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Studies on the induction and release of seed dormancy in wild oats (Avena fatua L.)

University of British Columbia

The induction and release of secondary dormancy by anaerobiosis in genetically pure dormant (AN-51, Mont 73) and nondormant (CS-40, SH-430) lines of Avena fatua L. and the role of alternative respiration in the regulation of its primary and secondary dormancy were studied. These lines differed with regard to the optimal period of anaerobiosis necessary for induction of dormancy and/or the degree (% of seeds acquiring dormancy) and duration of dormancy induced. Secondary dormancy could be induced more effectively in after-ripened seeds of dormant lines than in nondormant lines where only a short-term dormancy could be induced (in 5-7 week old seeds). As with primary dormancy, wild oat biotypes exhibit genetic variability in their secondary dormancy behaviour and factors such as temperature can modify the expression of this trait. The germination stimulants kinetin, isopentenyl adenine, sodium azide, potassium nitrate and ethanol, which break primary dormancy in wild oats, stimulated germination of secondarily dormant seeds (line AN-51). Since these chemicals are structurally diverse, primary and secondary dormancies appear to be regulated by similar mechanism(s). Salicylhydroxamate (SHAM), an inhibitor of alternative respiration, did not inhibit: 1. the respiration of embryos excised from after-ripened or secondarily dormant seeds, 2. the spontaneous release of secondary dormany in nondormant lines or 3. the release of secondary dormancy by a variety of chemicals (except azide), suggesting that alternative respiration is not involved in the induction or release of secondary dormancy. Azide and cyanide released seed dormancy at similar concentrations and treatment durations. While cyanide released primary dormancy in seeds with little after-ripening, azide was effective only in secondarily dormant seeds or seeds with more extensive after-ripening. Both inhibitors stimulated seed respiration to a similar extent. The release of dormancy by cyanide was always preceded by respiratory stimulation, but the latter appeared to be independent of germination. SHAM inhibited both the release of seed dormancy and the stimulation of seed respiration by azide but not by cyanide. Respiration was inhibited only when SHAM was applied concurrently with azide. When applied subsequent to azide treatment, SHAM had no effect. The respiration of seed pre-treated with azide and cyanide was insensitive to SHAM and therefore cannot be alternative. Studies were performed to determine the effect of pH on the stimulation of germination and respiration by cytochrome oxidase inhibitors. Although pH had little effect on seed respiration and germination in controls and in the presence of cyanide, it strongly affected the activity of azide. At pH 5, 1 mM azide inhibited both seed respiration and germination whereas at pH 7 it stimulated both. SHAM at pH 7 did not affect the stimulation of respiration by azide, but inhibited it in the unbuffered system and at pH 5. Thus, SHAM appears to alter azide activity by lowering pH, increasing the concentration of undissociated (active) azide, which then completely inhibits cytochrome oxidase and consequently, seed respiration and germination. The release of dormancy and the stimulation of respiration by cyanide and azide do not appear to be related to the inhibition of cytochrome-mediated respiration or the stimulation of alternative respiration.

Text

2010-06-30

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http://hdl.handle.net/2429/26092

Plant Science

University of British Columbia

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