Biology Reference
In-Depth Information
To achieve effective and efficient MAS, gene
effects and gene locations in genomes have to be
well characterized. Meanwhile, easily detected
and closely linked molecular markers should be
developed to implement MAS in breeding.
stage to the adult stage. Seedling resistance is
analyzed using cotyledon inoculation, whereas
adult-stage resistance is measured at a late devel-
opmental stage approaching maturity, especially
the development of the stem canker in green-
houses or under field conditions (Rimmer and
van den Berg 1992).
In genetic studies, blackleg-resistance segre-
gation in a doubled haploid (DH) line popu-
lation derived from a cross between 'Westar'
and 'Cresor' was tested under field conditions
with a dominant major locus identified (Dion
et al. 1995). Similarly, Pang and Halloran (1996)
detected a single dominant resistance gene locus
in 'Maluka' conferring adult stage resistance.
Blackleg resistance is commonly identified in
most Brassica species, for example,
B. rapa
(AA),
B. napus
(AACC),
B. juncea
(AABB),
B. nigra
(BB), and
B. carinata
(BBCC), while
all tested accessions in
B. oleracea
(CC) are
susceptible, suggesting that this diploid Bras-
sica species does not contain blackleg disease
resistance genes (Monteiro and Williams 1989).
Since
B. juncea
,
B. nigra,
and
B. carinata
show
strong resistance to
L. maculans
, the previous
reports suggest that resistance genes in these
three species may exist in the B genome of Bras-
sica species (Roy 1984; Chevre et al. 1997; Struss
et al. 1996).
Genetic analysis of the resistance genes
in the B genome has been performed, and
gene introgression via interspecific hybridiza-
tion has been extensively used to move the B
genome resistance genes into canola. For exam-
ple, Roy (1984) reported that blackleg resis-
tance to
L. maculans
from
B. juncea
had been
introduced into
B. napus
. Moreover,
B. napus-
B. nigra
and
B
.
oleracea
-
B
.
nigra
additional
lines were used to pinpoint the B genome chro-
mosomes that carry blackleg-resistance genes
(Chevre et al. 1996, Chevre et al. 1997).
Struss and colleagues (1996) reported that two
or three B chromosomes anchored blackleg-
resistance genes and Chevre and colleagues
(1997) illustrated that blackleg-resistance genes
Blackleg
Pathogenicity Groups and
Differentiation Hosts
Blackleg disease is caused by
L. manculans
,a
fungal pathogen with extensive pathogenicity
differentiation. The interaction of the blackleg
pathogen and plant resistance, first tested using
a cotyledon inoculation method (Williams and
Delwiche 1979), is commonly used to detect
sources of resistance and pathogenicity groups.
The first differential set including three canola
cultivars - 'Westar,' 'Glacier,' and 'Quinta' -
was established to classify pathogen isolates into
three pathogenicity groups, PG2, PG3, and PG4
(Mengistu et al. 1991). 'Westar' is susceptible
to all virulent isolates and accepted as the best
check that is used in most blackleg-resistance
studies. 'Glacier' is resistant to PG2 and sus-
ceptible to PG3 and PG4 isolates. 'Quinta' is
resistant to both PG2 and PG3 but susceptible
to PG4. With a different set of canola cultivars
including 'Lirabon,' 'Glacier,' 'Quinta,' and 'Jet
Neuf,' pathogen isolates were classified into A1
to A6 groups (Badawy et al. 1991). Actually in
the A-group classification, the susceptible canola
cultivar 'Westar' was replaced with 'Lirabon'
and PG2, PG3, and PG4 were subdivided into
two groups using 'Jet Neuf' as a host differential
cultivar. Later, the PGT group was added to the
PG groups. The PGT isolates were virulent to
'Quinta' but avirulent to 'Glacier.'
Genetics of Blackleg Disease
Resistance
There are two types of blackleg disease resis-
tance detected from the seedling (or cotyledon)
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