Metabolomic analysis for identification of biological functions associated with infection by and resistance to beet necrotic yellow vein virus in sugarbeet

Background: Rhizomania, caused by Beet necrotic yellow vein virus (BNYVV), is one of the most economically important diseases affecting sugarbeet, and is widely distributed in most sugarbeet growing areas of the world. Fields remain infested with BNYVV indefinitely in P. betae cystosori that can remain dormant up to 25 years. Rotation to nonhost crops or lengthening rotations is ineffective at reducing disease incidence, and to date the only viable means of control has been natural host-plant resistance. The Rz1 source of resistance was introduced widely to commercial sugarbeet in the 1990s, and for several years has effectively controlled the virus. However, this resistance does not completely eliminate virus replication, but rather suppresses it to low levels compared to what one would find in a susceptible variety. The low level of replication in Rz1 sugarbeet, has led to the emergence of new variants that overcome or “break” the resistance, since the main forms of the virus that can replicate in Rz1 varieties are those few variants that have the ability to replicate in the presence of Rz1. In the early 2000s an Rz1 resistance-breaking variant emerged in the Imperial Valley of California (Liu et al., 2005; Rush et al., 2006), and subsequent studies identified the presence of limited numbers of isolated resistance-breaking (RB) variants from most American production regions (Liu and Lewellen, 2007). RB isolates are increasingly affecting production throughout the US industry, and this can be expected to continue.