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oligogenic in nature. Thus, as many as three
different genes have been described that occa-
sionally show epistatic interaction (reviewed by
Pande et al. 2006a).
The locations of genomic areas controlling
resistance in the chickpea genetic map have been
identified by Anuradha and colleagues (2011).
Three QTLs were identified, with QTL1 sited on
LG6 (or LGVI), and QTL2 and QTL3 mapped on
LG3 (corresponding to LGVIII in the chickpea
consensus map, Table 11.1). QTL1 and QTL2
explained 12.8% and 9.5% of the total pheno-
typic variation for BGM. The strongest QTL for
BGM resistance was QTL3, explaining 48% of
the phenotypic variation, with a logarithm of
odds (LOD) score of 17.74. When BGM dis-
ease scores of 126 RILs were grouped into two
classes, a ratio of 54 (resistant):72 (susceptible)
was found, not significantly different (P
Rust symptoms are large pustules on leaves
that appear initially as small, round, brown
spots (Figure 11.1). In the mature pustule, when
the epidermis ruptures, uredospores are released
from the center of the spots (Singh et al.
2007). The fungus can affect various plant stages
(vegetative, flowering, or fruiting) and different
organs, including leaves, stems, pods, or even
seeds. In severely affected plants, lesions coa-
lesce, causing premature defoliation and consid-
erable reduction in yield (Jones 1983).
Host Resistance and QTL Mapping
The genetic basis of rust resistance in most cool-
season legumes is largely unknown. Evaluation
of germplasm collections reveals moderate levels
of incomplete and partial resistance in C. ariet-
inum and some resistant accessions in wild Cicer
relatives (Rubiales et al. 2001). Madrid and col-
leagues (2008) postulated that resistance is con-
trolled by one major gene located on LGVII; oli-
gogenic control of rust resistance is in agreement
with studies conducted on other legumes. For
example, recent mapping studies have yielded
identification of major QTLs for resistance to U.
viciae-fabae (Vijayalakshmi et al. 2005; Rai et al.
2011) and to U. pisi (Barilli et al. 2010). In lentil,
monogenic resistance to U. viciae-fabae has been
described (Erskine et al. 1994), and a sequence
related amplified polymorphism (SRAP) marker,
F7XEM4a, has been identified at 7.9 cM,
apart from the gene for resistance (Saha et al.
2010). Nevertheless, more studies are necessary
to elucidate the recessive/dominant nature of
this gene.
Only one study to date has been focused
on rust resistance in chickpea (Madrid et al.
2008). This research describes a QTL located
on LGVII of the chickpea genetic map, explain-
ing 31% of the total phenotypic variation in
seedlings and 81% of the area under the dis-
ease progress curve (AUDPC) in adult plant. It
was hypothesized that a single dominant gene
( Uca1/uca1) controlled resistance to rust, with
resistance regarded as a qualitative character.
0.1)
from 1:1 distribution. This result suggests the
presence of a major gene for BGM resistance
corresponding to QTL3. Markers linked to dif-
ferent QTLs are summarized in Table 11.1. Fur-
ther analysis using different sources of resistance
will facilitate the use of MAS to pyramid BGM
resistance genes in commercial varieties in order
to obtain higher levels of resistance.
=
Rust
Causal Agent
Several rust species can infect grain and forage
legumes, most of them belonging to the genus
Uromyces (Rubiales et al. 2001). In particular,
chickpea rust is caused by Uromyces ciceris-
arietini (Grogon) Jacz. & Beyer, and has been
described as a problem in central Mexico and
Italy (Ragazzi 1982; Dıaz-Franco and Perez-
Garcıa 1995) and also in India (Hiremath et al.
1987). Chickpea rust develops in cool and moist
weather conditions, although rain is not essen-
tial for its development. Environmental condi-
tions favoring rust occurrence are similar to those
for AB. Consequently, rust has been reported in
many of those countries where AB of chickpea
is a problem (Reddy et al. 1990).
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