Abstract
Inhibition of hypocotyl lengthening by phytochrome can be regarded as a prototype of a “negative” photoresponse (Mohr, 1966b). A characteristic feature of a negative photoresponse is the short lag-phase (Fig. 3). — The hypothesis has been advanced that “negative” photoresponses are the consequence of a differential gene repression which is exerted by P730, the active phytochrome (Fig. 1). In the present paper a number of experiments with the intact seedling are described which support this hypothesis. Continuous irradiation with far-red has been used to establish a stationary concentration of P730 over the whole period of experimentation. Under steady state conditions of hypocotyl lengthening P730 and actinomycin D (=Act) lower the growth velocity of the organ (Fig. 3, 4). The inhibitory action of Act (on a percentage basis) is the same with and without far-red (Fig. 5, 6). This fact means that Act and P730 act as two independent factors in a multiplicative system. Under steady state conditions of hypocotyl lengthening puromycin (=Pu) lowers the growth velocity of the organ (Fig. 7). The inhibitory action of Pu (on a percentage basis) is the same with and without far-red (Fig. 8, 9). This fact means that Pu and P730 act as two independent factors in a multiplicative system. The model in Fig. 10 agrees with all the facts which are available at the moment. The model is useful only if one can assume that the mRNA and enzymes which are coded by the repressible genes have a very short “life-time”. This assumption has not yet been proved. — The model is supported by the fact that RNA synthesis in the hypocotyl is strongly inhibited by P730 and is very sensitive toward Act (Weidner, unpublished data). — Furthermore Link (unpublished data) has shown that both P730 and Act suppress the incorporation of 14C-leucine into the protein fraction of the hypocotyl. It seems that in this case also, Act and P730 behave as two independent factors in a multiplicative system. Bei der “negativen” Photomorphose “Hemmung des Hypokotyllängenwachstums” kann gezeigt werden, daß die wachstumshemmenden Effekte von Phytochrom und Actinomycin D bzw. Puromycin keine Interaktion zeigen und multiplikativ miteinander verrechnet werden. Es wird die Hypothese begründet, daß Phytochrom über eine Reprimierung bestimmter Gene in die Steuerung des Wachstums eingreift. Das relative Ausmaß dieser Steuerung ist unabhängig vom Vorhandensein der Kotyledonen.