BackgroundCabbage Fusarium wilt is a major disease worldwide that can cause severe yield loss in cabbage (Brassica olerecea). Although markers linked to the resistance gene FOC1 have been identified, no candidate gene for it has been determined so far. In this study, we report the fine mapping and analysis of a candidate gene for FOC1 using a double haploid (DH) population with 160 lines and a F2 population of 4000 individuals derived from the same parental lines.ResultsWe confirmed that the resistance to Fusarium wilt was controlled by a single dominant gene based on the resistance segregation ratio of the two populations. Using InDel primers designed from whole-genome re-sequencing data for the two parental lines (the resistant inbred-line 99–77 and the highly susceptible line 99–91) and the DH population, we mapped the resistance gene to a 382-kb genomic region on chromosome C06. Using the F2 population, we narrowed the region to an 84-kb interval that harbored ten genes, including four probable resistance genes (R genes): Bol037156, Bol037157, Bol037158 and Bol037161 according to the gene annotations from BRAD, the genomic database for B. oleracea. After correcting the model of the these genes, we re-predicted two R genes in the target region: re-Bol037156 and re-Bol0371578. The latter was excluded after we compared the two genes’ sequences between ten resistant materials and ten susceptible materials. For re-Bol037156, we found high identity among the sequences of the resistant lines, while among the susceptible lines, there were two types of InDels (a 1-bp insertion and a 10-bp deletion), each of which caused a frameshift and terminating mutation in the cDNA sequences. Further sequence analysis of the two InDel loci from 80 lines (40 resistant and 40 susceptible) also showed that all 40 R lines had no InDel mutation while 39 out of 40 S lines matched the two types of loci. Thus re-Bol037156 was identified as a likely candidate gene for FOC1 in cabbage.ConclusionsThis work may lay the foundation for marker-assisted selection as well as for further function analysis of the FOC1 gene.

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Lipophilic extracts from flowers, leaves, and roots of Lamiophlomis rotata (Benth.) were analyzed using GC-MS. A total of 67 compounds were identified.Lamiophlomis (family Lamiaceae) is a monotypic genus with the species L. rotata (Benth.) Kudo, which is endemic to the Qinghai-Tibetan Plateau [1]. L. rotata is a nonstalk and perennial herb distributed in Bhutan, India (Sikkim), Nepal, and China [2]. In China, it has long been used as a folk medicinal plant to promote blood circulation, remove blood stasis, subdue swelling, and alleviate pain [3]. Current studies have indicated that L. rotata can be a remedy for a number of diseases, such as cancer, multidrug resistant tuberculosis (MDR-TB), rheumatic arthritis, and breast swelling [4][5][6][7][8][9]. More than ten compounds have been isolated from this species, in which four are phenylpropanoid glycosides and seven are iridoids [10,11]. However, lipophilic extracts in L. rotata have not been previously investigated.We identified a total of 67 compounds in the lipophilic extracts from flowers, leaves, and roots of L. rotata from three regions in the Qinghai-Tibetan Plateau, i.e., Tibetan Autonomous Region, Qinghai Province, and Yunnan Province (Table 1). The sixteen major compounds (> 4%) isolated included five common to flowers, leaves, and roots: linolenic acid methyl ester (8.77-11.90% in flowers, 11.19-18.23% in leaves, and 17.31-20.80% in roots), 9,12-octadecadienoic acid (6.90-15.78% in flowers, 2.75-9.36% in leaves, and 8.06-19.11% in roots), hexadecanoic acid (9.97-14.98% in flowers, 7.08-12.42% in leaves, and 9.65-18.54% in roots), β-sitosterol (13.72-16.63% in flowers, 15.04-18.00% in leaves, and 13.05-16.57% in roots), and stearic acid (2.41-4.07% in flowers, 2.02-4.52% in leaves, and tr -7.83% in roots); one common to flowers and roots, i.e., n-cetane (0.12-4.13% in flowers and 0.24-7.17% in roots); one common to flowers and leaves, i.e., n-hentriacontane (4.08-7.76% in flowers and 7.18-8.58% in roots); three in flowers only: myristic acid (0.94-4.09%), cyclohexenylacetic acid (2.41-4.07%) and n-nonacosane (4.33-4.80%); two in the leaves only: trimethyl-pentadecan-2-ol (5.06-7.50%) and n-tritriacontane (0.93-5.08%); and four in roots only: campesterol (3.92-8.83%), n-heptadecane (0.26-7.69%), n-pentadecane (1.15-5.71%), and n-octadecane (tr-4.93%). EXPERIMENTALFresh samples of L. rotata were collected from eight locations in three regions i.e., Tibet (four locations), Qinghai (two locations), and Yunnan (two locations) in August, 2004. The voucher specimens were deposited at the Ministry of Education Key Laboratory for Biodiversity Science and Ecological Engineering at Fudan University. Plant material was air dried at room temperature for about a month prior to analysis.

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Red-fleshed radish (Raphanus sativus L.) is a unique cultivar whose taproot is rich in anthocyanins beneficial to human health. However, the frequent occurrence of white-fleshed mutants affects the purity of commercially produced radish and the underlying mechanism has puzzled breeders for many years. In this study, we combined quantitative trait location by genome resequencing and transcriptome analyses to identify a candidate gene (RsMYB1) responsible for anthocyanin accumulation in red-fleshed radish. However, no sequence variation was found in the coding and regulatory regions of the RsMYB1 genes of red-fleshed (MTH01) and white-fleshed (JC01) lines, and a 7372 bp CACTA transposon in the RsMYB1 promoter region occurred in both lines. A subsequent analysis suggested that the white-fleshed mutant was the result of altered DNA methylation in the RsMYB1 promoter. This heritable epigenetic change was due to the hypermethylated CACTA transposon, which induced the spreading of DNA methylation to the promoter region of RsMYB1. Thus, RsMYB1 expression was considerably down-regulated, which inhibited anthocyanin biosynthesis in the white-fleshed mutant. An examination of transgenic radish calli and the results of a virus-induced gene silencing experiment confirmed that RsMYB1 is responsible for anthocyanin accumulation. Moreover, the mutant phenotype was partially eliminated by treatment with a demethylating agent. This study explains the molecular mechanism regulating the appearance of white-fleshed mutants of red-fleshed radish.

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