Nematode Resistance in Soybean - Translational Genomics for Crop Breeding: Biotic Stress - page 102

cultivar Forrest, which was developed from a
SCN-resistant plant introduction PI 548402
(Peking), prevented yield losses worth $405
million from 1975 to 1980 (Bradley and Duffy
1982).
With over 19,000 plant introductions (PIs),
the USDA Soybean Germplasm Collection
( http://www.ars-grin.gov) has been a valuable
resource in finding sources of SCN resistance.
Efforts have been made to evaluate this col-
lection for new sources of resistance to either
single- or multi-race SCN populations (Anand
and Gallo 1984; Anand et al. 1988; Arelli et al.
2000; Diers et al. 1997; Epps and Hartwig 1972;
Rao-Arelli et al. 1997; Ross and Brim, 1957;
Young 1990). In a field study conducted soon
after SCN was reported in the United States, Ross
and Brim (1957) reported PI 88788 and Peking
(PI 548402) as new sources of SCN resistance.
Subsequently, these two accessions were quickly
incorporated into many breeding programs, in
which PI 88788 became the predominant source
of SCN resistance in U.S. soybean production
areas (Diers and Arelli 1999).
Development of soybean varieties resistant to
SCN has been an effective and practical method
for controlling SCN. However, genetic shift of
SCN populations due to the continuous cultiva-
tion of the same sources of resistance, coupled
with a lack of diversity for SCN resistance genes
in soybean varieties, has created a need for fur-
ther investigation to discover new SCN genes
from other sources of resistance. Recently, soy-
bean scientists at the National Center for Soy-
bean Biotechnology (NCSB) at the University of
Missouri (MU), in cooperation with Dr. Nelson
of USDA-ARS in Urbana, Illinois, have eval-
uated a subset of over 600 soybean accessions
from maturity groups (MG) III to V for resistance
to six SCN races, including a synthetic SCN pop-
ulation, LY1. Of these, more than 20 exotic PIs
were identified and confirmed to be moderately
or highly resistant to either single or multiple
races of SCN (Nguyen Laboratory, unpublished
data). These PIs could be useful as new broad-
based SCN resistance sources in an effort to

discover novel or rare alleles of SCN resistance
using traditional QTL mapping or nested associ-
ation mapping (NAM) approaches.
Advances in molecular genetic and genomic
methodologies significantly facilitate the identi-
fication and mapping of QTL associated with
resistance to SCN. In early mapping studies,
Concibido et al. (1994) reported three RFLP
markers significantly associated with SCN resis-
tance and tentatively mapped these to soybean
chromosomes 8, 9, and 18 (corresponding to
molecular linkage groups (LGs) A2, K, and G)
( http://www.soybase.org). Later, additional SCN
resistance QTL have been detected and con-
firmed in several resistant sources of cultivated
soybean (Guo et al. 2005; Guo et al. 2006; Mek-
sem et al. 2001; Qiu et al. 1999; Vuong et al.
2010, 2011; Wu et al. 2009; Yue et al. 2001)
and wild annual species ( Glycine soja ) (Wang
et al. 2001; Winter et al. 2007). In a comprehen-
sive review of a decade of QTL analysis efforts,
Concibido et al. (2004) summarized 31 puta-
tive QTL for SCN resistance to various races,
which were mapped to 17 of 20 soybean chro-
mosomes (Chr.). Of these, the QTL on Chr. 18
has been well characterized and proven to be
the most important QTL because it contains the
rhg1 locus, which underlies resistance to most
of the existing SCN races: 1, 2, 3, 5, 14, and
LY1 (Concibido et al. 1997; Guo et al. 2005;
Guo et al. 2006; Vuong et al. 2011; Wu et al.
2009; Yue et al. 2001). A second important QTL
located on Chr. 8 was also identified in other
resistant PIs and corresponds to the dominant
locus Rgh4 , which was reported to play a dis-
tinct role in resistance to SCN race 3 (Concibido
et al. 1994; Heer et al. 1998; Webb et al. 1995;
Wu et al. 2009; Vuong et al. 2011). In addi-
tion to all of the QTL mapped to 17 soybean
chromosomes in early studies (Concibido et al.
2004), two new QTL controlling resistance to
multi-races of SCN were identified and mapped
to Chrs. 18 and 10 in PI 567516C (Vuong et al.
2010). The new QTL on Chr. 18 was located
at a new genomic region and was physically
distant from the known rhg1 locus. It was