Abstract

Rhizomania disease, caused by the Beet necrotic yellow vein virus (BNYVV), is considered as one of the major constraints for sugar beet production, worldwide. As a result of the introgression of major resistance genes (Holly, Rz2) in commercially available sugar beet varieties, the virus has endured strong selection pressure since the 90s'. Understanding the virus response and diversity to sugar beet resistance is a key factor for a sustainable management of only few resistance genes. Here we report rhizomania surveys conducted in a rhizomania hot spot, the Pithiviers area (France) during a 4-year period and complementary to the study of Schirmer et al. (2005). The study aimed at evaluating the intra- and inter-field BNYVV diversity in response to different sources of resistance and over the growing season. To follow rhizomania development over the sugar beet growing season, extensive field samplings combined with field assays were performed in this study. The evolution of the BNYVV diversity was assessed at intra- and inter-field levels, with sugar beet cultivars containing different resistance genes (Rz1, Rz1 + Heterodera schachtii resistance and Rz1Rz2). Intra-field diversity was analyzed at the beginning and the end of the growing season of each field. From more than one thousand field samples, the simultaneous presence of the different A, B and P types of BNYVV was confirmed, with 21 variants identified at positions 67–70 of the p25 tetrad. The first variant, AYHR, was found most commonly followed by SYHG. Numerous mixed infections (9.93% of the samples), mostly of B-type with P-type, have also been evidenced. Different tetrads associated with the A- or B-type were also found with a fifth RNA-genome component known to allow more aggressiveness to BNYVV on sugar beet roots. Cultivars with Rz1+Rz2 resistant genes showed few root symptoms even if the BNYVV titre was quite high according to the BNYVV type present. The virus infectious potential in the soil at the end of the growing season with such cultivars was also lower despite a wider diversity at the BNYVV RNA3 sequence level. Rz1+Rz2 cultivars also exhibited a lower presence of Beet soil-borne virus (BSBV), a P. betae-transmitted Pomovirus. Cultivars with Rz1 and nematode (N) resistance genes cultivated in field infected with nematodes showed lower BNYVV titre than those with Rz1 or Rz1+Rz2 cultivars. Overall, the population structure of BNYVV in France is shown to be different from that previously evidenced in different world areas. Implications for long-term management of the resistance to rhizomania is discussed.

Highlights

  • Rhizomania is one of the most challenging diseases of the sugar beet plant because of the difficulty in maintaining sustainable plant resistance sources against the causal virus, the Beet necrotic yellow vein virus (BNYVV), a soil-borne virus transmitted by the plasmodiophorid Polymyxa betae (Biancardi and Tamada, 2016)

  • A total of 1,058 samples were evaluated and 835 were found positive for BNYVV. Amongst these BNYVV-infected samples, 482 isolates were evaluated from individual sugar beet roots (Table 3) and 353 isolates were evaluated from a composite sample made of a mix of sugar beet roots collected from a single zone in the field

  • Amongst these 835 BNYVV positive samples, few mutations resulting in substitution of alanine with valine residue in the tetrad area of the RNA3 (0.65% of the total of 482 isolates from individual sugar beet roots) were detected

Read more

Summary

Introduction

Rhizomania is one of the most challenging diseases of the sugar beet plant because of the difficulty in maintaining sustainable plant resistance sources against the causal virus, the Beet necrotic yellow vein virus (BNYVV), a soil-borne virus transmitted by the plasmodiophorid Polymyxa betae (Biancardi and Tamada, 2016). The virus is associated with an additional RNA5, which is known to enhance both symptom developments in sugar beets and aggressiveness of the virus (Tamada et al, 1996). This RNA codes the protein p26, which contains a transcriptional activation domain (Covelli et al, 2009)

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call