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. During storage, 8656 genes, or 34% of all expressed genes, and 225 metabolites, equivalent to 59% of detected metabolites, were altered in expression or concentration, indicating extensive transcriptional and metabolic changes in stored roots. These genes and metabolites contributed to a wide range of cellular and molecular functions, with carbohydrate metabolism being the function to which the greatest number of genes and metabolites classified. Because respiration has a central role in postharvest metabolism and is largely responsible for sucrose loss in sugarbeet roots, genes and metabolites involved in and correlated to respiration were identified. Seventy-five genes participating in respiration were differentially expressed during storage, including two bidirectional sugar transporter SWEET17 genes that highly correlated with respiration rate. Weighted gene co-expression network analysis identified 1896 additional genes that positively correlated with respiration rate and predicted a pyruvate kinase gene to be a central regulator or biomarker for respiration rate. Overall, these results reveal the extensive and diverse physiological and metabolic changes that occur in stored sugarbeet roots and identify genes with potential roles as regulators or biomarkers for respiratory sucrose loss.

Sugar Beet Root Storage Properties Are Unaffected by Cercospora Leaf Spot.

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.

Methyl jasmonate effects on sugarbeet root responses to postharvest dehydration.

BACKGROUND: Sugarbeet (Beta vulgaris 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. Research was conducted to determine whether jasmonate treatment could mitigate physiological responses to dehydration in postharvest sugarbeet roots. METHODS: Freshly harvested sugarbeet roots were treated with 10 µM methyl jasmonate (MeJA) or water and stored under dehydrating and non-dehydrating storage conditions. Changes in fresh weight, respiration rate, wound healing, leaf regrowth, and proline metabolism of treated roots were investigated throughout eight weeks in storage. RESULTS: Dehydrating storage conditions increased root weight loss, respiration rate, and proline accumulation and prevented leaf regrowth from the root crown. Under dehydrating conditions, MeJA treatment reduced root respiration rate, but only in severely dehydrated roots. MeJA treatment also hastened wound-healing, but only in the late stages of barrier formation. MeJA treatment did not impact root weight loss or proline accumulation under dehydrating conditions or leaf regrowth under non-dehydrating conditions. Both dehydration and MeJA treatment affected expression of genes involved in proline metabolism. In dehydrated roots, proline dehydrogenase expression declined 340-fold, suggesting that dehydration-induced proline accumulation was governed by reducing proline degradation. MeJA treatment altered proline biosynthetic and catabolic gene expression, with greatest effect in non-dehydrated roots. Overall, MeJA treatment alleviated physiological manifestations of dehydration stress in stored roots, although the beneficial effects were small. Postharvest jasmonate applications, therefore, are unlikely to significantly reduce dehydration-related storage losses in sugarbeet roots.

Colocalization of sucrose synthase expression and sucrose storage in the sugarbeet taproot indicates a potential role for sucrose catabolism in sucrose accumulation.

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.