The development of sugar beet as an economically important field crop coincided with our increased understanding of modern genetic principles. It was developed in the late 1700s from white fodder beet; therefore, the genetic base of sugar beet is thought to be narrower than many open-pollinated crops. The wild sea beet is the progenitor of all domesticated beet and cross compatible with cultivated beet (domestic and cultivated are given subspecies level in the same species). The breeding system of sugar beet is complex and the crop is biennial, which lengthens the generation time to almost 1 year. A geneticcytoplasmic male sterility (CMS) system is utilized for commercial hybrid production. Early breeding objectives were to improve the concentration and extractability of sucrose and little emphasis was placed on host-plant resistance to insect, nematode, and disease pests. As production areas expanded, these pests limited production, sometimes severely. The first systematic L. Panella (

Rhizomania is an important virus disease of sugar beet and is caused by Beet necrotic yellow vein virus (BNYVV). During 2002-03, several sugar beet fields with cultivars partially resistant to BNYVV grown in the Imperial Valley of California were observed with severe rhizomania symptoms, suggesting that resistance conditioned by Rz1 had been compromised. Soil testing with sugar beet baiting plants followed by enzyme-linked immunosorbent assay (ELISA) was used to diagnose virus infection. Resistant varieties grown in BNYVV-infested soil from Salinas, CA, were ELISA-negative. In contrast, when grown in BNYVV-infested soil collected from the Imperial Valley, CA, all resistant varieties became infected and tested positive by ELISA. Based on host reaction, eight distinct BNYVV isolates have been identified from Imperial Valley soil (IV-BNYVV) by single local lesion isolation. Reverse transcription-polymerase chain reaction (RT-PCR) assays showed that the eight IV-BNYVV isolates did not contain RNA-5. Singlestrand conformation polymorphism banding patterns for the IV-BNYVV isolates were identical to A-type and different from P-type. Sequence alignments of PCR products from BNYVV RNA-1 near the 3′ end of IV-BNYVV isolates revealed that both IV-BNYVV and Salinas BNYVV isolates were similar to A-type and different from B-type. Our results suggest that the resistancebreaking BNYVV isolates from Imperial Valley likely evolved from existing A-type isolates.

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FC220 (Reg. No. GP‐263, PI 651015) and FC221 (Reg. No. GP‐264, PI 651016) sugarbeet (Beta vulgaris L.) germplasm were released from 05‐FC1030‐15 (Sp) and 05‐FC1030‐16 (Sp) seed lots, respectively, and tested under those designations and as 03‐FC1030‐15 and 03‐FC1030‐16, respectively. They were developed by the USDA–ARS, at Fort Collins, CO, and at Salinas, CA, in cooperation with the Beet Sugar Development Foundation, Denver, CO. FC220 and FC221 are multigerm sugarbeet germplasm in fertile cytoplasm, segregating for self‐fertility and hypocotyl color. Both have resistance to root‐rotting strains (AG‐2‐2) of Rhizoctonia solani Kühn and are segregating for the Rz1 gene, which confers resistance to some strains of Beet necrotic yellow vein virus, the causal agent of rhizomania. These germplasm have moderate resistance to Aphanomyces cochlioides Drechs., which causes aphanomyces root rot (aphanomyces black root). FC221 is moderately resistant to curly top caused by Beet severe curly top virus. FC220 is resistant to the sugarbeet root aphid (Pemphigus sp.). Both germplasm are moderately susceptible to cercospora leaf spot, caused by Cercospora beticola Sacc. FC220 and FC221 have favorable yield characteristics when evaluated as lines or in experimental hybrids under rhizomania conditions at Salinas, CA. Under these conditions, FC220, as a line and in hybrid combinations, had a slight to significantly higher sucrose concentration than FC221.

Beet necrotic yellow vein virus (BNYVV) is the causal agent of rhizomania in sugar beet (Beta vulgaris). The virus is transmitted by the plasmodiophorid Polymyxa betae. The disease is controlled primarily by the use of partially resistant cultivars. During 2003 and 2004 in the Imperial Valley of California, partially resistant sugar beet cultivars with Rz1 allele seemed to be compromised. Field trials at Salinas, CA have confirmed that Rz1 has been defeated by resistance-breaking isolates. Distinct BNYVV isolates have been identified from these plants. Rhizomania-infested sugar beet fields throughout the United States were surveyed in 2004–05. Soil surveys indicated that the resistance-breaking isolates not only existed in the Imperial Valley and San Joaquin Valley of California but also in Colorado, Idaho, Minnesota, Nebraska, and Oregon. Of the soil samples tested by baited plant technique, 92.5% produced infection with BNYVV in ‘Beta 6600’ (rz1rz1rz1), 77.5% in ‘Beta 4430R’ (Rz1rz1), 45.0% in ‘Beta G017R’ (Rz2rz2), and 15.0% in ‘KWS Angelina’ (Rz1rz1+Rz2rz2). Analyses of the deduced amino acid sequence of coat protein and P-25 protein of resistance-breaking BNYVV isolates revealed the high percentage of identity with non-resistance-breaking BNYVV isolates (99.9 and >98.0%, respectively). The variable amino acids in P-25 proteins were located at the residues of 67 and 68. In the United States, the two amino acids found in the non-resistance-breaking isolates were conserved (AC). The resistance-breaking isolates were variable including, AF, AL, SY, VC, VL, and AC. The change of these two amino acids cannot be depended upon to differentiate resistance-breaking and non-resistance-breaking isolates of BNYVV.