Rhizomania – what is to be learned from the fields?

Since the widespread use of rhizomania partially resistant cultivars, bearing the Rz1 gene along with high yield capacities, multiple Rz1 resistance-breaking events have been reported both in the USA and in Europe. A single mutation from alanine to valine in the p25 hypervariable amino acid tetrad was linked with such resistance breaking (Koenig et al., 2009). Although there are difficulties for determining the effect of virus variation along with the role of other soil-borne pathogens, inoculum densities as well as questions regarding a possible genetic erosion of the resistance enhancer genes, understanding the dynamic of the emergence of resistance breaking isolates as well as evaluating their fitness and ability to spread is of the uttermost importance. Between the 2007 and 2010 sugar beet growing season, rhizomania affected fields have been surveyed in France, in the Pithiviers region. More than 600 samples were collected both in disease and non-disease expressing areas. Samples were tested for the presence of BNYVV by RT-PCR targeting mostly the p14, p25 and p26 genes. The multiplex RT-PCR (Meunier et al., 2003) was also used to detect the rhizomania-associated pomoviruses Beet soil-borne virus and Beet virus Q, together with their vector Polymyxa betae. The presence of the Beet black scorch virus was also checked in selected samples. In the frame of a long-term study of rhizomania, field trials were set up in 2009 and 2010 to follow up the evolution of the disease within a single sugar beet growing seasons. The results confirmed the large presence of BNYVV type B and P in the surveyed areas, with mixed infections in single beets. Conversely to reports from other areas, the canonical p25 A-V mutation was almost not found while the AYHR and SYHG tetrads were frequently detected. The results stressed also the need to set up convergent survey methods to facilitate the exchange of data on viral resistance-breaking isolates.