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The Role of Starvation in Fenuron Injury to Shrub Live Oak

Published online by Cambridge University Press:  12 June 2017

Edwin A. Davis
Edwin A. Davis*
Affiliation:
Rocky Mountain Forest and Range Experiment Station, Forest Service, U. S. Department of Agriculture, with central headquarters maintained at Fort Collins in cooperation with Colorado State University
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Abstract

The hypothesis that leaf injury from applications of fenuron (3-phenyl-1,1-dimethylurea) is a direct result of a lack of photosynthate did not explain the results of experiments with seedlings of shrub live oak (Quercus turbinella Greene) supplied with an acorn food reserve supplemented with glucose solution, and with seedlings whose acorns were excised or left attached to the seedlings. An alternate hypothesis is offered: acute leaf injury from phenylurea treatment is due to one or more components of the electron transport chain, between the chlorophyll b pigment system and the reduction of triphosphopyridine nucleotide, which are left in a toxic oxidized state as a result of the phenylurea block in the oxygen-liberating system. Evidence also favors the above interpretation rather than the idea that toxicity results from the accumulation of a toxic oxidized product on the oxygen-liberating pathway. Although leaf injury appears to be due to toxic components of the inhibited photosynthetic apparatus, the ultimate cause of death of the entire plant is starvation.

Besides its effect on photosynthesis, fenuron at high concentrations also causes inhibition of root growth.

Type
Research Article
Information
Weeds , Volume 14 , Issue 1 , January 1966 , pp. 10 - 17
Copyright
Copyright © 1966 Weed Science Society of America 

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References

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