Transcriptomic and metabolomic changes in postharvest sugarbeet roots reveal widespread metabolic changes in storage and identify genes potentially responsible for respiratory sucrose loss.

Endogenous metabolism is primarily responsible for losses in sucrose content and processing quality in postharvest sugarbeet roots. The genes responsible for this metabolism and the transcriptional changes that regulate it, however, are largely unknown. To identify genes and metabolic pathways that participate in postharvest sugarbeet root metabolism and the transcriptional changes that contribute to their regulation, transcriptomic and metabolomic profiles were generated for sugarbeet roots at harvest and after 12, 40 and 120 d storage at 5 and 12°C and gene expression and metabolite concentration changes related to storage duration or temperature were identified.

Resistance to QoI and DMI Fungicides Does Not Reduce Virulence of Isolates in North Central United States.

Cercospora leaf spot (CLS) is a destructive disease limiting sugar beet production and is managed using resistant cultivars, crop rotation, and timely applications of effective fungicides. Since 2016, its causal agent, , has been reported to be resistant to quinone outside inhibitors (QoIs) and to have reduced sensitive to demethylation inhibitors (DMIs) in sugar beet growing areas in North Dakota and Minnesota. Isolates of resistant to QoIs, DMIs, and both QoIs and DMIs were collected from fields in Foxhome, Minnesota, in 2017.

Wounding rapidly alters transcription factor expression, hormonal signaling, and phenolic compound metabolism in harvested sugarbeet roots.

Injuries sustained by sugarbeet ( L.) roots during harvest and postharvest operations seriously reduce the yield of white sugar produced from stored roots. Although wound healing is critically important to reduce losses, knowledge of these processes is limited for this crop as well as for roots in other species.

Methyl jasmonate effects on sugarbeet root responses to postharvest dehydration.

Background: Sugarbeet ( L.) roots are stored under conditions that cause roots to dehydrate, which increases postharvest losses. Although exogenous jasmonate applications can reduce drought stress in intact plants, their ability to alleviate the effects of dehydration in postharvest sugarbeet roots or other stored plant products is unknown.

Age-Dependent Resistance to in Sugar Beet.

Rhizoctonia crown and root rot of sugar beet ( L.), caused by , continues to be one of the important concerns for the beet industry in Minnesota and North Dakota. Use of resistant cultivars is an important strategy in the management of in combination with seed treatment and timely fungicide application during the growing season.

Prevalence and Distribution of Beet Necrotic Yellow Vein Virus Strains in North Dakota and Minnesota.

Beet necrotic yellow vein virus (BNYVV) is the causal agent of rhizomania, a disease of global importance to the sugar beet industry. The most widely implemented resistance gene to rhizomania to date is , but resistance has been circumvented by resistance-breaking (RB) isolates worldwide. In an effort to gain greater understanding of the distribution of BNYVV and the nature of RB isolates in Minnesota and eastern North Dakota, sugar beet plants were grown in 594 soil samples obtained from production fields and subsequently were analyzed for the presence of BNYVV as well as coding variability in the viral P25 gene, the gene previously implicated in the RB pathotype.

Sensitivity of Rhizoctonia solani AG-2-2 from Sugar Beet to Fungicides.

Rhizoctonia damping-off and crown and root rot caused by Rhizoctonia solani are major diseases of sugar beet (Beta vulgaris L.) worldwide, and growers in the United States rely on fungicides for disease management. Sensitivity of R.

Characterization of Fusarium secorum, a new species causing Fusarium yellowing decline of sugar beet in north central USA.

This study characterized a novel sugar beet (Beta vulgaris L.) pathogen from the Red River Valley in north central USA, which was formally named Fusarium secorum. Molecular phylogenetic analyses of three loci (translation elongation factor1α, calmodulin, mitochondrial small subunit) and phenotypic data strongly supported the inclusion of F.

Efficacy of Variable Tetraconazole Rates Against Cercospora beticola Isolates with Differing In Vitro Sensitivities to DMI Fungicides.

Cercospora leaf spot (CLS) of sugar beet is caused by the fungus Cercospora beticola. CLS management practices include the application of the sterol demethylation inhibitor (DMI) fungicides tetraconazole, difenoconazole, and prothioconazole. Evaluating resistance to DMIs is a major focus for CLS fungicide resistance management.

Comparative Pathogenicity and Virulence of Fusarium Species on Sugar Beet.

In all, 98 isolates of three Fusarium spp. (18 Fusarium oxysporum, 30 F. graminearum, and 50 Fusarium sp.

Temperature, moisture, and fungicide effects in managing Rhizoctonia root and crown rot of sugar beet.

Rhizoctonia solani AG-2-2 is the causal agent of Rhizoctonia root and crown rot in sugar beet; however, recent increases in disease incidence and severity were grounds to reevaluate this pathosystem. To assess the capacity at which other anastomosis groups (AGs) are able to infect sugar beet, 15 AGs and intraspecific groups (ISGs) were tested for pathogenicity on resistant ('FC708 CMS') and susceptible ('Monohikari') seedlings and 10-week-old plants. Several AGs and ISGs were pathogenic on seedlings regardless of host resistance but only AG-2-2 IIIB and AG-2-2 IV caused significant disease on 10-week-old plants.