Reducing the economic impact of crop disease is a global effort. Here are some tools we offer researchers working to reduce the impact:
- Necrotrophic Effectors
- Genetic Markers for SNB and Yellow Spot Resistance
- Unified nomenclature for target-site mutations associated with resistance to fungicides
The CCDM is a specialist centre in effector biology and is one of the few organisations in Australia studying necrotrophic effectors of crop fungal pathogens. At the CCDM we work on the model that a wheat line insensitive to all relevant necrotrophic effectors will be extremely resistant to a given disease.
How can effectors be used in breeding programs?
Breeders can contact the CCDM for an effector sensitivity screening kit including ToxA for yellow spot and ToxA, Tox1 and Tox3 for SNB. These effectors can be infiltrated directly onto wheat varieties. Breeders can see necrosis within a few days, and can rapidly discard sensitive varieties from the breeding program.
Benefits of using effectors
- A rapid assay – Once infiltrated, necrosis caused by sensitivity to effectors appears in a few days. Wheat cultivars that are insensitive to effectors possess the genetic potential to confer greater SNB and yellow spot resistance. No need to test in different locations, as the cultivar is either sensitive or insensitive to the effector.
- Save costs – effectors are provided to breeding companies without charge. The only cost for leaf infiltrations is the labour involved, which is minimal when compared to field trials. It is possible to carry out up to 2000 infiltrations per day.
- Save on space – leaf infiltrations can be carried out on seedlings, as young as nine days old.
- Simplicity – infiltrations only require a needleless 1cc syringe and non-toxic marker pen. As a result, operating costs are kept to a minimum.
- Take out the guess work – breeders will know exactly which effector is causing symptoms on the plant.
Genetic Markers for SNB and Yellow Spot Resistance
Through national and international collaboration programs, the CCDM also develops both gene-specific and closely-linked reliable QTL markers that can be passed on to breeders to assist in germplasm enhancement breeding and high-throughput genotype screening.
Our provision of gene specific markers for Tsn1 has successfully enabled breeders to remove this effector sensitivity gene from wheat germplasm, eliminating fungal virulence associated with ToxA in SNB and yellow spot, without affecting yield. The CCDM also provides closely-linked effector-complementary markers for Snn1 and Snn3 that confer sensitivity to Tox1 and Tox3 respectively.
In addition, we anticipate new genetic markers for SNB and yellow spot to become available once novel effectors are discovered. At present, we have identified QTLs in chromosomes 2A and 2D that respond to SNB. In the near future, we expect more genetic markers to be available.
The CCDM is currently developing wheat genetic resources using modern SNP marker technology to identify novel disease QTLs, as well as implementing KASP genotyping to screen wheat varieties for known dominant sensitivity genes. These approaches will complement our effector-assisted breeding (above) and offer greater versatility to cereal breeders.
In collaboration with the National Institute of Agricultural Botany, UK, reliable markers for Snn1 and Snn3 which confer sensitivity to Tox1 and Tox3 of SNB have been developed and will be made available shortly.
Unified nomenclature for target-site mutations associated with resistance to fungicides
In 2016, CCDM’s Fungicide Resistance Group published a paper on a proposal for a unified nomenclature for target-site mutations associated with resistance to fungicides. This paper can be found here.
The purpose of this paper was to propose a system for unifying the labelling of mutant amino acids in fungicide target proteins. The advantages of a unified system is that it would be easier to memorise common changes to determine whether the changes were novel or were repetitions of what has already been seen in other species and to link changes to particular active ingredients. We favour basing alignment on the species with the most currently described resistance mutations, but also taking into account using the longer gene when alternative species are candidates.
We are proposing the following genes are fitted to the corresponding pathogens:
|Gene||Pathogen||Table of amino acid substitutions|
|Cyp51A||Aspergillus fumigatus||Refer to table 2|
|Cyp51B and Cytb||Zymoseptoria tritici||Refer to table 1 and 3|
|b-tubulin||Aspergillus nidulans||Refer to table 4|
|SDH proteins||Pyrenophora teres||Refer to table 5, 6 and 7|
|CesA3||Phytophthora infestans||Refer to table 8|
|Os-1||Botrytis cinerea||Refer to table 9|