LITMIR.BIZ

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resistance to cucurbit leaf crumple virus, conferred by a single gene, culcrv. Another single recessive gene, nsv, confers resistance to melon necrotic spot virus. Resistance to this virus is also attributed to two independent dominant genes, Mnr-1 and Mnr-2 (McCreight et al., 1993; Lopez-Sese and Gomez-Guillamon, 2000; Frantz and Jahn, 2004).

      Several melon genes for insect resistance have been identified. Af influences resistance to red pumpkin beetle. Tolerance to melon aphid is provided by the dominant allele at gene Ag, and Vat conditions resistance to viruses transmitted by that pest. Two complementary genes, dc-1 and dc-2, govern resistance to melon fruit fly. Genes controlling foliar cucurbitacin content, including cb and Bi, influence insect resistance; plants homozygous recessive at both of these loci are resistant to cucumber beetles. A single dominant gene, Lt, confers antibiosis resistance to leafminer (Liriomyza trifolii) (Dogimont et al., 1999).

      Many genes influence melon plant habit, several of which have been identified. Compact habit can be obtained by breeding for the homozygous recessive state at one of the short internode loci, si-1, si-2 or si-3 (Knavel, 1990) or short lateral branching, slb (Fukino et al., 2012). Fine mapping of short internode loci identified a region on chromosome 7 (Hwang et al., 2014). Allele Imi increases internode length on the main stem, and ab (abrachiate) inhibits lateral branch development.

      Genes a (andromonoecious) and g (gynomonoecious) interact to influence sex expression in the following manner: monoecy (a⁺/- g⁺/-), andromonoecy (a/a g⁺/-), gynomonoecy (a⁺/- g/g) and hermaphrodism (a/a g/g). Stable gynoecious sex expression can be achieved by combining homozygous recessive gy (gynoecious) at a third locus with a dominant allele at the a locus and the g allele in the homozygous state at the g locus (i.e. a⁺/- g/g gy/gy). Genetic markers for the a, m, and g loci have been developed (Noguera et al., 2005; Feng et al., 2009; Gao et al., 2011). Melon plants are male sterile if homozygous recessive for alleles at one of the independent genes ms-1, ms-2, ms-3, ms-4 or ms-5.

      Fruit of some melon cultivars detach (slip) from the vine at maturity due to the presence of an abscission layer, but other cultivars, lacking this trait, have persistent (non-slip) fruit. Two dominant alleles, Al-1 and Al-2, control formation of the abscission layer.

      Fruit quality is a polygenic trait, but several individual genes have a major effect. In wild melon populations, fruit may be bitter due to Bi and have mealy flesh texture because of the Me allele. Sour taste is dominant to sweet and conditioned by the So gene. A recessive allele (if) for juicy flesh and a dominant allele (Mu) for musky flavour have been reported. A recessive gene (suc) has been reported to condition high sucrose accumulation in melon.

      Many genes influence the intensity of flesh colour, but individual major genes may determine whether the flesh is orange (which is dominant), green or white. Recessive alleles of two genes govern green flesh (gf) and white flesh (wf), with wf⁺ epistatic to gf⁺/gf.

      External fruit colour is influenced by Mt (mottled rind), st (striped epicarp), w (white mature fruit), Wi (white immature fruit) and Y (yellow epicarp). Fruit shape genes include O (oval), s (‘sutures’ or vein tracts) and sp (spherical fruit shape).

      A molecular linkage map of melon with 12 linkage groups, corresponding to the 12 chromosomes, has been assembled by groups in Texas, France and Spain. Additionally, the melon genome has been sequenced in Spain and is now available to further enhance the genetic map saturation (Oliver et al., 2001).

      Squash

      Most descriptions of genes with links to the primary literature can be found in Paris and Padley (2014). In the most recent update, a number of new disease resistance genes have been added for squash. Powdery mildew resistance of C. okeechobeensis (Small) L. H. Bailey and C. lundelliana L. H. Bailey is controlled by dominant alleles of the Pm-0 and Pm loci, respectively, and modifier genes may influence expression of these alleles. Two recessive resistance genes (pm-1 and pm-2) have been characterized in C. moschata. Three dominant complementary genes (Crr-1, Crr-2 and Crr-3) for resistance to crown rot (caused by Phytophthora capsici) were introgressed from C. lundelliana and C. okeechobeensis ssp. okeechobeensis into C. moschata. Six genes plus modifiers originating from C. moschata have been reported to affect resistance to zucchini yellow mosaic virus. For four loci, the resistant allele is dominant, whereas for the other two loci, alleles are recessive. Zym-0 and zym-6 appear to act independently, whereas Zym-1, Zym-2 and Zym-3, and Zym-4 and zym-5 form complementary sets. A modifier of zym-6 (m-zym-6) alters recessive expression to dominant expression. Recessive resistance (zymecu) has also been found in C. ecuadorensis to ZYMV. Watermelon mosaic virus resistance has been described from two different species with Wmv from C. moschata and Wmvecu identified in a C. maxima × C. ecuadorensis interspecific cross. A pair of complementary genes (prv-1 and Prv-2) identified in C. moschata confer resistance to papaya ringspot virus. Two genes (dominant Slc-1 and recessive slc-2) independently confer resistance to squash leaf curl virus in C. pepo. A single gene for cucumber mosaic virus resistance (Cmv) was identified in C. moschata. In some cases, such as for Zym-1 and Wmv, resistance to different viruses may be conferred by genes at the same locus, or genes that are tightly linked in a complex locus. Homology among resistance genes to the same pathogen from different species has yet to be resolved.

      Resistance to the melon fruit fly is provided by allele Fr in C. maxima. C. pepo plants homozygous for cu, which reduces foliar cucurbitacin content, are not preferred by cucumber beetles since these insects are attracted by cucurbitacins. Resistance to silver leaf disorder caused by whitefly (Bemisia tabaci) is found in both C. pepo and C. moschata with resistance conferred by recessive sl.

      A number of genes are associated with domestication traits in Cucurbita. Bitterness caused by cucurbitacin is under the control of several genes. In addition to cu which conditions bitter cotyledons, Bi-0 conditions bitter fruit in C. pepo. Three bitter fruit loci (Bi-1, Bi-2 and Bi-3) were found in an interspecific cross of C. pepo × C. argyrosperma. Bi-0 and either Bi-1 or Bi-2 may be allelic. In C. maxima and C. maxima × C. ecuadorensis crosses, Bimax conditions bitterness. Wild Cucurbita species and some summer squash cultivars have a hard fruit rind. Rind hardness is influenced by the Hr (hard rind) gene of C. pepo and Hi (hard rind inhibitor) of C. maxima. In the presence of Hr, Wt confers wartiness in C. pepo. Wartiness is also found in C. maxima but has not been characterized genetically. Bush habit due to short internodes is conditioned by allele Bu in C. pepo; expression of Bu is dominant in early stages of plant development and recessive as plants vine out. Bush habit of C. moschata is also under monogenic control, whereas two to three incompletely dominant genes have been implicated in different bush phenotypes of C. maxima. There is extreme variation in bush growth habit among species, but only one gene has been definitively described and additional ones may await discovery. While most genes affecting fruit size and shape are quantitative, two qualitative genes

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