Biology Reference
In-Depth Information
Chickpea plants may be infected at any
growth stage. High temperature is critical for
development of fusarium wilt, and disease sever-
ity is higher at 25-30
◦
C. Nevertheless, optimal
temperatures vary for different race and culti-
var combinations (Jimenez-Diaz 2011). Typical
wilting symptoms include drooping of the peti-
oles and leaflets, followed by a dull-green dis-
coloration, desiccation, and collapse of the entire
plant (Figure 11.1). Sometimes partial wilting of
a few branches is seen, owing to restriction of
the pathogen within infected vascular bundles.
An important diagnostic feature of the disease is
internal discoloration of xylem in root and stems,
without external root discoloration or mycelial
growth on the surface.
In the absence of host plants the pathogen can
survive for several years as chlamydospores in
infected chickpea debris in soil. It can also infect
seeds and become seed borne. Infected seeds
are the primary source for introduction of the
pathogen into new production areas. Infested soil
and infected debris serve as inoculum for local
spreading through cultivation and other human
activity.
The pathogen is host-specific and is known to
infect
Cicer
species only. The pathogen invades
feeder roots directly without wounds. After
reaching the xylem tissue, the fungus spreads
up in the vessels and to adjacent vessels. The
development of the pathogen clogs the xylem
vessels, restricting movement of nutrients and
water through the vascular tissue.
In addition to chickpea genotypes (cultivars),
pathogen races, and inoculum density, the other
important factor affecting development of the
disease is soil temperature. High temperature is
critical for development of Foc.
colleagues (1987) found that resistance to race
1 was governed by three independent genes.
The combination of any two of the three genes
(
h1h1
or
h2h2
or
h1H3
or
h2H3
) was required
for complete resistance to race 1. Nevertheless,
Sharma and colleagues (2005) and Gowda and
colleagues (2009) reported a single gene govern-
ing resistance to race 1, using the resistant lines
WR315 and Vijay, respectively. The presence of
one favorable allele in the genotype causes the
symptom of late wilting (reviewed by Sharma
and Muehlbauer 2007).
Similarly, as many as three genes have been
described as controlling resistance to race 2; a
combination of recessive alleles of two of these
genes confers resistance, whereas when only
one gene is present in a recessive state, late
wilting reaction occurs (Kumar 1998; Sharma
and Muehlbauer 2007). Sharma and colleagues
(2005) suggested that a single recessive gene in
WR315 also governs resistance to this race, simi-
lar to that reported in the RIL population derived
from JG62 x Vijay, Vijay being the source of
resistance (Gowda et al. 2009).
Resistance to race 3 has been found to be
monogenic (Sharma et al. 2005; Gowda et al.
2009), but its dominant or recessive nature
remains unknown. Resistance to race 4 was
observed to be controlled by either one or two
genes, with the resistant allele being recessive
(Tullu et al. 1998, Tullu et al. 1999). In the
case of resistance to race 5, several authors have
proposed monogenic inheritance using differ-
ent sources of resistance (Tekeoglu et al. 2000;
Sharma et al. 2005; Iruela et al. 2007; Cobos
et al. 2009). Assays developed at the Univer-
sity of Cordoba (Spain) revealed the recessive
nature of resistance to race 5 (Dr. P. Castro and
Dr. J. Gil, personal communication). Two genes
were reported to control resistance to race 0,
one in the genotype JG62 (the same as ICC
4951) and another in CA2139 (Rubio et al.
2003).
The slow wilting resistance reaction in
chickpea seems to be controlled by minor
genes (Sharma and Muehlbauer 2007). Different
Host Resistance
Fusarium wilt resistance in chickpea has been
reported as race-specific and controlled by a
maximum of three major genes, which are reces-
sive for the majority of favorable alleles. Upad-
hyaya and colleagues (1983) and Singh and
Search WWH ::
Custom Search