Abstract
Norflurazon, an inhibitor of the carotenoid biosynthesis, was used to modify the thylakoid structure of Euglena gracilis. Cells grown in the presence of norflurazon reveal an altered pigment composition as well as a decrease in photosynthetic activity. The reduced level of carotenoids caused a diminishing of some pigment–protein complexes . Besides the loss of oligomeric LHC II proteins, the content of a special pigment–protein complex consisting of LHC II and LHC I proteins was markedly decreased. The importance of this complex for the photosynthesis of E. gracilis was underlined by an altered fluorescence spectrum at 77 K and a modification of non-photochemical fluorescence quenching in NF-treated cells. The loss of a long wavelength fluorescence emitter (711 nm) resulted in a fluorescence spectrum (77 K) similar to that in higher plants. Furthermore, we observed the complete loss of a component of non-photochemical fluorescence quenching characterised by its relaxation half-time of about 6 min. In a previous paper (Photosynth. Res. 63 (2000) 159) this quenching mechanism was attributed to a spill over-mechanism. In contrast to the non-treated control cells, qE clearly dominates the non-photochemical quenching in NF-treated cells of E. gracilis under limiting actinic light (AL) conditions. At light intensities of above light saturation, non-photochemical quenching is determined mainly by qI. From the measured data, there is no evidence that the mechanism of qE is localised in E. gracilis in the antennae, but rather in the RC II.
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