Biology Reference
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genes, such as LepR1 , LepR2 , LepR3, and LepR4,
into B. napus (Yu et al. 2005, 2008, 2012).
The gene introgression was first performed in
the development of the canola cultivar 'Surpass
400' and this canola cultivar was then used to
develop a series of commercial canola cultivars
in Australia. All sylvestris-derived canola culti-
vars theoretically contained blackleg-resistance
genes introduced from the wild B. rapa subsp.
sylvestris. Currently, 'Surpass 400' is commonly
used in canola breeding programs by Cana-
dian breeding organizations. Yu and colleagues
(2008) mapped a dominant blackleg-resistance
locus, named LepR3 on linkage group N10 in
'Surpass 400.' More recently, in the same region
on linkage group N10 in 'Surpass 400,' two sepa-
rate resistance genes, BLMR1 and BLMR2, were
identified, and BLMR1 was fine mapped (Long
et al. 2010). Using a map-based cloning strategy,
BLMR1 was successfully cloned and function-
ally confirmed through complementary transfor-
mation of the susceptible cultivar 'Westar.' This
is the first blackleg-resistance gene that has ever
been cloned in B. napus (Li et al. 2010 and
unpublished data).
The B genome Brassica species, including B.
nigra , B. juncea, and B. carinata , have a high
level of resistance to L. maculans . Gene intro-
gression from the B genome to B. napus has
been extensively performed with the blackleg-
resistance genes introduced into canola. Using
RAPD markers and B. napus-B. nigra additional
lines, the B8 chromosome of B. nigra was shown
to carry blackleg-resistance genes. A genetic
map constructed with RFLP molecular markers
was used to illustrate that a blackleg-resistance
gene locus is located on linkage group JR13,
suggesting that the blackleg-resistance gene in
B. juncea belongs to the B genome. In general,
genetic mapping of blackleg-resistance genes
introgressed from the B genome into the A and
C genomes in B. napus has not been successful,
since the B genome is quite different from the A
and C genomes and recombination between the
B and A, B, and C genomes is very low.
Mapping and Cloning of Avirulence
Genes in L.maculans
Based on a gene-for-gene interaction theory, sev-
eral avirulence genes, such as Avrlm1 to Avrlm9,
have been successfully identified using cultivars
and breeding lines harboring resistance genes to
blackleg (Balesdent et al. 2006), and Avrlm1 ,
Avrlm6, and Avrlm4-7 have been characterized
(Gout et al. 2006, Fudal et al. 2007, Parlange
et al. 2009). These cloned avirulence genes are
coded for secreted small proteins (SSPs) as fun-
gal effectors in the interactions of plant host and
pathogen. More recently, after the whole genome
of L. maculans was assembled, 651 SSP genes
in the genome of L. macunlans were predicted
(Rouxel et al. 2011). The authors suggested that
122 SSP genes in AT-blocks might correspond
to avirulence genes to blackleg or other biotic
stresses, and those SSPs in GC-blocks might
not belong to avirulence genes, since they lack
the features of known effectors (Rouxel et al.
2011). Obviously, the numbers of SSP genes in
the genome of L. maculans are more than those of
the mapped resistance-gene loci described pre-
viously in Brassica species; it is highly possible
that not every SSP gene belongs to an aviru-
lence gene. Otherwise, one blackleg-resistance
gene might interact with more than one SSP
gene. Therefore, after resistance genes to black-
leg are cloned in the future, the interactions of
effectors and resistance genes can be investigated
further.
QTL Mapping for Blackleg Resistance
Disease resistance is commonly classified into
qualitative and quantitative traits that are con-
trolled by major and minor genes respectively.
All mapped blackleg-resistance genes described
previously are major genes, which display a
typical Mendelian segregation ratio in map-
ping populations. Since these dominant or reces-
sive resistance genes are considered to be race
specific, this resistance might be overcome by
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