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Fusarium wilt (FW) is a very serious soil-borne disease worldwide, which usually results in huge yield losses in cucumber production. However, the inheritance and molecular mechanism of the response to FW are still unknown in cucumber (Cucumis sativus L.). In this study, two inbred cucumber lines Superina (P1) and Rijiecheng (P2) were used as the sensitive and resistant lines, respectively. A mixed major gene plus polygene inheritance model was used to analyze the resistance to FW in different generations of cucumber, namely, P1, P2, F1 (P1×P2), B1, and B2, obtained by backcrossing F1 plants with Superina (B1) or Rijiecheng (B2), and F2, obtained by self-crossing the F1 plants. After screening 18 genetic models, we chose the E-1 model, which included two pairs of additive-dominance-epistatic major genes and additive-dominance polygenes, as the optimal model for resistance to FW on the basis of fitness tests. The major effect quantitative trait locus (QTL) fw2.1 was detected in a 1.91-Mb-long region of chromosome 2 by bulked-segregant analysis. We used five insertion/deletion markers to fine-map the fw2.1 to a 0.60 Mb interval from 1,248,093 to 1,817,308 bp on chromosome 2 that contained 80 candidate genes. We also used the transcriptome data of Rijiecheng inoculated with Fusarium oxysporum f. sp. cucumerinum (Foc) to screen the candidate genes. Twelve differentially expressed genes were detected in fw2.1 , and five of them were significantly induced by FW. The expression levels of the five genes were higher in FW-resistant Rijiecheng inoculated with Foc than in the control inoculated with water. Our results will contribute to a better understanding of the genetic basis of FW resistance in cucumber, which may help in breeding FW-resistant cucumber lines in the future. [ABSTRACT FROM AUTHOR]

Cucumber (Cucumis sativus L.) is an important vegetable crop worldwide, and Fusarium wilt (FW), caused by Fusarium oxysporum f. sp. cucumerinum (Foc), severely restricts cucumber growth and yield. Accumulating lines of evidence indicate that chitinases play important roles in attacking the invading fungal pathogens through catalyzing their cell wall degradation. Here, we identified the chitinase (Chi) genes in cucumber and further screened the FW-responsive genes via a comparative transcriptome analysis and found that six common genes were predominantly expressed in roots but also significantly upregulated after Foc infection. Expression verification further conformed that Chi2 and Chi14 were obviously induced by Foc as well as by hormone treatments, compared with the controls. The purified Chi2 and Chi14 proteins significantly affected the growth of Foc in vitro, compared with the controls. Knockdown of Chi2 in cucumber by virus-induced gene silencing (VIGS) increased susceptibility to FW, compared with the Chi14-silenced and control plants, and silencing of Chi2 drastically impaired gene activation in the jasmonic acid pathway, suggesting that the Chi2 gene might play positive roles in cucumber FW defense and, therefore, can provide a gene resource for developing cucumber-FW-resistance breeding programs. [ABSTRACT FROM AUTHOR]

Fusarium wilt (FW) of cucumber (Cucumis sativus L.) caused by Fusarium oxysporum f. sp. cucumerinum (Foc) is a destructive soil-borne disease that severely decreases cucumber yield and quality worldwide. MicroRNAs (miRNAs) are small non-coding RNAs (sRNAs) that are important for regulating host immunity because they affect target gene expression. However, the specific miRNAs and the miRNA/target gene crosstalk involved in cucumber resistance to FW remain unknown. In this study, we compared sRNA-seq and RNA-seq data for cucumber cultivar 'Rijiecheng', which is resistant to FW. The integrated analysis identified FW-responsive miRNAs and their target genes. On the basis of verified expression levels, we detected two highly expressed miRNAs with down-regulated expression in response to Foc. Moreover, an analysis of 21 target genes in cucumber inoculated with Foc indicated that JRL3 (Csa2G362470), which is targeted by miR319a, and BEE1 (Csa1G024150), DAHP1 (Csa2G369040), and PERK2 (Csa4G642480), which are targeted by miR6300, are expressed at high levels, but their expression is further up-regulated after Foc inoculation. These results imply that miR319a-JRL3, miR6300-BEE1, miR6300-DAHP1 and miR6300-PERK2 regulate cucumber defenses against FW, and provide the gene resources that may be useful for breeding programs focused on developing new cucumber varieties with enhanced resistance to FW. [ABSTRACT FROM AUTHOR]

Fusarium wilt (FW) in cucumber (Cucumis sativus L.), caused by Fusarium oxysporum f. sp. cucumerinum (Foc), poses a major threat to cucumber growth and productivity. However, lack of available natural resistance resources for FW restricts the breeding of resistant cultivars via conventional approaches. Susceptibility (S) genes in susceptible host plants facilitate infection by the pathogen and contribute to susceptibility. Loss of function of these S genes might provide broad-spectrum and durable disease resistance. Here, we screened S genes via comparative proteomic analysis between cucumber cultivars Rijiecheng and Superina, which exhibited resistance and high -susceptibility to FW, respectively. We identified 210 and 243 differentially regulated proteins (DRPs) in the Rijiecheng and Superina, respectively, and further found that 32 DRPs were predominantly expressed in Superina and significantly up-regulated after Foc inoculation. Expression verification found that TMEM115 (CsaV3_5G025750), encoding a transmembrane protein, TET8 (CsaV3_2G007840), encoding function as a tetraspanin, TPS10 (CsaV3_2G017980) encoding a terpene synthase, and MGT2 (CsaV3_7G006660), encoding a glycosyltransferase, were significantly induced in both cultivars after Foc infection but were induced to a higher expression level in Superina. These candidate genes might act as negative regulators of FW resistance in cucumber and provide effective FW-susceptibility gene resources for improving cucumber FW resistance through breeding programs. [ABSTRACT FROM AUTHOR]