Inhalt: International Common Bunt Consortium
Up to now, Bt1-15 and Btp are known resistance genes. Since we need complete resistance stacking of several genes together is the only durable and reliable strategy
Gaining more knowledge about resistance genes, as well as finding new ones and combining them is the overall goal in the common bunt research.
In the ICBC, we get together, share our experiences and work together on the next step.
Every member brings a different set of skills and capacity with them. Therefore, we try to divide and concur to make the most progress.
The ICBC is an association of breeders and scientists, we all have a passion for common bunt and dedicate a part of our time to the consortium on a voluntary basis.
Common bunt (Tilletia caries) is a seed-borne disease of wheat. We received reports that the disease spread even more widely across Germany, Europe and the world. Although the chemically-synthesized seed treatments are generally effective, the socio-politically desired in organic farming tends to lead to an increased occurrence. Breeding for complete resistance in adapted genetic background with high yield potential is becoming more and more important.
Background information on common bunt
Common bunt (Tilletia caries) is a seed- and soil-borne disease of wheat. Although the chemically-synthesized seed treatments are generally effective, the socio-politically desired in organic farming tends to lead to an increased occurrence. Resistance breeding is a sustainable strategy of preventing bunt infections. Up to now, Bt1-15 and Btp are known resistance genes.
Sufficient resistance against this seed borne diseases need to be ensured.
The spores of common bunt are in the soil or directly on the seed surface. At temperatures around 5°C to 10°C, the spores germinate and penetrate the leaf sheaths of the seedlings. The pathogen then grows to the growing point of seedlings and grows with the plants until ears are formed. In the ears common bunt leads to the development of bunts instead of grains. First typical symptoms are only visible after ear emergence: infected plants have somewhat shorter stalks, remain green for longer and are more heavily tufted. Before ripening, common bunt ears can be recognized by their blue-green discoloration and often more elongated growth. The formed bunts are filled with spores, which break open during harvest and contaminate other plants, machines and the soil. Bunt spores produce trimethylamine, which leads to a fishy small and taste. This passes into animal products, like eggs and milk, making the infected wheat unusable for animal feed. Common bunt reduces yield up to 40%. At the moment fungicides or brushing of the spores are the mode of action against common bunt. So the search for resistances moves to the spotlight.
References: Borgen, 2004; Borgen and Kristensen, 2001; Borgen and Davanlou, 2000 ; Borgen, 2001; Nielsen et al., 2000
Status for European Virulence Races
Infection in a resistant variety is not a final proof of the presence of a race being virulent to a resistance gene. Infection in a line may be caused by impurity in the line, or by the resistance gene being partly depending on environmental factors. To document presence of true virulence, spores need to be collected from resistant lines and used for re-inoculation to demonstrate increased infection rate.
Diseases that spread with soil, wind or by water are normally linked to a specific geographical region, but common bunt is mainly spread via seed and may therefore spread over long distances following seed trade rather than from neighbouring fields. Therefore, the virulence of common bunt is more relevant to relate to a seed system or continent rather than a single country or climatic zone. Seed is traded freely within the EU, and it is therefore relevant to consider Europe as one zone of bunt dispersal, and North America another, since seed exchange of infected seed between the continents are limited.
Dwarf bunt on the contrary is more likely to stay stable in virulence within a smaller region.
Virulence is found against most resistance genes in Europe. Bt11 and Bt12 have so far being considered safe genes in Europe, but as described below, these genes are not single genes, but combinations of several genes. The differential lines used to describe Bt11 contains a mixture of several genes, and it is still unknown if virulence is present in Europe against any of these single genes. The same is the situation with Bt12.
Several genes are called Bt8 but comes from different sources and are most likely quite different. The differential line for Bt8 suggested by Blaire Goates is PI 554120 (with PI 173438 as source). Virulence against “Bt8” in PI 554120 is present in Europe. In both USA and Europe, PI 178383 has been used in breeding as a source of “Bt8”, but this “Bt8” is most likely different from the Bt8 in the differential line. It is unknown if virulence is present in common bunt in Europe against “Bt8” coming from PI 178383 or from the original source ‘Yayla 305’, but virulence against “Bt8” coming from PI 178383 is most likely present in dwarf bunt on the island Gotland (Sweden). More research is ongoing about the understanding of Bt8 complex and possible virulence to the genes involved.
Bt9 has been properly mapped confirming that it is a single gene. There are indications of infection in lines having Bt9, but the efficiency of Bt9 is partly climate dependent and it still needs to be confirmed that it is true virulence under field conditions, and not just random infection in off type plants.
Most other genes can be infected by bunt spores from Europe, including Bt1-7, Bt10, Bt13-15 and BtZ. We have not found any virulence to BtP, but little is known about this gene, based on the results from other genes, it may be worth investigating if BtP is really just a single gene or if it could be another example of a combination of other genes.