Phytochrome-controlled Nyctinasty in Albizzia julibrissin

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Abstract
Indole-3-acetic acid, alpha-naphthylacetic acid, and 2,4-dichlorophenoxyacetic acid (0.001 to 1.0 mm) inhibit the nyctinastic closure of excised Albizzia leaflet pairs; antiauxins and auxin analogs are ineffective, and the auxin effects seem not to be mediated by ethylene. Indoleacetic acid (0.001 to 0.1 mm) also promotes rhythmic opening in the dark, but is ineffective during that phase of rhythmic closure ("leaky phase") which is insensitive to azide. At these concentrations, all of the indoleacetic acid effects are reversible upon transfer of the tissue to water and are linked to alteration of potassium flux in pulvinule motor cells.A supraoptimal concentration of indoleacetic acid (1 mm) inhibits rhythmic opening as well as nyctinastic closure, although it has little or no effect on potassium flux in motor cells. These inhibitions cannot be completely reversed by transferring the leaflets to water.Although indoleacetic acid (0.01 to 1.0 mm) inhibits leaflet opening and potassium flux in dorsal and ventral motor cells when leaflets are transferred from darkness to light, it has no effect during other portions of the light period, implying that changes in endogenous auxin do not control leaflet angle in the light. Neither does auxin seem to be involved in the phytochrome-regulated process, since it does not alter phytochrome control of leaflet movement or potassium flux. However, endogenous auxin probably plays an important role in controlling potassium flux into ventral motor cells during the opening phase of rhythmic leaflet movement in the dark.