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Storage rots are a significant cause of postharvest losses for the sugar beet crop, however, intrinsic physiological and genetic factors that determine the susceptibility of roots to pathogen infection and disease development are unknown. Research, therefore, was carried out to evaluate the disease development in sugar beet roots caused by two common storage pathogens as a function of storage duration and storage temperature, and to identify changes in the expression of defense genes that may be influencing the root susceptibility to disease. To evaluate root susceptibility to disease, freshly harvested roots were inoculated with Botrytis cinerea or Penicillium vulpinum on the day of harvest or after 12, 40, or 120 d storage at 5 or 12 °C and the weight of rotted tissue present in the roots after incubation for 35 d after inoculation were determined. Disease susceptibility and progression to B. cinerea and P. vulpinum increased with storage duration with elevations in susceptibility occurring more rapidly to B. cinerea than P. vulpinum. Also, B. cinerea was more aggressive than P. vulpinum and caused greater rotting and tissue damage in postharvest sugar beet roots. Storage temperature had minimal effect on root susceptibility to these rot-causing pathogens. Changes in defense gene expression were determined by sequencing mRNA isolated from uninoculated roots that were similarly stored for 12, 40 or 120 d at 5 or 12 °C. As susceptibility to rot increased during storage, concurrent changes in defense-related gene expression were identified, including the differential expression of 425 pathogen receptor and 275 phytohormone signal transduction pathway-related genes. Furthermore, plant resistance and hormonal signaling genes that were significantly altered in expression coincident with the change in root susceptibility to storage rots were identified. Further investigation into the function of these genes may ultimately elucidate methods by which storage rot resistance in sugar beet roots may be improved in the future., (© 2024. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.)

Cultivated beet (Beta vulgaris L. ssp. vulgaris) originated from sea beet (B. vulgaris ssp. maritima (L.) Arcang), a wild beet species widely distributed along the coasts of the Mediterranean Sea and Atlantic Ocean, as well as northern Africa. Understanding the evolution of sea beet will facilitate its efficient use in sugarbeet improvement. We used SNPs (single nucleotide polymorphisms) covering the whole genome to analyze 599 sea beet accessions collected from the north Atlantic Ocean and Mediterranean Sea coasts. All B. maritima accessions can be grouped into eight clusters with each corresponding to a specific geographic region. Clusters 2, 3 and 4 with accessions mainly collected from Mediterranean coasts are genetically close to each other as well as to Cluster 6 that contained mainly cultivated beet. Other clusters were relatively distinct from cultivated beets with Clusters 1 and 5 containing accessions from north Atlantic Ocean coasts, Clusters 7 and Cluster 8 mainly have accessions from northern Egypt and southern Europe, and northwest Morocco, respectively. Distribution of B. maritima subpopulations aligns well with the direction of marine currents that was considered a main dynamic force in spreading B. maritima during evolution. Estimation of genetic diversity indices supported the formation of B. maritima subpopulations due to local genetic drift, historic migration, and limited gene flow. Our results indicated that B. maritima originated from southern Europe and then spread to other regions through marine currents to form subpopulations. This research provides vital information for conserving, collecting, and utilizing wild sea beet to sustain sugarbeet improvement., Competing Interests: The authors have declared that no competing interests exist., (Copyright: This is an open access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.)

Cercospora leaf spot (CLS; causal agent Cercospora beticola Sacc.) is endemic in many sugar beet production regions due to the widespread distribution of C. beticola and the inability of current management practices to provide complete control of the disease. Roots harvested from plants with CLS, therefore, are inevitably incorporated into sugar beet root storage piles, even though the effects of CLS on root storage properties are largely unknown. Research was conducted to determine the effects of CLS on storage properties including root respiration rate, sucrose loss, invert sugar accumulation, loss in recoverable sucrose yield, and changes in sucrose loss to molasses with respect to CLS disease severity and storage duration. Roots were obtained from plants with four levels of CLS severity in each of three production years, stored at 5°C and 95% relative humidity for up to 120 days, and evaluated for storage characteristics after 30, 90, and 120 days storage. No significant or repeatable effects of CLS on root respiration rate, sucrose loss, invert sugar accumulation, loss in recoverable sucrose yield, or change in sucrose loss to molasses were detected after 30, 90, or 120 days storage regardless of the severity of CLS disease symptoms. Therefore, no evidence was found that CLS accelerates sugar beet storage losses, and it is concluded that roots harvested from plants with CLS can be stored without additional or specialized precaution, regardless of CLS symptom severity., Competing Interests: The author(s) declare no conflict of interest.

