Biology Reference
In-Depth Information
MAS is a tool that could increase the efficacy
and efficiency of chickpea breeding programs,
accelerating development of new varieties
adapted to different environmental conditions or
market requirements. In recent years, improve-
ment of genetic maps and identification of
markers targeting genes or quantitative trait
loci (QTLs) has progressed rapidly in chickpea.
Thus, numerous sequence tagged microsatellite
site (STMS) markers have been developed,
allowing for unified nomenclature for different
linkage groups (LGs) and the establishment
of reference maps (Winter et al. 2000; Millan
et al. 2010; Gaur et al. 2011). Additionally,
gene-based single nucleotide polymorphisms
(SNP) marker loci from transcript sequences
have been included in chickpea genetic maps,
providing anchor points for comparison of
chickpea LGs with chromosomes of the model
species Medigaco truncatula (Nayak et al.
2010; Gujaria et al. 2011; Thudi et al. 2011).
In addition, bacterial artificial chromosome
(BAC) libraries and the generation of BAC-end
sequence markers are facilitating the availability
of genome-wide physical maps in C. arietinum
(Rajesh et al. 2004; Lichtenzveig et al. 2005;
Zang et al. 2010; Thudi et al. 2011). Integration
of genomic tools for marker-assisted breeding,
high-resolution mapping, and positional cloning
of genes and QTLs are expected to enhance
genetic
(teleomorph: Didymella rabiei ). The disease
affects all aerial parts of the plant, causing brown
lesions with concentric rings of black pycnidia
on stems, leaves, flowers, pods, and seeds (Bayaa
and Chen 2011) (Figure 11.1). A. rabiei propa-
gates both asexually through conidia (pycnid-
iospores) and sexually through ascospores pro-
duced in pseudothecia. It requires two mating
types for sexual reproduction and both mating
types have been found in many chickpea pro-
duction areas. Sexual reproduction requires a
cold and moist period and usually occurs off sea-
son (between chickpea crops) on chickpea debris
(Trapero-Casas and Kaiser 1992). The sexual
spores mature and are ready for release when
the next chickpea growing season starts. Dur-
ing storm and moist conditions, the ascospores,
which serve as the primary inoculum, are ejected
from pseudothecia and carried by wind to chick-
pea plants, where they initiate primary infec-
tion. Conidia on overwintering debris and on
seeds may also serve as the local primary
inoculum and initiate infection (Navas-Cortes
et al. 1995). Secondary spread of the pathogen
within chickpea fields is through rain splash of
conidia.
The pathogen as well as the disease are
favored by cool (15-25 C) and moist condi-
tions (Bayaa and Chen 2011). The disease is
particularly severe in growing areas with a pro-
longed rainy season. A. rabiei causes economic
losses only on chickpea, but it readily infects
wild chickpea relatives ( Cicer spp.), and it may
infect a range of other plant species occasionally
or under artificial inoculation.
Considerable variation in A. rabiei has been
reported, both in terms of virulence and in
neutral genetic markers. Several systems are
available to classify or categorize the virulence
forms, ranging from 3 pathotypes to 14 virulent
forms. The current trend is to reduce the num-
ber of categories of virulence forms (Chen et al.
2004). More virulent isolates have been reported
recently (Imtiaz et al. 2011). It should be noted
that no genetic bases for virulence differences
in the systems have been found, although genes
or QTLs in chickpea for resistance to different
and
genomic
research
and
breeding
applications in chickpea.
This chapter will focus on the current sta-
tus and future potential of genomic tools for
MAS in chickpea for resistance to major biotic
stresses such as ascochyta blight (AB) and fusar-
ium wilt (Foc), which currently impose major
constraints on stable productions. Botrytis gray
mold (BGM) and rust diseases, biotic stresses
that are becoming increasingly important, will
be also considered.
AscochytaBlight (AB)
Causal Agent
Ascochyta blight of chickpea is caused by the
fungal pathogen Ascochyta rabiei (Pass) Lab.
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