Disease Resistance in Chickpea - Translational Genomics for Crop Breeding: Biotic Stress - page 207

studies using both an RIL population and near-
isogenic lines (NILs) suggest that in race 5, apart
from a major gene, additional genomic areas
influence slow wilting resistance (Cobos et al.
2009; Castro et al. 2010). Larger segregating
populations are required to clarify the nature of
genetic control of slow wilting. Likewise, further
studies are necessary to identify the genetics of
resistance to races 1B/C and 6.

ers to pyramid genes in a single variety and thus
provide durable resistance.

BotrytisGrayMold (BGM)

Causal Agent

Botrytis gray mold of chickpea is caused by
Botrytis cinerea Pers. Ex. Fr. Its teleomorph (sex-
ual stage) is Botryotinia fuckeliana , although the
sexual stage has not been reported on chick-
pea. The pathogen attacks all the aerial parts of
the plant but most frequently the growing tips
and flowers (Davidson et al. 2004). The dis-
ease initially appears as water-soaking lesions,
which turn gray or dark brown (Figure 11.1).
Sometimes tiny black sclerotia may develop on
the dead infected tissues (Pande et al. 2011b).
Infected chickpea pods result in no seeds at all
or only shriveled seeds.
B. cinerea has a very wide host range of more
than 100 plant species including many econom-
ically important vegetable and field crops, orna-
mentals, and pre- and post-harvest fruits (David-
son et al. 2004).
The pathogen survives between crops in
infested soil and infected plant debris as mycelia,
chlamydospores, and sclerotia. It may also sur-
vive in infested or infected seeds. Seeds carrying
the fungus may not show any visible symptoms.
Because of its wide host range, other alterna-
tive hosts are also important inoculum sources
(Pande et al. 2011b).
Relative humidity, leaf wetness, and temper-
ature are the most important factors for disease
infection and development. The effects of the
disease on yield depend on the growth stage of
the crop at onset of the disease and its severity
(Davidson et al. 2004). Isolates show variation in
virulence on chickpea, but no host-specialization
has been reported.

Gene Mapping

Markers identified early on as linked to a Foc
reistance gene were RAPD UBC-170 550 and CS-
27 700 , which each target one of the three loci
controlling resistance to race 1 ( foc-1 ) (Mayer
et al. 1997). An allele-specific associated primer
(ASAP) was designed, based on CS-27 700 . Later,
Tullu and colleagues (1998) demonstrated that
foc-1 was linked to foc-4 and suggested the pres-
ence of a gene cluster for Foc resistance sited
in LGII of chickpea map. Winter and colleagues
(2000) mapped a RIL population segregating for
resistance to Foc-4 and Foc-5 located in the same
gene cluster on LGII previously mentioned, with
ASAP CS27, STMS TA27, TA59, and TA96
included as indicative markers. These markers
have been validated in different genetic back-
grounds (Table 11.1). Similarly, single genes for
foc-0 , foc-2, and foc-3 have been mapped in the
same genomic area (Table 11.1). Apart from this
gene cluster, a different gene controlling resis-
tance to race 0 ( foc-0 1 ) was previously mapped
on LGV (Table 11.1).
Near isogenic lines recently developed for
Foc resistance confirmed the efficacy of the
STMS marker TA59 for targeting resistance
genes for races 1A, 2, 3, 4, and 5 (Castro et al.
2010). On the other hand, TR59 (targeting foc0 1
on LGV) and TA59 (targeting foc0 2 on LGII)
were useful in determining which of those genes
were segregating in five chickpea RIL popula-
tions (Halila et al. 2010). Nevertheless, there
are still genes for different races that have not
been mapped; knowledge of their locations in
the chickpea map is essential to enable breed-

Host Resistance Inheritance and QTL
Mapping

Information available on the genetic inheri-
tance of resistance to BGM suggests that it is