Chromosome localisation of genes for resistance to Heterodera schachtii, Cercospora beticola and Polymyxa betae using sets of Beta procumbens and B. patellaris derived monosomic additions in B. vulgaris

Abstract

Beet cyst nematodes (BCN, Heterodera schachtii), Cercospora beticola, and rhizomania, caused by the beet necrotic yellow vein virus (BNYVV) and vectored by the soil-borne fungus Polymyxa betae, are the most serious diseases of sugar beet ( Beta vulgaris subsp. vulgaris). The wild Beta species of section Procumbentes are known to be completely resistant to H. schachtii, C. beticola and P. betae. Alien monosomic additions (2n=19), plants of cultivated beet (2n=18) carrying different individual chromosomes of B. procumbens (2n=18) or B. patellaris (2n=36), were tested in greenhouse experiments for resistance to these pathogens. Gene(s) conferring full resistance to the beet cyst nematode in B. patellaris are located on chromosome 1.1, and the other tested chromosomes of B. patellaris are not involved in the expression of resistance. Artificial inoculation under greenhouse conditions, with in vitro produced inoculum of C. beticola and spot-percentage rating of the disease intensity, showed that the high level of resistance that was observed in the wild species B. procumbens and B. patellaris was not found in any of the monosomic additions tested. It was suggested that genes on various chromosomes of the wild species are needed to express full resistance, and that the chromosomes of group 7 of B. patellaris and chromosome 7 of B. procumbens have the largest effect. The greenhouse tests for resistance to P. betae in B. patellaris derived monosomic additions showed that the addition families of group 4.1 have a strong partial resistance, while the addition families of group 8.1 appeared to be completely resistant to the pathogen. Resistance to P. betae in the two wild species as well as in the two resistant addition types did not exclude infection with BNYVV, but resulted in a considerable reduction of the virus concentration. It was concluded that resistance to the vector would complement virus resistance, and may provide a more effective and durable control of rhizomania.