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of the pathogen have been identified worldwide
based on reaction on a standard set of twelve
host differential cultivars (Pastor-Corrales 1991).
Races are assigned a binary code according to
their pathogenicity on members of the differ-
ential series (Melotto et al. 2000). The use of
the same twelve differentials by scientists has
resulted in a uniform and useful characterization
of pathogenic variability of
C. lindemuthianum
in different countries and continents. Knowl-
edge of pathogenic variability has allowed for
a planned approach to breeding for resistance
(Kelly et al. 1994). The genetics of anthracnose
resistance has been studied in many bean geno-
types since Barrus (1911) described a differen-
tial response in the host-pathogen interaction.
Several resistance genes that condition resis-
tance against specific isolates or races have been
described in common bean. These include the
Co-1
,
Co-2
,
Co-3
,
Co-4
,
Co-5
,
Co-6
,
Co-7
,
Co-
8
,
Co-9
,
Co-10
,
Co-11
,
Co-12
,
Co-13
,
Co-14
,
Co-u
,
Co-v
,
Co-w
,
Co-x
,
Co-y
, and
Co-z
genes.
Multiple resistance alleles were also reported at
the
Co-1
,
Co-3
,
Co-4
, and
Co-5
loci. The major-
ity of these loci were described based on the
interpretation of allelism tests challenged against
different anthracnose races. However, recent
molecular and genetic evidence suggests that the
classical interpretation of the
C. lindemuthianum
- P. vulgaris
interaction should be reconsidered
because:
This chapter reviews limitations of the classical
genetic analysis of resistance based on allelism
tests and the current state of knowledge about
resistance to anthracnose in common bean.
The Pathogen,
Colletotrichum
lindemuthianum
Colletotrichum lindemuthianum
(Sacc. & Mag-
nus) Lams.- Scrib., the causal agent of bean
anthracnose, is a serious seed-borne pathogen of
common bean (
P. vulgaris
) that has also been
reported to attack other species of
Phaseolus
(Zaumeyer and Thomas 1957; Sicard et al. 1997).
Bean anthracnose has worldwide distribution,
but it occurs in temperate regions and at higher
elevations in the tropics where beans are grown
in cooler, more humid environments (Pastor-
Corrales and Tu 1989).The pathogen is seed
borne and is particularly problematic for small
seed producers who save their own seed. Clean-
seed programs are the most effective means to
control the disease, but these require organized
seed production in areas where the disease is
not endemic. Local spread of the pathogen can
occur by wind-driven rain and by movement of
animals and machinery through infected fields.
Long-distance spread in infected seed has been
reported to occur both within and between coun-
tries (Tu 1994). Disease control measures that
include seed and foliar treatment with fungi-
cides, as well as crop rotation, are not very
effective. Genetic resistance can offer a long-
term solution, but the appearance of new physio-
logical races of
C. lindemuthianum
continuously
poses a challenge to breeders and producers mak-
ing resistance appear elusive and short-lived.
The symptoms of anthracnose are most dis-
tinctive on bean pods appearing as round black
shrunken lesions containing flesh-colored spores
(Figure 9.1). Lesions will expand and coalesce
to cover the entire pod under extreme condi-
tions (Schwartz and Pastor-Corrales 2005). Seed
harvested from infected pods will exhibit simi-
lar lesions particularly obvious on light-colored
seeds.
1. Resistance to different isolates or races
of anthracnose in bean genotype(s) can
be controlled by different genes although
monogenic segregation ratios are commonly
observed in response to different races.
2. Anthracnose resistance genes are located in
specific regions of genome and are organized
in groups or clusters of loci in which individ-
ual gene(s) confers resistance to one specific
isolates or race.
3. Molecular analysis revealed an organization
of gene clusters that encode for proteins con-
taining leucine-rich repeat motifs involved in
the response to pathogens.
Foliar
lesions
are
dark
brown/black
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