Читать книгу Cucurbits - James R. Myers - Страница 36

Many loci governing disease resistance of melon have been investigated. A single gene, Ac, governs Alternaria leaf blight resistance in melon line MR-1. Resistance to races 0 and 2 of Fusarium wilt is provided by Fom-1 or Fom-3, and there is an allele of another gene (Fom-2) for resistance to races 0 and 1. Allele Mc confers a high level of resistance to gummy stem blight, and Mc-2 a moderate degree of resistance to that disease. Five independent dominant genes, Gsb-1 through Gsb-5, have also been reported to confer high levels of gummy stem blight resistance, from PIs 140471, 157082, 511890, 482398 and 482399, respectively. Eight loci have been postulated to influence resistance to the powdery mildew disease caused by Podosphaera xanthii and three more to the powdery mildew incited by Erysiphe cichoracearum. Four genes have been reported for downy mildew resistance. Two alleles (Prv¹ and Prv²) of a single gene provide resistance to papaya ringspot virus from PI 180280, but they differ in reaction to some strains of that virus. Prv² is recessive to Prv¹ but dominant to Prv⁺. Resistance to pathotype O of zucchini yellow mosaic virus is provided by dominant allele Zym from PI 424723. A single dominant gene, Wmr, confers partial resistance to watermelon mosaic virus. Although polygenic resistance to cucumber mosaic virus has been known, recently a single dominant gene, Creb-2, has been reported to confer resistance to CMV-B2 strain. Two complementary recessives genes, cab-1 and cab-2, confer resistance to cucurbit aphid-borne yellows virus (CABYV). Resistance to cucurbit yellow stunting disorder virus (CYSDV) has been attributed to a single dominant gene (Cys) from TGR-1551. Subsequent studies have suggested that a single recessive gene may provide stronger resistance. Another dominant gene, Liy from PI 313970, confers resistance to the related Crinivirus, lettuce infectious yellows virus. The same PI has recessive 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).