine, restored growth of the mutant. The purC mutation also significantly enhanced the production of an unknown purine synthesis associated pigment and extracellular polysaccharides by the bacterium. In addition, comparative proteomic analyses of bacteria grown on rich and minimal media revealed that the purC mutation affected the expression levels of diverse proteins involved in purine and pyrimidine synthesis, carbon and energy metabolisms, iron uptake, proteolysis, protein secretion, and signal transduction. These results provided clues to understanding the contributions of purine synthesis to bacterial virulence and interactions with host immune systems.展开更多
文摘Black rot, caused by Xanthomonas campestris pv. campestris (Xcc) is possibly the most important disease of Brassica worldwide. To compare chromosomal positions of Xcc resistance loci in Brassica oleracea between the present and published studies and to develop marker assisted selection (MAS) to resistance against Xcc race 1, we constructed a B. oleracea map, including pW, pX and BoCL markers that were closely linked to previously reported Xcc resistance QTLs. We also analyzed Xcc resistance QTLs by improving our previously reported map derived from the cross of a susceptible double-haploid line (GC P09) with a resistant double-haploid line (Reiho P01). In the nine linkage groups obtained (C1-C9), the major QTL, XccBo(Reiho)2, was derived from Reiho with a maximum LOD score (7.7) in C8. The QTL (LOD 4.4) located in C9, XccBo(GC)1 was derived from the susceptible GC. The other QTL (LOD 4.4), XccBo(Reiho)1, was found in C5. Based on common markers, it was possible to compare our finding Xcc resistance QTLs with the B. oleraceaXcc loci reported by previous authors;XccBo(Reiho)1 and XccBo(GC)1 may be identical to the Xcc resistance QTLs reported previously or a different member contained in the same resistance gene cluster. Our map includes public SSR markers linked to Xcc resistance genes that will promote pyramiding Xcc resistance genes in B. oleracea. The present study will also contribute to a better understanding of genetic control of Xcc resistance.
基金supported by the grants from the National Basic Research Program of the Ministry of Science and Technology of China(No.2011CB100700)the National Science Foundation of China(Nos.31100065 and 31070081)the Basic Research of Frontiers of the Chinese Academy of Sciences(No.KSCX2-EW-J-6)
文摘Bacterial proliferation in hosts requires activation of a number of housekeeping pathways, including purine de novo biosynthesis. Although inactivation of purine biosynthesis genes can attenuate virulence, it is unclear which biochemical or virulence factors are associated with the purine biosynthesis pathway in vivo. We report that inactivation of purC, a gene encoding phosphoribosylaminoimidazole-succinocarboxamide synthase, caused complete loss of virulence in Xanthomonas campestris pv. cam- pestris, the causal agent of black rot disease of cruciferous plants. The purC mutant was a purine auxotroph; it could not grow on minimal medium, whereas addition of purine derivatives, such as hypoxanthine or adenine plus guanine, restored growth of the mutant. The purC mutation also significantly enhanced the production of an unknown purine synthesis associated pigment and extracellular polysaccharides by the bacterium. In addition, comparative proteomic analyses of bacteria grown on rich and minimal media revealed that the purC mutation affected the expression levels of diverse proteins involved in purine and pyrimidine synthesis, carbon and energy metabolisms, iron uptake, proteolysis, protein secretion, and signal transduction. These results provided clues to understanding the contributions of purine synthesis to bacterial virulence and interactions with host immune systems.
