Biology Reference
In-Depth Information
inducing the extension of plant cell walls by
weakening the noncovalent interactions that help
maintain their integrity. Nematodes produced
expansin to loosen cell walls when invading host
plants (Qin et al. 2004).
Auxin, a plant hormone that is a major reg-
ulator of organogenesis, plays an important role
in the successful establishment of nematode life.
Increased auxin has been detected when galls
and syncytia of RKN and SCN are initiated.
Chorismate mutase was first cloned from RKN
and also has been found in SCN (Bekal et al.
2003; Lambert et al. 1999). Chorismate mutase
is a key branch-point regulatory enzyme in the
shikimate pathway, in which auxin and salicylic
acid were produced. Overexpression of nema-
tode gene MjCM-1 suppresses lateral root for-
mation and the development of the vascular
system by reducing auxin levels (Doyle and
Lambert 2003). If the auxin signaling and trans-
port pathway was interrupted, mutants had sig-
nificantly lower rates of infection by nema-
todes (Grunewald et al. 2009a). Recently, the
role of polar auxin transport has been elucidated
(Grunewald et al. 2009b). PIN1-mediated auxin
transport is needed to deliver auxin to the initial
syncytial cell, whereas PIN3 and PIN4 distribute
the accumulated auxin laterally and are involved
in the radial expansion of the syncitum. In pin3
mutant, syncytia and cysts are smaller and less
developed. LAX3, an auxin influx transporter, is
upregulated in the developing syncytia. Recent
studies showed that SCN effector Hs19C07 inter-
acted with LAX3 and may increase LAX3 activ-
ity by binding to it (Lee et al. 2011). Overexpres-
sion of Hs19c07 resulted in an increased rate of
lateral root emergence, indicating an enhanced
auxin influx. Previous studies showed LAX3
can upregulate cell-wall-degrading enzymes in
developing syncytia, indicating different path-
ways jointly regulate the development of feeding
cells (Lee et al. 2011).
Beside the cell wall and auxin pathways, ethy-
lene and the SA pathway is also involved in the
development of syncytia (Tucker et al. 2010).
Arabidopsis
less susceptible to H. schachtii , while ethylene-
overproducing lines attract more nematodes
(Wubben et al. 2004). But no convincing evi-
dence suggests ethylene is involved in root-knot
infection because M. incognita affects ethylene-
related mutants in a similar way to controls
(Lohar and Bird 2003). Successful cyst nematode
parasitism may involve a local suppression of SA
signaling in roots. SA-deficient mutants ( sid2-1 ,
pad4-1 , and NahG ) exhibited increased suscep-
tibility to H. schachtii . In contrast, SA-treated
wild-type plants showed decreased H. schachtii
susceptibility. The npr1-2 and npr1-3 mutants,
which are impaired in SA signaling, also showed
increased susceptibility to H. schachtii , whereas
the npr1-2 suppressor mutation sni1 showed
decreased susceptibility (Wubben et al. 2008).
The starch metabolic pathway is involved in
the establishment of nematode feeding sites. The
formation of feeding sites is accompanied by a
massive solute import into syncytia, leading to
highly elevated sucrose levels (Hofmann et al.
2008). The authors found that the syncytia use
starch as intermediate carbohydrate storage to
compensate for fluctuating sugar levels in vivo .
Twenty of 56 genes known to be related to starch
synthesis and degradation were upregulated in
nematode-induced syncytia. Loss of function
mutation of Atss1 results in a decreased number
of nematodes in nematode infection tests, indi-
cating the importance of the starch metabolic
pathway for the function of feeding sites.
Breeding Strategy and Variety
Developmentfor Nematode
Resistance and Tolerance
Among several practices applied to control and
prevent yield losses caused by these nematode
species, use of nematode-resistant and -tolerant
varieties is a primary and efficient tactic to sup-
press losses. Thus, breeding for resistance is
a major goal of most soybean breeding pro-
grams. Resistant cultivars are advantageous by
suppressing nematode reproduction, reducing
the need for toxic nematicides and shortening
ethylene-insensitive
mutants
are
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