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new virulence genes evolved in the pathogen
based on the gene-for-gene interaction model.
In contrast, quantitative resistance is conferred
by race nonspecific minor genes, the resistance
is thought to be more durable even though quan-
titative resistance genes are not individually as
strong as race-specific resistance genes, and
quantitative resistance is much more difficult to
manipulate.
Quantitative trait loci (QTLs) are analyzed
through QTL mapping. Ferreira and colleagues
(1995) detected two QTLs for blackleg disease
resistance in
B. napus
under field conditions.
Similarly, Pilet and colleagues (1998) described
ten field resistance QTLs in one cross and later
ten QTLs in another cross; however, only four
QTLs were common to the previously reported
ones in
B. napus
(Pilet et al. 2001). In a recent
report, more than a dozen QTLs of resistance to
blackleg have been identified (Kaur et al. 2009).
The genomic regions controlling race nonspe-
cific QTLs and race-specific resistance genes are
not commonly co-located, but there is one QTL
sharing a similar genomic region where a race-
specific resistance gene Rlm2 is mapped on link-
age group N10 (Pilet et al. 2001, Delourme et al.
2006) and another QTL was co-located with a
dominant resistance gene locus
Rlm4
(Raman
et al. 2012).
Downy mildew is a serious disease in broc-
coli and Chinese cabbage, and resistance sources
have been identified in Brassica vegetables. Farn-
ham and colleagues (2002) observed a single
dominant resistance gene in broccoli that seg-
regated in a Mendelian fashion in F2 and BC1
populations.
For turnip mosaic virus disease, Hughes and
colleagues (2002) screened 42
B. rapa
and
B. napus
accessions to identify resistance to
turnip mosaic virus (TuMV) isolates represent-
ing the three major pathotypes in Europe. Most
tested accessions were found to be resistant to
TuMV disease, and 14 out of 42 accessions were
resistant to all three used pathogen pathotypes.
Genetic analysis in individual accessions indi-
cated that the resistance might be controlled by
single or multiple, dominant or recessive resis-
tance gene loci in various accessions, based on
the interaction between genotypes and patho-
types observed.
Genetic mapping of resistance genes has been
performed for several Brassica diseases such as
downy mildew, TuMV. In
B. napus
and
B. rapa
,
several dominant and recessive resistance gene
loci have been mapped with RFLP and SSR
markers (Walsh et al. 1999; Hughes et al. 2003;
Rusholme et al. 2007). Two gene loci,
ConTR01
and
retr01
were located on chromosome R4
and R8 (Rusholme et al. 2007). Another TuMV-
resistance gene locus,
TuRB03
, was assigned to a
region on chromosome N6 where two other gene
loci,
TuRB01
and
TuRB01b,
were mapped, sug-
gesting that these three resistance gene loci might
be allelic (Walsh et al. 1999; Hughes et al. 2003).
In genetic mapping of resistance genes for
downy mildew, a genetic map constructed with
RFLP, SSR, ISSR, and RAPD markers was used
to map a major dominant resistance-gene locus
in a cross of rapid cycling kale and broccoli
(Farinho et al. 2004). In Chinese cabbage, Yu
and colleagues (2009) used SSR, STS, SRAP,
and enzyme markers to perform QTL mapping
of downy mildew resistance and identified a
major downy mildew resistance QTL on chro-
mosome A8.
Genetic Mapping of Resistance
to Other Brassica Diseases
Compared with the previously described major
diseases in canola, other Brassica diseases are not
well characterized, since the losses due to these
diseases in Brassica species are, in general, not as
great as those caused by sclerotinia, clubroot, and
blackleg in canola. Ren and colleagues (2001)
performed genetic analysis of resistance to bac-
terial soft rot caused by
Erwinia carotovora
with
25 accessions of
B. rapa
vegetable and oilseed
types. The results showed that the resistance was
quantitative, whereas the narrow-sense heritabil-
ity of the resistance ranged from 42% to 60% in
a Griffing's diallel analysis.
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