Abstract
The late flowering, quantitative long day habit of wild type pea (Pisum sativum L.) is conferred by the joint presence of dominant genes Sn, Dne and Ppd. Grafting studies have shown that flowering in wild type plants is delayed under short days by formation of a graft‐transmissible inhibitor and that the early flowering, day neutral mutants sn and dne are deficient in this inhibitor. However, the physiological action of the Ppd gene has not been examined by grafting and the possibility exists that the ppd mutation causes early flowering and a day neutral habit by blocking response to, rather than synthesis of, the inhibitor. We here identify a second, more severe (probably null) mutant allele (ppd‐2) at the Ppd locus and show that flowering was delayed by 4 nodes in a ppd‐2 shoot grafted to a wild type stock, and promoted by 13 nodes in a wild type shoot grafted to a ppd‐2 stock. Thus a ppd‐2 shoot can respond to inhibitor donated by a wild type stock but a ppd‐2 stock is unable to provide sufficient inhibitor to prevent early flower initiation in a wild type shoot. We conclude genes Sn, Dne and Ppd each control steps in the synthesis of the flower inhibitor. Grafts among the sn, dne and ppd mutants gave an indication that the three genes may act in the sequence Sn, Ppd, Dne, but possible cases of physiological complementation need to be tested using null mutants in the same genetic background.
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