Control of rhizomania in sugar beet—A success story made possible by resistance breeding

Abstract The economic success of sugar beet production depends largely on the control of various pathogens and pests. Beet necrotic yellow vein virus (BNYVV) has historically been a major threat to sugar beet growers because of the high yield losses and the fact that the virus is transmitted by a soilborne protist vector that cannot be controlled. Resistance breeding began after the disease was first described in 1959 and led to the identification of two monogenic resistance genes. Rz1 was the first resistance gene to be introduced into all varieties, enabling sugar beet production under high disease pressure. However, the widespread use of a single resistance gene resulted in high selection pressure on the virus population. As a result, resistance‐breaking of Rz1 was first reported in the early 2000s in the United States and later in many other countries. The mechanism of resistance‐breaking is based on mutations in the viral pathogenicity factor P25 and the presence of an additional RNA5 species. The second resistance gene being used in breeding is Rz2 , which is based on a different resistance mechanism and is highly effective at sites where Rz1 has been overcome by the virus. In addition, Rz2 was the first rhizomania resistance gene to be cloned, and the triple gene block I of BNYVV was identified as the corresponding avirulence gene. This article highlights that resistance breeding has been key to the control of rhizomania, but history also shows that re‐emergence of the disease due to resistance‐breaking remains a permanent threat.