Agriculture Reference
In-Depth Information
tional proteins interact (Dodds et al., 2007), will
lead to greater understanding and potential
exploitation of gene-for-gene specifi city in the
wheat rusts. Of course any of these strategies will
depend on the eventual governmental, regulatory,
and consumer acceptance of transgenic wheat.
In the meantime the frequency and severity of
rust epidemics on wheat can be reduced by greater
utilization of resources that are already available.
Diagnostic markers for genes such as
Lr34/Yr18
should greatly simplify selection of these genes,
potentially allowing genes with durable rust resis-
tance to become fi xed in wheat germplasm.
Increased planting of wheat cultivars with high
levels of leaf rust resistance in the US, and removal
of susceptible cultivars, will reduce the size of the
P. triticina
population that regularly overwinters,
thus reducing the chance of mutation for increased
virulence to newly deployed resistance genes.
Australia has adopted minimum disease standards
for release of wheat cultivars (Wallwork 2007),
with the specifi c goal to reduce the amount of rust
inoculum and thus prolong the effective life span
of a rust resistance gene by reducing the chances
of new virulent races emerging. The effectiveness
of this approach can be seen in comparing the
effective life span of
Lr24
in the US versus Aus-
tralia. In the US, virulence to
Lr24
appeared
almost immediately after the release of cultivars
with this gene, while in Australia races of
P. tri-
ticina
with virulence to
Lr24
did not appear until
17 years after cultivars with this gene were fi rst
grown (Park et al., 2002). Genes
Lr1
and
Lr13
have also been much more effective in Australia
compared with the US due to the greater use of
highly resistant cultivars and the reduced size of
the
P. triticina
population.
For the stem rust race Ug-99, the challenge
will be to incorporate
Sr2
into wheat germplasm
in regions where this race poses an immediate
threat. This gene was common in older CIMMYT
wheat cultivars such as Pavon 76, but more recent
germplasm releases appear to lack
Sr2
. Although
Ug-99 is virulent to many genes that were origi-
nally derived from hexaploid wheat, several genes
derived are from wild wheat relatives that condi-
tion resistance to this race. It should be feasible
to add these genes into wheat germplasm by using
tightly linked molecular markers and testing with
avirulent stem rust races.
The reproductive capacity, long-distance aerial
dispersal, and high degree of genetic variation in
the wheat rust fungi almost certainly ensure that
new races with virulence to important and widely
used resistance genes will continue to arise and
pose a threat to wheat production. Ultimately
losses due to these pathogens can be avoided only
by continued vigilance by wheat breeders and
plant pathologists.
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