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  • Author or Editor: James D. McCreight x
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Cucurbit yellow stunting disorder virus (CYSDV) is a devastating viral disease of melon that can cause significant yield and quality losses. This disease has recently emerged as a major concern in the southwest United States and major melon-growing regions across the world. Coinfection of melon by Cucurbit chlorotic yellows virus (CCYV) was recognized in Imperial Valley and neighboring production areas of California and Arizona in 2018, but its importance remains largely unknown. Identifying and deploying CYSDV resistance from elite germplasm is an economical and effective way to manage the disease. A F2:3 population was developed from a cross of susceptible ‘Top Mark’ with CYSDV-resistant PI 313970, which was shown to possess a single recessive gene for resistance to CYSDV. The F2:3 population was phenotyped in the field in response to natural, mixed infections by the two viruses, CYSDV and CCYV in the Fall melon seasons of 2018 and 2019. Phenotypic data (foliar yellowing) from both years were not useful for mapping CYSDV resistance quantitative trait loci (QTL), as PI 313970 and CYSDV-resistant F2:3 plants exhibited yellowing symptoms from CCYV coinfection. QTL analysis of the relative titer of CYSDV calculated from reverse transcriptase quantitative polymerase chain reaction (RT-qPCR) data identified one locus on chromosome 3 at the physical location of S5-28,571,859 bp that explained 20% of virus titer variation in 2018 but was undetected in 2019. A locus on chromosome 5 between S5-20,880,639 to S5-22,217,535 bp explained 16% and 35% of the variation in CYSDV titer in 2018 and 2019, respectively. One or both of the markers were present in six of 10 putative melon CYSDV resistance sources. Markers flanking the 2019 QTL were developed and can be used in marker-assisted breeding of CYSDV-resistant melons.

Open Access

Nineteen polymorphic and eleven monomorphic isozyme loci were identified in thirteen enzyme systems in a survey of four-hundred melon (Cucumis melo L.) accessions. Segregation of allozymes in F2 and backcross (BC) families for isozyme loci agreed with the expected 1:2:1 and 1:1 segregation ratios (P <0.01). Eleven isozyme loci were linked and were integrated to form a map containing two linkage groups spanning 98 cM with a mean linkage distance of ≈9 cM. Linkage groups (A and B) contain the following loci in the order: A Fdp-2, Pgd, Pgm, Mpi-1, Idh, and Ac, and B Pep-gl, Mdh-2, Mdh-4, Mdh-5, Mdh-6. The remaining eight loci (Acp-1, Acp-4, Ak-4, Fdp-1, Gpi, Mpi-2, Pep-la, and Pep-pap) segregated independently. The isozyme map constructed in this study provides genomic information for future linkage studies with economically important traits and concensus map construction through map merging.

Free access

Abstract

Lettuce (Lactuca sativa L.) cultivars and breeding lines differed in tolerance to lettuce infectious yellows virus. Correlations of symptom severity in field tests with fresh weight of control plants in a greenhouse test indicate a relationship between symptom severity and the inherent vigor of a cultivar. ‘Climax’ had the mildest symptoms and was the most vigorous cultivar. The level of tolerance exhibited by ‘Climax’ and a few other cultivars will not prevent occurrence of lettuce infectious yellows, but could ameliorate its effect on lettuce production.

Open Access

Abstract

Greenhouse and field tests showed casaba melon, (Cucumis melo L. cv. Deserta Naja) to be highly susceptible to the western spotted cucumber beetle (Diabrotica undecimpunctata ssp. undecimpunctata Mannerheim). F1 and F2 progenies derived from a cross between ‘Deserta Naja’ and a comparatively resistant melon aphid-resistant breeding line ‘Top-Mark’ were nearly as susceptible as ‘Deserta Naja’, indicating a dominance of susceptibility. The mean damage to the progeny was significantly different from that of ‘Deserta Naja’; however, this indicated that dominance was incomplete. Greater numbers of the beetles on ‘Deserta Naja’ than on other entries in a field trial indicated that preference is associated with its high susceptibility. Differential damage to ‘Top-Mark’ in free-choice and no-choice tests supported the theory that resistance includes non-preference.

