Organization of Genes Conferring Resistance to Anthracnose in Common Bean - Translational Genomics for Crop Breeding: Biotic Stress - page 157

resistance gene as is present in the differen-
tial cultivar Kaboon, a widely recognized resis-
tance source that provided resistance to race 73.
Within five years the new race 105 (reported
in 2008; Dongfang et al. 2008) emerged that
attacked Envoy and overcame the Co-1 2 resis-
tance gene. The most likely scenario was that
race 73 acquired additional virulence gene(s) to
overcome the Co-1 2 resistance gene that evolved
into race 105 (Table 1). Race 105 has never been
reported in North America and is relatively rare
in South and Central America (Balardin et al.
1997). Fortunately, many of the resistance genes
that control race 73 are also effective against race
105. The speed with which race 73 evolved into
race 105 that defeated the Co-1 2 gene was rapid
as all the conditions favorable for the develop-
ment of a new race of anthracnose existed in
Manitoba. These included favorable cool wet
weather conditions, planting of infected seed of
susceptible cultivars that produced an abundance
of inoculum of race 73, and the widespread plant-
ing of a highly resistant host variety in adjacent
fields in the localized production area. The poten-
tial of this pathogen to rapidly evolve under-
scores the risk of planting resistance cultivars
with single resistance genes, and breeders should
be encouraged to develop cultivars with multiple
resistance genes to ensure more durable resis-
tance to anthracnose in the future bean cultivars.

tions. Genetic evidence for one dominant gene
is generally deduced from resistant reaction in
F 1 plants or 3R:1S or 15R:1S observed ratios
in F 2 segregating populations derived from R
x S crosses. Recessive resistances genes were
also described in the literature based on suscep-
tible reaction of F 1 plants or 1R:3S or 13R:3S
observed ratios in descendents derived from R x
S crosses. Genes conferring recessive resistance
were described for race beta in the crosses Tus-
cola x Montcalm and Tuscola x Swedish Brown
(Muhalet et al. 1981) or in the reaction of cultivar
AB136 to race 73 in the population derived from
the cross AB136 x Cornell 49242 (Alzate-Marin
et al. 1997). Recessive resistance genes to race
beta were also described in the cultivars Miche-
lite or Brazilian Red (Cardenas et al. 1964). In
those instances where recessive resistance was
reported these observations were later explained
as a reversal of dominance between different
resistance alleles at the same locus when chal-
lenged with different pathogenic races (Melotto
and Kelly 2000).
The majority of resistance genes to anthrac-
nose exhibit an epistatic interaction of dupli-
cate dominant loci controlling resistant reac-
tions to a specific pathogenic variant of C.
lindemuthianum . Complementary mode of
action between two genes was described and
deduced in F 2 populations from observed ratios
such as 9R:7S, 57R:7S or 249R:7S (Cardenas
et al. 1964; Muhalet et al. 1981). Genetic mech-
anism conditioning resistance to beta, gamma,
and delta races conferring by duplicate and com-
plementary genes was described in F 2 popula-
tions involving cultivar Kaboon (Muhalet et al.
1981; Melotto and Kelly 2000). Two dominant
and complementary genes conditioning resis-
tance to race 31 were also found and mapped
in cv. Kaboon (Campa et al. 2011). Expression
of this complementary mode of action depends
on genetic background and is more common in
Andean genotypes. If two genotypes only dif-
fer in one complementary gene, a more common
monogenic dominant segregation pattern would
be expected.

Genetic Resistance to
Anthracnose

3.1 Modes of Action of Genes
Conferring Resistance

Genetic analysis of resistance to C. lindemuthi-
anum generally follows a qualitative mode of
inheritance where resistant and susceptible reac-
tions are clearly differentiated. Alleles at a
locus can interact in several ways either through
complete dominance, partial dominance, addi-
tive effect, or overdominance. The majority of
described genes conferring resistance to bean
anthracnose show complete dominance where
the dominant allele conditions resistance reac-