Contents - Faperta

Mechanisms and Inheritance of Resistance to Insect Pests 137
and Livers, 1980; Hollenhorst and Lappa, 1983; Weng and Lazar, 2002). The gene Gb5 located
on wheat chromosome 7A in CI 17882 was introgressed from A. speltoides (Hollenhorst and
Lappa, 1983; Tyler, Webster, and Merkle, 1987), while Gb6 was identifi ed in GRS 1201 (Porter,
Webster, and Friebe, 1994). Gbx and Gbz from A. tauschii are allelic or tightly linked to Gb3
(Zhu et al., 2004), and are inherited as single dominant genes (Zhu et al., 2004). Gby is located
on the wheat chromosome 7A (Boyko, Starkey, and Smith, 2004). Rsgla confers inducible
S. graminum resistance in barley, and is triggered by feeding of avirulent S. graminum
biotype (Carver et al., 1988; Hays et al., 1999).
Twelve genes confer resistance to the Russian wheat aphid, Diuraphis noxia (Kurdj.) in barley,
rye, and wheat. The dominant genes Dnl and Dn2 were identifi ed in Triticum aestivum L.
accessions PI 137739 (Dn1) and PI 262660 (Dn2) from Iran and Azerbaijan, respectively (du
Toit, 1987, 1988, 1989). The recessive gene dn3 is present in an amphiploid wheat parent derived
from crosses between A. tauschii and durum wheat. The Dn5 was identifi ed in PI 294994 (du
Toit 1987; Saidi and Quick, 1996; Zhang, Quick, and Liu, 1998), while Dn4 and Dn6 originated
from PI 372129 and PI 243781, respectively (Nkongolo et al., 1989, 1991a, 1991b; Saidi and
Quick, 1996). The gene Dn7 from rye has been transferred to the wheat cultivar Gamtoos
(Marais and du Toit, 1993; Marais, Horn, and du Toit, 1994; Marais, Wessels, and Horn, 1998).
The genes Dn8 and Dn9 are coexpressed with Dn5 in PI 294994 (Liu et al., 2001), while Dnx
from PI 220127 is inherited as a dominant trait (Harvey and Martin, 1990; Liu et al., 2001).
Resistance to D. noxia biotype I in barley line STARS-930IB (derived from PI 573080) is controlled
by dominant alleles at two loci (Momhinweg, Porter, and Webster, 1995). An incompletely
dominant allele at the Rdnl locus and a dominant allele at the Rdn2 locus confer a
high level of resistance to D. noxia in barley.
Maize
Several genes condition resistance to the European corn borer, O. nubilalis (G.E. Scott and
Guthrie, 1967; Chiang and Hudson, 1973). Different genes condition resistance to fi rst and
second broods, but some genes condition resistance to both broods (Jennings, Russell,
and Guthrie, 1974). Resistance to ear damage by H. zea in sweetcorn involves multiple
genes, and is controlled by epistatic as well as additive-dominance effects (Warnock,
Davis, and Gingera, 1998). Resistance to H. zea and S. zeamais is largely controlled by additive
effects rather than dominance or epistatic effects (Widstrom, 1972; Widstrom,
Wiseman, and McMillian, 1972; Widstrom and McMillian, 1973). Both GCA and SCA
effects explain signifi cant amounts of variation in different maize populations for resistance
to fall armyworm, S. frugiperda and the sugarcane borer, Diatraea grandiosella (Dyar)
(Williams, Buckley, and Davis, 1995; Williams, Davis, and Buckley, 1998). More than one
pair of genes control maize silk resistance to H. zea, and some of these genes interact in a
nonallelic manner (Wiseman and Bondari, 1992, 1995). Inheritance of maysin content in
maize, which imparts resistance to H. zea, is governed by the presence of a major modifi er
gene (Widstrom and Snook, 2001). The locus for maysin production is governed by a
single modifi er gene in GT 114 GT 119 (Widstrom and Snook, 1994). However, some
accessions of maize, such as PI 245138, which have low levels of maysin, are also resistant
to H. zea (Wilson, Wiseman, and Snook, 1995). Stalk resistance to the stem borer, Sesamia
nonagrioides (leFebvre) is inherited quantitatively (Cartea et al., 1999, 2001), and additive,
dominant, and epistatic effects control the gene action. Both additive and dominant effects
explain the variation in expression of resistance to the corn leaf aphid, Rhopalosiphum
maidis (Fitch.) (Bing and Guthrie, 1991), and to the spotted stem borer, C. partellus
(R.S. Pathak, 1991).