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.

Inhibitors of tri- and tetra- polyamine oxidation, but not diamine oxidation, impair the initial stages of wound-induced suberization.

The mechanisms regulating, and modulating potato wound-healing processes are of great importance in reducing tuber infections, reducing shrinkage and maintaining quality and nutritional value for growers and consumers. Wound-induced changes in tuber polyamine metabolism have been linked to the modulation of wound healing (WH) and in possibly providing the crucial amount of H2O2 required for suberization processes. In this investigation we determined the effect of inhibition of specific steps within the pathway of polyamine metabolism on polyamine content and the initial accumulation of suberin polyphenolics (SPP) during WH. The accumulation of SPP represents a critical part of the beginning or inchoate phase of tuber WH during closing-layer formation because it serves as a barrier to bacterial infection and is a requisite for the accumulation of suberin polyaliphatics which provide the barrier to fungal infection. Results showed that the inhibitor treatments that caused changes in polyamine content generally did not influence wound-induced accumulation of SPP. Such lack of correlation was found for inhibitors involved in metabolism and oxidation of putrescine (arginine decarboxylase, ornithine decarboxylase, and diamine oxidase). However, accumulation of SPP was dramatically reduced by treatment with guazatine, a potent inhibitor of polyamine oxidase (PAO), and methylglyoxal-bis(guanylhydrazone), a putative inhibitor of S-adenosylmethione decarboxylase which may also cross-react to inhibit PAO. The mode of action of these inhibitors is presumed to be blockage of essential H2O2 production within the WH cell wall. These results are of great importance in understanding the mechanisms modulating WH and ultimately controlling related infections and associated postharvest losses.

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.