| Résumé | Yellow‐cedar (Chamaecyparis nootkatensis [D. Don] Spach) seeds exhibit prolonged coat‐imposed dormancy following their dispersal from the parent plant. Analyses were undertaken using S‐(+)‐[³H] abscisic acid (ABA) to monitor the capacity of embryos to metabolize ABA following their isolation from seeds subjected to various dormancy‐breaking and control treatments. Radiolabelled phaseic acid (PA) and dihydrophaseic acid (DPA) were detected in embryos and, to a greater extent in the surrounding media, by 48 h regardless of whether the embryos had been excised from seed previously subjected to only a 3 d soak or to a full dormancy‐breaking treatment. Of the two enantiomers of ABA, only the natural S‐(+)‐ABA effectively inhibited germination of isolated embryos. A metabolism‐resistant synthetic ABA analogue S‐[8′,8′,8′,9′,9′,9′]‐hexadeuteroabscisic acid, S‐(+)‐d6‐ABA, consistently slowed the germination rate of excised embryos to a greater extent than that caused by natural S‐(+)‐ABA. The deuterium‐labelled ring methyl groups of the analogue made it more resistant to oxidation by yellow‐cedar embryos and thus rendered the analogue more persistent and possessing greater activity. With increasing time of exposure to moist chilling, yellow‐cedar embryos became increasingly insensitive to both ABA and to the analogue. Subjecting seed to chemical treatments (GA₃ in combination with 1‐propanol) prior to moist chilling strongly enhanced the germinability of whole seeds. This treatment also had a relatively greater impact on ABA metabolism than did moist chilling alone, as indicated by a greater capacity of S‐(+)‐d6‐ABA to inhibit the germination of embryos as compared to S‐(+)‐ABA. Moist chilling was most critical for reduced ABA sensitivity of embryos. A change in the embryo's ability to metabolize ABA and reduced embryo sensitivity to ABA are two factors associated with dormancy termination of whole seeds of yellow cedar; a change in only one of these factors is insufficient to elicit high germinability. |
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