Is the onset of senescence in leaf cells of intact plants due to low or high sugar levels?

• Published in: Journal of Experimental Botany 2008-05, Vol.59 (8), p.1963-1972
• Main Author: van Doorn, Wouter G.
• Format: Article
• Language: English
• Subjects: beta-Fructofuranosidase - metabolism; Biological and medical sciences; Carbohydrate Metabolism; Carbon Dioxide - metabolism; Cell Wall - enzymology; Cell walls; Cellular Senescence; Chloroplast; Chloroplasts; Chloroplasts - genetics; Chloroplasts - physiology; cytokinin; Cytokinins; fructose; Fundamental and applied biological sciences. Psychology; Gene expression regulation; Genes; glucose; hexokinase; Hexokinase - metabolism; Leaves; nitrogen partitioning; photosynthesis; Plant cells; Plant Leaves - genetics; Plant Leaves - physiology; Plant Physiological Phenomena; Plant physiology and development; Plants; Plants - genetics; programmed cell death; Review Paper; senescence; Senescence and abscission; Signal Transduction; sucrose; Sugars; Vegetative apparatus, growth and morphogenesis. Senescence; yellowing
• ISSN: 0022-0957; 1460-2431
• DOI: 10.1093/jxb/ern076

This review examines the hypotheses that developmental programmed cell death in leaves is mediated (i) by sugar starvation in the leaf cells or (ii) by sugar accumulation in these cells. Experimental evidence for both hypotheses is critically discussed and found to be lacking. For example, some papers show that sugars prevent senescence of cut leaves placed in darkness, and prevent low sugar levels in the leaves. In these tests, the sugars seem to replace photosynthesis, hence the results have little relevance to leaf senescence in intact plants in the light. Low nitrogen nutrition and high light results in earlier senescence than the low nitrogen treatment alone. This is accompanied by high sugar levels in the leaves. The results have led to the idea that accumulation of sugars is the cause of the additional effect, or more generally, that sugar accumulation is always the direct cause of leaf senescence. Results from over-expressing, or knocking out, hexokinase genes tend to support the high sugar hypothesis, but pleiotropic effects confound this conclusion. In addition, several experiments show the effects of treatments on senescence without the increase in leaf sugar levels. Nonetheless, sugar levels are usually measured in whole leaves. Such an overall level does not reflect the differences in the onset of senescence between tissues and cells, and can therefore not be used as an argument for or against either of the two hypotheses. It is argued that future work should determine the time line of the concentrations of various sugars in various cells and cellular compartments, in relation to senescence processes in the same cells. Taken together, the data are not decisive. It is possible that neither of the two hypotheses is correct.