Agriculture Reference
In-Depth Information
resistance gene,
Yr17
located on chromosome 2NS of
T. ventricosum
Tausch. has
been translocated to the short arm of bread wheat chromosome 2AS (Helguera et al.
2003
), and this chromosomal segment also conferred resistance to leaf rust (
Lr37
)
and stem rust (Sr38). The
Lr19
gene, originated from decaploid
Th. ponticum
, was
transferred into durum wheat, and widely conferring resistance to leaf rust in wheat
(Gennaro et al.
2009
).
Ae. tauschii
Cosson was the donor of the
Lr21
that is a du-
rable and highly effective leaf rust resistance gene, and it has been incorporated into
wheat cultivar and is available for breeding (Talbert et al.
1994
). The leaf rust resis-
tance gene
Lr47
confers resistance to a wide spectrum of leaf rust strains. This gene
was recently transferred from chromosome 7S of
T. speltoides
Tausch to chromo-
some 7A of common wheat (Helguera et al.
2000
). Leaf rust resistance gene
Lr51
,
located within a segment of
T. speltoides
Tausch chromosome 1S, was translocated
to the long arm of chromosome 1B of bread wheat, which is resistant to the cur-
rent predominant races in USA (Helguera et al.
2005
). The gene-specific markers
Xucw108
and
Xuhw89
for
Gpc-B1
and
Yr36
originated from chromosome 6BS of
T. turgidum
ssp. dicoccoides. They were identified and validated in a collection of
117 cultivated tetraploid and hexaploid wheat germplasm (Uauy et al.
2006
).
Molecular Basis of Disease Resistance
It is important to understand the molecular mechanism of disease resistance to
devise sustainable control (Bux et al.
2012b
). The earlier findings of Flor (
1956
)
proposing gene-for-gene hypothesis provided basis for predicting the molecular ba-
sis of disease resistance. The molecular interpretation of Flor's findings, avirulent
(
Avr
) genes encode signal transduction that is perceived by the products of plant
R
genes, are regarded as foundation concept in disease resistance. The
R
-gene/aviru-
lence factor complex is thought to instigate a series of signaling cascades leading
to disease resistance. Rapid oxidative bursts, cell wall strengthening, induction of
defense gene expression and rapid cell death at the site of infection are the down-
stream cellular events that confer resistance state (Morel and Dangl
1997
). In more
elaborated form, the direct or indirect recognition of pathogen by host '
R
' genes
lead to a resistance response known as effector-triggered immunity (ETI), which
includes localized programmed cell death (PCD), known as the hypersensitive re-
sponse (HR) which ultimately restrict pathogen growth (Dangl et al.
1996
).
R
gene
proteins serve to recognize pathogen effectors either through direct interaction or as
guards for target molecules and are known to confer resistance to bacteria, viruses,
nematodes, oomycetes, insects, and biotrophic fungi (Martin et al.
2003
). Genes for
resistance, their protein products, and underlying mechanism are being investigated
(Hammond-Kosack and Jones
1996
). Sufficient progress has been made in these
aspects that will facilitate developing effective control strategies.
Most of the
R
genes cloned so far, revealed a nucleotide-binding site (NBS)
and a leucine-rich-repeat (LRR) region. These are the most abundant types in
plant species (Meyers et al.
1998
). These plant
R
genes encode proteins that have
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