The most important rhizomania-resistance gene in sugar beet is the Rz1 gene from the Holly Sugar Company in California, the source widely used to breed partially resistant varieties. Other important gene sources are WB41 and WB42, which both originate from Beta vulgaris subsp. maritima collected in Denmark, and which have been reported to be similar. The major resistance gene in WB42 is known as Rz2. We studied the resistance in WB41 and used markers to map the major resistance gene in this source, which we call Rz3. It was identified on chromosome III. This is the chromosome that Rz1 and Rz2 have been mapped to. Data from greenhouse tests and ELISA showed that Rz3 had incomplete penetrance, with heterozygotes varying widely in resistance levels. The involvement of additional minor genes in the strong resistance of the original WB41 source cannot be excluded.

Nucleotide sequence analyses revealed that the genomes of the various European types of Beet necrotic yellow vein virus (BNYVV), i.e. the A, B and P types, are strongly conserved. Almost identical sequences were found, for instance, for A types originating from The Netherlands, Italy and former Yugoslavia; these sequences were also almost identical to those determined c. 15 years ago by Bouzoubaa et al. (1985; 1986 and 1987). This sequence stability of BNYVV types is in contrast to a pronounced sequence variability observed with Beet soil-borne pomovirus, another Polymyxa-transmitted sugar beet virus with rod-shaped particles. Sequences of RNA 1, 2 and 4 of BNYVV sources from Kazakhstan were almost identical to those of the P type of BNYVV which so far had been found only in a small area around the French town of Pithiviers. RNA 5, which in Europe is found also only in the Pithiviers area, was detected in the bait plants grown in two out of three soil samples from different fields in Kazakhstan. It closely resembled RNA 5 from the Pithiviers area, but was very different from RNA 5 from various East Asian BNYVV sources.

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Rhizomania of sugar beet, caused by Beet necrotic yellow vein virus (BNYVV), is characterized by excessive lateral root (LR) formation leading to dramatic reduction of taproot weight and massive yield losses. LR formation represents a developmental process tightly controlled by auxin signaling through AUX/IAA-ARF responsive module and LATERAL ORGAN BOUNDARIES DOMAIN (LBD) transcriptional network. Several LBD transcription factors play central roles in auxin-regulated LR development and act upstream of EXPANSINS (EXPs), cell wall (CW)-loosening proteins involved in plant development via disruption of the extracellular matrix for CW relaxation and expansion. Here, we present evidence that BNYVV hijacks these auxin-regulated pathways resulting in formation LR and root hairs (RH). We identified an AUX/IAA protein (BvAUX28) as interacting with P25, a viral virulence factor. Mutational analysis indicated that P25 interacts with domains I and II of BvAUX28. Subcellular localization of co-expressed P25 and BvAUX28 showed that P25 inhibits BvAUX28 nuclear localization. Moreover, root-specific LBDs and EXPs were greatly upregulated during rhizomania development. Based on these data, we present a model in which BNYVV P25 protein mimics action of auxin by removing BvAUX28 transcriptional repressor, leading to activation of LBDs and EXPs. Thus, the evidence highlights two pathways operating in parallel and leading to uncontrolled formation of LRs and RHs, the main manifestation of the rhizomania syndrome.

Rhizomania caused by Beet necrotic yellow vein virus (BNYVV) is one of the most devastating sugar beet diseases. Sugar beet plants engineered to express a 0.4 kb inverted repeat construct based on the BNYVV replicase gene accumulated the transgene mRNA to similar levels in leaves and roots, whereas accumulation of the transgene-homologous siRNA was more pronounced in roots. The roots expressed high levels of resistance to BNYVV transmitted by the vector, Polymyxa betae. Resistance to BNYVV was not decreased following co-infection of the plants with Beet soil borne virus and Beet virus Q that share the same vector with BNYVV. Similarly, co-infection with the aphid-transmitted Beet mild yellowing virus, Beet yellows virus (BYV), or with all of the aforementioned viruses did not affect the resistance to BNYVV, while they accumulated in roots. These viruses are common in most of the sugar beet growing areas in Europe and world wide. However, there was a competitive interaction between BYV and BMYV in sugar beet leaves, as infection with BYV decreased the titres of BMYV. Other interactions between the viruses studied were not observed. The results suggest that the engineered resistance to BNYVV expressed in the sugar beets of this study is efficient in roots and not readily compromised following infection of the plants with heterologous viruses.