Open Access

Races 1 and 2 of Podosphaera xanthii (syn. Sphaerotheca fuliginea) were defined in Imperial Valley, Calif. 1938 when P. xanthii overcame genetic resistance in `PMR 45'. Race 3 was first observed in the U.S. in 1976 in Texas; 15 additional races of P. xanthii have been reported in the literature since 1996. Races 1 and 2 have been common in Arizona and California based upon the effectiveness of the powdery mildew resistance genes in commercially available melon cultivars grown in these states. Field data from 11 commonly used melon P. xanthii race differentials in 2001 and 2002 indicated the presence of race 1 in the Imperial Valley and San Joaquin Valley of California, and Yuma, Arizona. In spring 2003, the powdery mildew race situation changed. The first evidence was the occurrence of a severe and widespread infection of powdery mildew in a commercial cantaloupe field. The 11 powdery mildew race differentials were susceptible to powdery mildew in a nearby replicated field test. PI 313970, a melon from India, was resistant to this apparent new race of powdery mildew.

Free access

Three races of Fusarium oxysporum f.sp. lactucae, cause of fusarium wilt of lettuce, are known in Japan, where the pathogen was first observed in 1955. Fusarium wilt first affected commercial U.S. lettuce production in 1990 in Huron, Calif., but did not become a serious problem in the U.S. until 2001 when it reappeared in Huron and appeared in the Yuma, Arizona lettuce production area. Reactions of three fusarium wilt differentials (`Patriot', susceptible to races 1, 2 and 3; `Costa Rica No. 4', resistant to race 1, and susceptible to races 2 and 3; and `Banchu Red Fire', susceptible to races 1 and 3, and resistant to race 2) in a naturally-infected commercial field test and artificially-inoculated greenhouse tests, indicated presence of race 1 in the Yuma lettuce production area. Reactions of these differentials to an isolate from Huron confirmed the presence of race 1 in that area. Consistent with previous results from the U.S. and Japan, `Salinas' and `Salinas 88' were resistant to the Yuma and Huron isolates of race 1, whereas `Vanguard' was highly susceptible. Limited F1 and F2 data indicate that resistance to race 1 in `Costa Rica No. 4' and `Salinas' is recessive. `Calmar' is the likely source of resistance in `Salinas' and `Salinas 88'.

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Genetic variation among 378 melon (Cucumis melo L.) germplasm accessions collected in India in 1992 and 26 accessions in China in 1994 was evaluated with 19 isozyme loci. `Top Mark' and `Green Flesh Honeydew', which represented two distinct C. melo ssp. melo L. groups, Cantalupensis and Inodorus, respectively, were used as reference cultivars. Genetic distances among accessions were calculated, and an initial cluster analysis using these distances resulted in 148 groups of varying size, ranging from two to 47 accessions. One accession from each of the 148 groups was chosen at random and used in a second cluster analysis that identified 11 accession groups. Group 1 was unique and consisted of only two C. melo ssp. agrestis (Naudin) Pangalo accessions. Two large branches were detected at cluster node 2. One branch was comprised of three groups of 3, 12, and 34 accessions, while the other branch contained seven groups of 2, 3, 14, 16, and 47 accessions, and the reference cultivars. Of the 148 accessions, 132 were from 41 sites in Rajasthan and Madhya Pradesh, India, which were distributed unequally across the 11 groups. The 14 Chinese accessions originating from seven provinces were also dispersed unequally in the four major cluster groups. `Top Mark' and `Green Flesh Honeydew' were genetically distinct and uniquely clustered in the same group. These results indicate that additional collections of melon germplasm should be made in eastern and southern India.

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The spread of watermelon mosaic virus by the melon aphid (Aphis gossypii Glover) was 31%, 74%, and 71% less to a melon aphid-resistant muskmelon (Cucumis melo L.) breeding line than to the susceptible recurrent parent in a field cage study. Aphid-resistant and susceptible plants served equally well as the virus source. The highest rate of infection (97.9%) was noted when target plants were all melon-aphid susceptible, least (26.7%) when the target plants were all melon-aphid resistant, and intermediate (69.4%) when the target plants were an equal mix of aphid-resistant and susceptible plants. The number of viruliferous aphids per plant required to cause a 50% infection varied from five to 20 on susceptible controls and from 60 to possibly more than 400 on a range of melon aphid-resistant populations. An F family from a cross of the melon aphid-resistant AR Topmark (AR TM) with the susceptible `PMR 45' had significantly less resistance to virus transmission than AR TM. Breeding line AR 5 (an aphid-resistant population with `PMR 5' as the recurrent parent) had significantly greater resistance to transmission than other aphid-resistant populations.

Free access