Summary
The inhibition of hypocotyl lengthening in intact mustard seedlings is controlled by two photosensitive systems which can be experimentally separated.
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1.
Kinetics of the growth response in the dark after red and far-red irradiation (Figs. 1, 2) demonstrate the operation of Pfr in the ground state via a threshold mechanism similar to the regulation of lipoxygenase synthesis in the mustard cotyledons (c. f. ref. [27]). This threshold mechanism determines the duration of the growth inhibition (Δt) following irradiation (Fig. 1, 2). Δt is dependent on the relative Pfr concentration at the beginning of the dark period and on the half life of Pfr destruction, but it is independent of the quantum flux density of far-red light (Fig. 4). The effect of 5 min red light on Δt can be fully reversed by 5 min far-red light (Fig. 3). The data reveal a quantitative relationship between the relative Pfr concentration and the photomorphogenetic response, Δt (Fig. 6). This relationship may explain in principle the logarithmic correlation between the percentage of phytochrome converted to Pfr by an initial irradiation and the subsequent response which has also been reported in the literature.
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2.
In continuous far-red light the velocity constant of the steady state growth is controlled by a “high intensity reaction” which shows the usual logarithmic dependence on quantum flux density (Fig. 4, 5), but no phytochrome destruction is apparent (Fig. 2). According to Hartmann (ref.[11–13]) this “high intensity reaction” can also be attributed to Pfr, which in this case acts through some excited state, P *fr .
It is concluded that the two photoreactive systems involve separate populations of phytochrome, which inhibit cell lengthening by independent control mechanisms.
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Schopfer, P., Oelze-Karow, H. Nachweis einer Schwellenwertsregulation durch Phytochrom bei der Photomodulation des Hypokotylstreckungswachstums von Senfkeimlingen (Sinapis alba L.). Planta 100, 167–180 (1971). https://doi.org/10.1007/BF00385217
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DOI: https://doi.org/10.1007/BF00385217