Progress towards the understanding and control of sugar beet rhizomania disease

Abstract

Rhizomania is a soil-borne disease that occurs throughout the major sugar beet growing regions of the world, causing severe yield losses in the absence of effective control measures. It is caused by Beet necrotic yellow vein virus (BNYVV), which is transmitted by the obligate root-infecting parasite Polymyxa betae. BNYVV has a multipartite RNA genome with all natural isolates containing four RNA species, although some isolates have a fifth RNA. The larger RNA1 and RNA2 contain the housekeeping genes of the virus and are always required for infection, whereas the smaller RNAs are involved in pathogenicity and vector transmission. RNA5-containing isolates are restricted to Asia and some parts of Europe, and these isolates tend to be more aggressive. With no acceptable pesticides available to restrict the vector, the control of rhizomania is now achieved almost exclusively through the use of resistant cultivars. A single dominant resistance gene, Rz1, has been used to manage the disease worldwide in recent years, although this gene confers only partial resistance. More recently, new variants of BNYVV have evolved (both with and without RNA5) that are able to cause significant yield penalties on resistant cultivars. These isolates are not yet widespread, but their appearance has resulted in accelerated searches for new sources of resistance to both the virus and the vector. Combined virus and vector resistance, achieved either by conventional or transgenic breeding, offers the sugar beet industry a new approach in its continuing struggle against rhizomania.

Figure 1

Symptoms of Beet necrotic yellow vein virus (BNYVV) on sugar beet, and Polymyxa betae, the plasmodiophorid vector of rhizomania. (a) Rhizomania‐infected patch (indicated by arrow) typical of BNYVV infection in the field. (b) Classical ‘root madness’ symptoms in BNYVV‐infected sugar beet. (c) A virus‐free root. (d) Necrotic yellow vein symptom only observed under optimal disease conditions. (e) Long‐lived resting spores in sugar beet roots viewed under the light microscope. (f) Multilobed zoosporangium (solid arrows) inside host root cells after secondary zoospore release. Exit tubes where zoospores were released are visible (dotted arrows). The P. betae zoosporangium had been fixed in situ in 10% formaldehyde, pH 7.2, for at least 3 years prior to being visualised and photographed under the microscope with ultraviolet illumination.

Figure 2

Beet necrotic yellow vein virus (BNYVV), the cause of rhizomania. (a) Electron micrograph of BNYVV particles [courtesy Descriptions of Plant Viruses No. 391 (Tamada, 2002), http://www.dpvweb.net/dpv/showdpv.php?dpvno=391, with permission from the Association of Applied Biologists). Scale bar represents 100 nm. (b) BNYVV genome map showing multipartite organisation of viral proteins. CP, coat protein; HEL, helicase; MTR, methyltransferase; POL, polymerase; PRO, protease; RT, read‐through protein.

Figure 3

Interaction between Beet necrotic yellow vein virus (BNYVV) and Beet mild yellowing polerovirus (BMYV). Plants susceptible to rhizomania and infected with both BNYVV and BMYV are severely diseased, often leading to plant loss (left), whereas plants with partial resistance to BNYVV (conferred by Rz1; right) do not appear as affected. Plants were sown in a UK rhizomania‐infested field in April 2003 and inoculated with BMYV viruliferous aphids in June 2003. Photograph was taken in October 2003.