Abstract

Rhizomania is one of the most destructive sugar beet diseases. It is caused by Beet necrotic yellow vein virus (BNYVV) vectored by the soilborne protoctist Polymyxa betae Keskin. The studies in this thesis evaluated natural and transgenic resistances to rhizomania in sugar beets. Also the genetic variability in the coat protein genes of BNYVV, Beet soil-borne virus, Beet virus Q and Beet soil-borne mosaic virus isolates was studied. Several natural sources of resistance to BNYVV are known, such as the "Holly" source with resistance gene Rz1, WB42 carrying Rz2, and WB41. We mapped the major gene called Rz3 in WB41 to a locus on chromosome 3. In hybrids with combined resistance of Rz1 and Rz3, the resistance level to BNYVV was improved as compared to plants carrying Rz1 only. Transgenic sugar beets resistant to BNYVV were produced. The resistance was based on RNA silencing. The level of resistance to BNYVV in the transgenic plants was compared to the natural sources of resistance in greenhouse experiments and in the field and found to be superior to the resistance conferred by Rz1. When plants were grown in soil containing highly virulent strains of BNYVV, the transgenic plants contained significantly less BNYVV than all tested hybrids carrying the natural resistance genes Rz1, Rz2 and Rz3. The transgenic resistance to BNYVV was durable in plants infected with heterologous viruses, such as Beet yellows virus (BYV) and Beet mild yellowing virus (BMYV) that might suppress gene silencing. It is concluded that resistance to BNYVV can be improved by combining different natural resistance genes, but the transgenic sugar beet plants, produced in this study, expressed the strongest resistance to BNYVV observed so far.