Sucrose metabolism is believed to have a central role in promoting sink strength and sucrose storage in the sugarbeet taproot. How sucrose accumulation is increased by sucrose-degrading enzymes, however, is a paradox. To elucidate roles for sucrose-degrading activities in sucrose accumulation, relationships between the intercellular location of sucrose-catabolizing enzymes and sites of sucrose accumulation were determined in the sugarbeet taproot. Sucrose storage was evident in parenchyma cells of the outer cortex, rays, and rings of parenchyma tissue, but was absent in phloem, the vascular cambium, cells surrounding these tissues, or cells surrounding xylem. Sucrose synthase, which was primarily responsible for sucrose catabolism throughout the taproot, was expressed in similar cell and tissue types to those accumulating sucrose. Colocalization of sucrose synthase with sucrose accumulation, as well as sucrose synthase localization near the tonoplast, suggests a role for the enzyme in generating metabolic energy to fuel sucrose sequestration in the vacuole. Localization near the plasma membrane also suggests a role for sucrose synthase in supplying substrates for cell wall biosynthesis. By utilizing sucrose for ATP or cell wall biosynthesis, sucrose synthase likely maintains the source-to-sink sucrose gradient that drives sucrose transport into the root, thereby promoting sugarbeet root sink strength., (Published by Elsevier GmbH.)

Injury to plant products by harvest and postharvest operations induces respiration rate and increases the demand for respiratory substrates. Alterations in primary carbon metabolism are likely to support the elevated demand for respiratory substrates, although the nature of these alterations is unknown. To gain insight into the metabolic changes that occur to provide substrates for wound-induced increases in respiration, changes in the concentrations of compounds that are substrates, intermediates or cofactors in the respiratory pathway were determined in sugarbeet (Beta vulgaris L.) roots in the 4days following injury. Both wounded and unwounded tissues of wounded roots were analyzed to provide information about localized and systemic changes that occur after wounding. In wounded tissue, respiration increased an average of 186%, fructose, glucose 6-phosphate, ADP and UDP concentrations increased, and fructose 1,6-bisphosphate, triose phosphate, citrate, isocitrate, succinate, ATP, UTP and NAD(+) concentrations decreased. In the non-wounded tissue of wounded roots, respiration rate increased an average of 21%, glucose 6-phosphate, fructose 6-phosphate, glucose 1-phosphate and ADP concentrations increased, and isocitrate, UTP, NAD(+), NADP(+), and NADPH concentrations declined. Changes in respiration rate and metabolite concentrations indicated that localized and systemic changes in primary carbon metabolism occurred in response to injury. In wounded tissue, metabolite concentration changes suggested that activities of the early glycolytic enzymes, fructokinase, phosphofructokinase, phosphoglucose isomerase, and phosphoglucomutase were limiting carbon flow through glycolysis. These restrictions in the respiratory pathway, however, were likely overcome by use of metabolic bypasses that allowed carbon compounds to enter the pathway at glycolytic and tricarboxylic acid (TCA) cycle downstream locations. In non-wounded tissue of wounded roots, metabolic concentration changes suggested that glycolysis and the TCA cycle were generally capable of supporting the small systemic elevation in respiration rate. Although the mechanism by which respiration is regulated in wounded sugarbeet roots is unknown, localized and systemic elevations in respiration were positively associated with one or more indicators of cellular redox status., (Published by Elsevier Ltd.)