Cucurbit Genetics Cooperative Report 7:86-87 (article 38) 1984

Linkage between an Isozyme Locus and One of the Genes Controlling Resistance to Watermelon Mosaic Virus 2 in Cucurbita ecuadorensis

Weeden, N.F., R.W. Robinson and F.Ignart^*

Dept. Horticultural Sciences, New York Agricultural Experiment Station, Geneva NY 14456

Resistance to watermelon mosaic virus 2 (WMV-2) has been found in Cucurbita ecuadorensis (2). The resistant phenotype appears to be controlled by more than one locus (1), but little is known regarding the number of loci involved or the interactions between these loci.

As part of an on-going program to transfer multiple virus resistance from Cucurbita ecuadorensis to C. maxima two backcross populations [(C. maxima x C. ecuadorensis) x C. maxima] were grown in field plots at the New York State Agricultural Experiment Station, Geneva NY. Each plant was inoculated in the first true leaf stage with WMV- 2, and natural infection of WMV-2 also occurred in the field. Plants were phenotyped for 12 different isozyme systems (acid phosphatase, aldolase, aspartate aminotransferase, esterase, galactosidase, leucine aminopeptidase, malate dehydrogenase, phosphoglucomutase, peroxidase, shikimic dehydrogenase. superoxide dismutase and triose phosphate isomerase), permitting the observation of products from at least 21 segregating loci.

Correlation was found between resistance to WMV-2 and an allele of Aldo-p, the isozyme locus specifying the plastid- specific aldolase (3). A majority of the plants displaying a heterozygous Aldo-p phenotype at Aldo-p were resistant while all except one plant exhibiting the aldolase phenotype of C. maxima (homozygous slow) were susceptible (Table 1). We interpret these results to indicate that C. ecuadorensis possessed a WMV-2 resistance gene closely linked to Aldo-p. In the genetic background of the backcross population, the possession of this gene appeared to be a required but not a sufficient condition for expression of the resistant phenotype. The one individual exhibiting the slow aldolase allozyme in combination with the resistant phenotype could have resulted from a recombination event. The considerable number of WMV-2 susceptible plants heterozygous at Aldo-p may be due to an absence in these plants of other genes from C. ecuadorensis which contribute to the resistant phenotype. All other isozyme loci appeared to be assorting randomly with respect to WMV-2 resistance.

Table 1. Backcross segregation for watermelon mosaic virus 2 resistance and allozymes at the Aldo-D locus.
Population	n	WMV-2 susceptible		WMV-2 resistant		Chi-square	P
		aldolase		aldolase
		slow	het.	slow	het.
83-978	25	10	1	7	7	6.84	0.05<P<O.1
83-979	19	10	0	2	7	13.2**	P<0.01
Total	44	20	1	9	14	17.6**	P<0.01

Literature Cited

1. Greber, R.S. and M.E. Herrington. 1980. Reaction of interspecific hybrids between Cucurbita ecuadorensis, C. maxima and C. moschata to inoculation with cucumber mosaic virus and watermelon mosaic virus 1 and 2. Australian Plant Pathology 9:1-2.
2. Provvidenti, R., R.W. Robinson and H.M. Munger. 1978. Resistance in feral species to six viruses infecting Cucurbita. Plant Dis. Reptr. 62:326-329.
3. Weeden, N.F. 1984. A nuclear gene codes for the plastid-specific aldolase in Cucurbita species. Cucurbit Genet. Coop. Rpt. 7:88.

^*Present address: Institut de Recherches TEZIER, Domaine de Maninet, Route de Beaumont, B.P. 336, 26003 Valence- Cedex, Franc