CHROMOSOME LOCALIZATION OF GENES FOR RESISTANCE TO HETERODERA-SCHACHTII, CERCOSPORA-BETICOLA AND POLYMYXA-BETAE USING SETS OF BETA-PROCUMBENS AND BETA-PATELLARIS DERIVED MONOSOMIC ADDITIONS IN BETA-VULGARIS

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 ser ious diseases of sugar beet (Beta vulgaris subsp. vulgaris). The wild Beta species of section Procumbentes are known to be completely resist ant to H. schachtii, C. beticola and P. betae. Alien monosomic additio ns (2n=19), plants of cultivated beet (2n=18) carrying different indiv idual chromosomes of B. procumbens (2n=18) or B. patellaris (2n=36), w ere tested in greenhouse experiments for resistance to these pathogens . Gens(s) conferring full resistance to the beer cyst nematode in B. p atellaris are located on chromosome 1.1, and the other tested chromoso mes of B. patellar-is are not involved in the expression of resistance . Artificial inoculation under greenhouse conditions, with in vitro pr oduced inoculum of C. beticola and spot-percentage rating of the disea se intensity, showed that the high level of resistance that was observ ed in the wild species B. procumbens and B. patellaris was not found i n any of the monosomic additions tested. It was suggested that genes o n various chromosomes of the wild species are needed to express full r esistance, and that the chromosomes of group 7 of B. patellaris and ch romosome 7 of B. procumbens have the largest effect. The greenhouse te sts for resistance to P. betae in B. patellaris derived monosomic addi tions showed that the addition families of group 4.1 have a strong par tial 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 n ot exclude infection with BNYVV, but resulted in a considerable reduct ion of the virus concentration. It was concluded that resistance to th e vector would complement virus resistance, and may provide a more eff ective and durable control of rhizomania.