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tentatively named Chr. 18 2nd locus. The second
QTL mapped on Chr. 10 has not been reported in
other SCN resistance sources studies to date. Pre-
vious studies have reported that it is essential to
have both genes from Chrs. 18- and 8-QTL asso-
ciated with the rhg1 and Rhg4 loci, respectively,
for the development of new varieties derived
from any resistance source (Cregan et al. 1999;
Meksem et al. 1999). However, results reported
by Vuong et al. (2010) indicated that other than
rhg1 and Rhg4 loci, comprehensive resistance to
multiple SCN races can be conveyed by other
genomic regions from different SCN-resistant
sources, as shown in other studies (Guo et al.
2006; Winter et al. 2007; Wu et al. 2009).
ductive adult stage (Davis and Mitchum 2005).
In many host plants, pericycle and cortical root
cells immediately surrounding the giant cells are
stimulated to divide (hyperplasia), giving rise
to the “gall” or “knot” characteristic of RKN
infection.
However, similar to cyst nematode, RKN
uses a protrusible style to secret parasitism pro-
teins into the host roots, where giant cells are
formed and required for its development and
reproduction. The secretory parasitism proteins
mediate the dynamic interaction of the RKN
with the plant hosts. The broad host range of
the RKN suggests that the RKN affects fun-
damental processes within plant cells (Davis
et al. 2004). When using a gland-cell-specific
cDNA of M. incognita (Mi), Huang et al.
(2003) successfully isolated a parasitism gene
encoding a putative signaling peptide, which
significantly expressed itself in the subven-
tral esophageal secretory gland cells. Further
investigations of transgenic expression of this
gene and its interaction with host plant tran-
scription factors are also reviewed later in this
chapter.
Root-Knot Nematode
LifeCycleandParasiticBiology
Root-knot nematode ( Meloidogyne spp.) is an
obligate sedentary endoparasitic pest and has a
wide host range of at least 1,700 plant species
(Cook 1991). Although SCN and RKN share
many common features in their life cycles, they
differ in many aspects of parasitism. In the soil,
the life cycle of RKN starts with developed J1
juvenile in its egg. A second-stage J2 juvenile
hatches from the egg and mechanically pene-
trates the root near the root tip at the zone of
elongation (Hussey and Grundler 1998). The
parasitic J2 juvenile migrates through the root
intercellularly in the root cortex to reach the
root vascular cylinder. The esophageal gland
cell of the J2 nematode actively synthesizes
and mobilizes secretions from its stylet during
migration within tissues and subsequently ini-
tiates the formation of feeding cells (Hussey
1989). Unlike cyst nematode, the RKN J2 juve-
nile induces the formation of three or six multin-
ucleate giant cells through repeated nuclear divi-
sion uncoupled from cytokinesis. The giant cells
can develop up to 100 times the size of normal
root vascular parenchyma cells and serve as the
feeding site, where the sedentary nematode goes
through three successive molts to reach the repro-
GeneticVariationforVirulence
Among four common RKN species, southern
Mi ( M. incognita) and peanut Ma (M. arenaria)
are the most important because increasing levels
of damage has been observed in the southeast-
ern U.S., where soybean, peanut, and cotton are
major crop plants.
For southern Mi nematode, four races have
been recognized based on morphological char-
acteristics of male head and female stylet shape
(Sasser 1972). But various studies also reported
that races of Mi nematode can be differenti-
ated according to their parasitism on specific
host plants, like tomato, soybean, alfalfa, and
lima bean. Thus, it was essential to establish a
race classification scheme for each crop (Canto-
Saenz and Brodie 1986). In a study of two Mi
populations originating from North Carolina and
Georgia, these authors identified these nematode
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