Biology Reference
In-Depth Information
obligate parasitic pests of thousands of plant
species and were first reported by Cornu (1879)
and later by Neal (1889). The Meloidogyne genus
includes more than 50 described species (Trudg-
ill and Blok 2001) and has greater worldwide
distribution than other major groups of plant-
parasitic nematodes (Sasser 1980). Among these,
four species— Meloidogyne incognita (Kofoid
& White) Chitwood (Mi), M. arenaria (Neal)
(Ma), M. javanica (Treub) Chitwood (Mj), and
M. hapla (Chitwood) (Mh)—are the most com-
mon nematodes, causing 95% of the incidence of
RKN parasitism on important crop plants world-
wide (Doucet and Pinochet 1992; Hussey and
Janssen 2002). In the southeastern United States,
however, two RKN species, Mi and Ma, are the
most concerning nematodes to soybean, tobacco,
peanut, and cotton growers (Boerma and Hussey
1992; Rodriquez-Kabana et al. 1991), as they
cause annual yield losses of an estimated $30
million (Sciumbato 1993). Once established in
crop roots, using pest controls to prevent yield
losses can be difficult. In past decades, due to the
cancellation of permits for the use of fumigant
nematicides, the development and deployment
of RKN-resistant cultivars, in conjunction with
crop rotation, became the most effective mea-
sure to control nematode damage (Boerma and
Hussey 1992).
Results of a genetic study of the Forrest culti-
var showed that resistance to Mi was controlled
by a single gene, named Rmi1 (Luzzi et al.
1994a). Since then, many efforts have been made
to identify new sources of resistance, which have
subsequently been utilized for further investiga-
tion of how soybeans inherit RKN resistance
(Harris et al. 2003; Yates et al. 2010). How-
ever, genetic analysis in different soybean geno-
types, when challenged with other RKN species
(i.e., Ma, Mj, and Mi), indicated that the resis-
tance to RKN was quantitatively inherited, with
moderate to high heritability (Luzzi et al. 1994b,
1995a, 1995b). With the availability and acces-
sibility of different molecular marker technolo-
gies, a number of QTL-underlying resistances to
RKN species were identified and mapped (Ha
et al. 2004; Li et al. 2001; Tamulonis et al.
1997a). Advances in microarray gene expression
and transcriptional profiling enabled soybean
researchers to characterize candidate genes for
nematode parasitism, as well as plant host genes
resistant to RKN infection (Huang et al. 2003,
2005; Ibrahim et al. 2011a, 2011b). Genetic map-
ping, host plant resistance genes, and candidate
genes for parasitism are presented in more detail
later in this chapter.
Reniform Nematode
Reniform nematode (RN, Rotylenchulus reni-
formis Linford and Oliveira) occurs primarily
in tropical and subtropical regions in Australia,
Southeast Asia, the Middle East, Africa, and
South America, where it parasitizes a wide range
of crop plants (Gaur and Perry 1991; Herald
and Robinson 1990). This nematode species was
first described in 1931 in Hawaii (Linford and
Oliveira, 1940) and was first detected in the
continental United States in Georgia in 1940
(Smith 1940). Since then, the nematode has been
found throughout the southern United States in
South Carolina, Arkansas, Louisiana, Missis-
sippi, Florida (Herald and Thames 1982; Her-
ald and Robinson 1990; Starr 1998), and as far
north as Missouri (Wrather et al. 1992). Among
important crop plants, cotton has been known
to be a major host of RN, but many other veg-
etable and field crops, such as tomato, peanut,
and soybean, are also infested by this nematode
species (Davis et al. 2003; Herald and Robinson
1990). Parasitized plants exhibit varying degrees
of stunting and chlorosis, resulting in moderate
to heavy yield suppression (Koenning et al. 1999;
Laurence and McLean 1996). In soybean, an
average of 33% of yield reduction was reported
in both moderately resistant and susceptible cul-
tivars tested (Rebois et al. 1975).
Improving the genetic resistance of host
plants has been demonstrated to be the most effi-
cient approach to control the damage of this pest,
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