Agriculture Reference
In-Depth Information
the pathogen population may be many millions in size,
so such a mutant will arise! New races of pathogen have
overcome vertical resistance to air-borne diseases partic-
ularly quickly. In other cases, for example the single gene
(H
1
) in potato which gives vertical resistance to potato
cyst nematode (
Globodera rostochiensis
), have proved
very durable probably as a result of the much lower
degree of mobility of the earth dwelling eelworm pest.
One technique used by plant breeders is to
pyramid
single gene resistance where there are a number of qual-
itative genes available. This technique was attempted
in potato for late blight (
Phytophtra infestans
) using a
series of single resistance genes (R genes) derived from
Solanum demissum
. To date, nine R genes have been
identified, and up to six of these combined into a single
potato clone. However, the late blight pathogen was able
to overcome the pyramiding of R genes quickly and the
technique was not successful. Pyramiding single gene
resistance to diseases and pests, with the use of molecu-
lar markers that avoids the need to have suitable virulent
pathotypes to screen for multiple resistance genes, has
recently kindled interest.
Horizontal resistance is determined by many alleles
acting collectively with each allele only having a small
contribution to overall resistance. Because of the multi-
plicity of genes involved, horizontal resistance tends to
be far more durable than vertical resistance. The advan-
tage of horizontal resistance is in its ability to control a
wide spectrum of races and, new races of the pathogen
have difficulty overcoming the alleles at all loci control-
ling the resistance. The main disadvantage of horizontal
resistance is that it is often difficult to transfer from
parent to offspring. The probability of transferring all
the resistant alleles from a resistant parent to a sus-
ceptible one can be very low. Breeding for horizontal
resistance therefore tends to be a cyclic operation with
the aim of increasing the frequency of desirable resistant
genes.
By far the most numerous examples of inhibition
of infection in crop plants are related to hypersensitiv-
ity. Infection of the host plant causes a rapid localized
reaction at the infection site. Host plant cells surround-
ing the infection point die, and hence the pathogen is
effectively isolated from the live plant tissue and can-
not spread further in the host plant. Hypersensitivity is
usually associated with a necrotic flecking at the infec-
tion site and the host plant is totally immune to the
pathogen as a result. Plant resistance through hyper-
sensitivity is controlled by single genes and hence can
usually be easily incorporated into breeding lines. In
cases of high disease infection, cell death in the host
plant can cause a significant reduction in plant pho-
tosynthesis and in extreme cases, plant death through
lethal necrosis.
Other examples of disease infection inhibitors are
less numerous and are usually associated with physical
or morphological barriers. For example, the resistance
to cabbage seedpod weevil found in yellow mustard
(
Sinapis alba
) has been attributed to the very hairy
surface of its pods and other parts, a feature not
appreciated by the weevils that are deterred from lay-
ing their eggs. Similarly, leaf wax mutants of cabbage
can deter insect feeding, and tightly wrapped corn
husks can prevent insect pests from feeding on the
developing seed.
Growth inhibition after infection is caused by the
host plant restricting the development of a pathogen
after initial infection. The pathogen is not able to repro-
duce in a resistant host plant as rapidly after infecting
compared to a susceptible one. For example, Russian
wheat aphids feeding on susceptible wheat plants inject
toxins into leaves causing the leaves to fold. Adult Rus-
sian wheat aphids lay eggs in the folded leaves and the
developing larvae gain protection from within the folds.
Resistance genes have been identified that do not deter
the adult Russian wheat aphids from feeding or injecting
toxins into the leaves. However, the toxins do not cause
the leaves of resistant wheat to fold, and hence there
is greater mortality of developing Russian wheat aphid
larvae, and reduced populations of the pest. Resistance
to lack of spread of disease after infection can result
from
antibiosis
, where the resistance reduces survival,
growth, development or reproduction of the pathogens
or insects feeding on the plant, or by
antixenosis
, where
the resistant host plant has reduced preference or accep-
tance to the pest, usually insects. Resistance due to
Mechanisms for disease resistance
Two
main
disease
resistance
mechanisms
exist.
These are:
•
Resistance due to lack of infection
•
Resistance due to lack of subsequent growth or spread
after initial infection
