| dc.description.abstract | Senescent sweetening is a storage disorder that typically occurs following medium to
long-term storage of potato tubers in the presence of sprout suppressors at moderate
storage temperatures. It represents a significant issue for the processing industry where
reducing sugar accumulation results in problems of dark fry colour. Furthermore, the
Maillard reaction between reducing sugars and asparagine results in the accumulation of
the potential neurotoxin and carcinogen acrylamide in processed products. At present
almost nothing is known regarding the mechanisms promoting senescent sweetening
which differs from cold-induced sweetening in that it is not reversible by transfer of
tubers to higher temperatures. In the present work we set out to test the hypothesis that
oxidative damage caused during long term storage is linked to senescent sweetening. A
marked difference in storage induced reducing sugar accumulation was observed
between a sweetening resistant and a sweetening sensitive cultivar. However, markers
of oxidative damage and activities of antioxidant enzymes did not exhibit any specific
correlation with reducing sugar accumulation indicating that oxidative damage and
senescent sweetening may not be linked. To identify the underlying biochemical causes
of sugar accumulation GC/MS was used to quantify a range of primary metabolites in
sweetened and unsweetened tubers. Few differences were observed in metabolite
profiles however, labelling with [
13C] glucose indicated a greater capacity for sucrose
synthesis in the sweetening resistant compared with the sweetening sensitive cultivar. In
addition, differences in specific activity of carbohydrate metabolism enzymes as well as
microarray data suggest starch re-synthesis and alternative metabolic sinks for carbon as
potential traits linked to sweetening resistance. Moreover, we identified GPT2 as a
potential candidate gene associated with the accumulation of sugars during long-term
storage. These findings will lead to a better understanding of the mechanisms, processes
and genes involved in senescent sweetening and will provide insights into improved
storage management in the short-term and the development of senescent sweetening
resistant cultivars in the longer term. | en |
