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In-Depth Information
the genetic variability of nematode species,
as well as the complex involvement of resis-
tance genes (Niblack et al. 2002; Williamson
1998). Advancements in molecular marker tech-
nologies have greatly facilitated the detec-
tion and characterization of genomic regions
associated with broad resistance to nematodes
(Concibido et al. 2004; Ha et al. 2004; Ha
et al. 2007; Li et al. 2001; Tamulonis et al.
1997a; Vuong et al. 2010; Wu et al. 2009).
Such genetic marker-trait associations can be
efficiently utilized for marker-assisted selection
(MAS) or genomic selection (GS), in which sev-
eral resistance genes/genomic regions can be
pyramided to select elite backgrounds, leading
to the improvement of nematode-resistant vari-
eties of soybean.
In this chapter, we summarize and highlight
current knowledge about the parasitic biology
of these three nematode species, genetic vari-
ation for virulence, candidate genes for host
plant resistance, and host-nematode interactions.
We also discuss soybean-breeding strategies and
variety development for resistance and tolerance
to nematodes. Finally we mention the prospects
and applications of new genomic approaches and
next-generation sequencing (NGS) technologies
in future research to understand parasitic nema-
todes and their soybean host.
adapt to resistant soybean genotypes. SCN was
first reported in Japan in 1915, in Korea in 1936,
and in the United States in 1954 (Winstead et al.
1955). In the United States, it was reported that
H. glycines field isolates in North Carolina were
found to be different than isolates collected in
Tennessee (Ross 1962). Since then, a number
of studies have reported the genetic diversity
among and within populations of SCN in vari-
ous soybean production areas (Anand et al. 1994;
Colgrove et al. 2002; Golden and Epps 1965;
Niblack et al. 1993; Rao-Arelli et al. 1991; Riggs
et al. 1968; Sugiyama et al. 1968; Zhang et al.
1998).
Regarding the inheritance of resistance to
SCN, early studies indicated SCN resistance is
genetically controlled by three recessive genes
designated rhg1 , rhg2 , and rhg3 (Caldwell
et al. 1960). Later, Matson and Williams (1965)
reported one dominant gene and designated it as
Rhg4 . Analyzing a new source of resistance, PI
88788, Rao-Arelli (1994) identified an additional
dominant gene and designated it as Rhg5 .How-
ever, further genetic studies of different sources
of resistance showed that inheritance of SCN
resistance was oligogenic and complex (Anand
and Rao-Arelli 1989). Multiple alleles at a sin-
gle locus could be involved in SCN resistance
(Hancock et al. 1987; Hartwig 1985). For
decades, advances in molecular genetics and
biotechnology made it possible to identify and
characterize genomic regions quantitatively con-
ditioning SCN resistance, indicating that resis-
tance to SCN is a complex trait conveyed by
quantitative trait loci (QTL), with either small
effects or epistatic interaction. Since then, many
efforts have been made to screen more resistance
sources, which were subsequently utilized for
QTL mapping and characterization. QTL analy-
sis and marker association are discussed in more
detail later in this chapter.
Overview of Nematode Problems
inSoybean Production
Soybean Cyst Nematode
Among the plant-parasitic nematode species
causing severe annual soybean yield losses, cyst
nematode (SCN, Heterodera glycines )isthe
most devastating worldwide. It was estimated
that this nematode species causes nearly $1 bil-
lion annually in yield losses in U.S. soybean
production alone (Koenning and Wrather 2010).
Once an SCN infestation is established in a
soybean field, it is very difficult to eradicate it
because of the genetic diversity of H. glycines
field populations and their ability to eventually
Root-Knot Nematode
Root-knot nematodes (RKN, Meloidogyne spp.)
belong to the genus Meloidogyne , which are
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