Abstract

Malonic acid (10−2 M) promoted germination of excised dormant embryos of Avena fatua L. but inhibited germination of non-dormant embryos. Malonate inhibited oxygen consumption and carbon dioxide evolution of dormant embryos which resulted in an increased respiratory quotient and a decrease in the glucose C6/C1 ratio. Germination is oxygen-dependent, and malonate-sensitive oxygen consumption decreased during afterripening. Succinic acid (5 × 10−2 M) promoted germination of dormant embryos. Gibberellic acid (GA) (1.0 ppm) and succinate (5 × 10−2 M) interacted synergistically in promoting germination. Adenosine diphosphate also promoted germination but only after a considerable lag period. Germination of non-dormant embryos was inhibited by 2,4-dinitrophenol indicating the importance of adenosine triphosphate for germination. Storage of caryopses in various gaseous environments indicated that the response of dormant embryos to GA treatment was dependent on the operation of oxidative processes during afterripening. A model is proposed, indicating the nature of the regulation of the oxidative systems involved in the control of dormancy. The model accounts for the known effects of oxygen treatments on seeds, provides an explanation of the mechanism of afterripening, and explains the survival of imbibed dormant caryopses during adverse conditions. Such a model may be of widespread significance and is discussed in relation to its interaction with GA in developmental processes.

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