Potato dry rot is one of the potato storage diseases caused by Fusarium species and is a representative pathological disorder that induced post-harvest loss during storage. Chlorpropham treatment for sprouting inhibition is mainly used for room temperature storage of potatoes for processing. In this study, the inhibitory effect of chlorpropham on Fusarium-induced dry rot of potato ‘Dano’. To investigate the mycelial growth rate of the dry rot fungus (Fusarium solani Appel & Wollenw), mycelial growth was investigated in a chlorpropham (5.0, 50.4, 503.8, and 5,038 ppm) and prochloraz (0.1, 1.0, 10.0, and 100.0 ppm) medium containing F. oxysporum mycelia. Mycelia were more inhibited as the concentration of chlorpropham and prochloraz increased during incubation at 20°C, and the inhibition rate was 98.2% and 100% when treated with 503.8 ppm of chlorpropham and 10ppm of prochloraz in 14 days, respectively. Potato Dano tubers inoculated with F. oxysporum were dipped in chlorpropham (5.0, 50.4, and 503.8 ppm) and prochloraz (100 ppm) to investigate the effect of preventing dry rot during cold storage at 20°C and 4°C in vivo. The disease diameter of potatoes stored at room temperature (about 20°C) was reduced to 13.0 mm in the prochloraz 100 ppm teatment, and 10.7 mm in the chlorpropham 50.4 ppm treatment compared to 13.7 mm in the control tuber at 70 days of storage. The disease progression in all treatments including control was similar with no statistically significant difference at 4°C air temperature. From the results of this study, it is considered that treatment with 50.4 ppm of chlorpropham after harvest will be useful for suppressing dry rot of stored potatoes.

Fusarium crown root rot (FCRR) is a severe fungal disease caused by Fusarium oxysporum f. sp. radicis-lycopersici (FORL) in tomato. Resistance to FORL is conferred by single dominant locus Frl on chromosome 9, but its precise genomic location is not clearly determined. In this study, detailed location of Frl was assessed by using a set of molecular markers physically anchored on Chr.9 and F2 and RIL population derived from FORL-resistant inbred AV107-4 (S.lycopersicum) x susceptible L3708 (S. pimpinellifolium). Bioassay of the two populations with a FORL strain isolated from Korea resulted in single dominant heritance of the resistance. Two SCAR and 11 CAPS markers encompassing 3.6Mb~72Mb of Chr.9 were developed from the Tomato-EXPEN 2000 map and SolCAP SNP-array analysis. These markers were genotyped on 345 F2 plants. A high level of cosegregation with the resistance were observed for 5 markers which were mapped at a large physical interval of 5.1Mb (T1212) to 46.4Mb (SSR237), indicating that genetic recombination was highly suppressed in this region. Cosegregation of these markers with Frl was confirmed by using 126 RILs. The results implied that, in contrast with the previously reported long arm, Frl is present on a pericentromeric region of short arm of Chr. 9, in which crossing-over is severely suppressed. The marker set was further tested on 12 FORL-resistance or susceptibility commercial cultivars. Unlike the biparental populations, frequent linkage break was observed for T1212 and D4 in commercial cultivars. T1212 and D4 showed 50% and 100% match with the phenotype, respectively. D4, a CAPS, was converted to a high resolution melting (HRM) marker and tested on 55 breeding lines from private seed companies (Fig.3). All breeding lines showed the HRM genotype for resistance allele, indicating that D4 can be useful for selecting FORL-resistance tomato plants.