NO releases caryopsis dormancy in Avena fatua, the effect being dependent on the level of dormancy. The NO effect involves also the reduction of caryopsis sensitivity to ABA and to a decrease in the ABA to GAs ratio due to a decrease in ABA levels and the lack of effect on GAs levels before germination is completed. Nitric oxide (NO) from various donors (i.e. SNP, GSNO and acidified KNO2), applied to dry caryopses or during initial germination, released primary dormancy in caryopses. Dormancy in caryopses was gradually lost during dry storage (after-ripening) at 25 °C, enabling germination at 20 °C in the dark. The after-ripening effect is associated with a decrease in NO required for germination. In addition, NO decreased the sensitivity of dormant caryopses to exogenous abscisic acid (ABA) and decreased the embryos' ABA content before germination was completed. However, NO did not affect the content of bioactive gibberellins (GAs) from non-13-hydroxylation (GA4, GA7) and 13-hydroxylation (GA1, GA3, GA6.) pathways. Paclobutrazol (PAC), commonly regarded as a GAs biosynthesis inhibitor, counteracted the dormancy-releasing effect of NO and did not affect the GAs level; however, it increased the ABA content in embryos before germination was completed. Ascorbic acid, sodium benzoate and tiron, scavengers of reactive oxygen species (ROS), reduced the stimulatory effect of NO on caryopsis germination. This work provides new insight on the participation of NO in releasing A. fatua caryopses dormancy and on the relationship of NO with endogenous ABA and GAs.
Keywords: Abscisic acid; After ripening; Avena fatua; Dormancy; Gibberellins; Nitric oxide.
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