The aphototropic mutant line ptr116 of the moss todon purpureus shows characteristics of a deficiency in the phytochrome chromophore. Photoreversibility measurements indicate an approximately 20 time lower concentration of spectrally active phytochrome compared to wildtype, whereas normal phytochrome apoprotein levels are found on immunoblots. Feeding with the tetrapyrroles biliverdin, the proposed precursor of the phytochrome chromophore, or phycocyanobilin, which may replace the phytochrome chromophore, resulted in the rescue of ptr116 phototropism. The ptr116 mutant and the phenotypically-related mutant ptr1 contain lower chlorophyll levels than the wildtype. Chlorophyll content of wildtype and mutant tissue grown under different light conditions was estimated using conventional spectrophotometry of extracts and fluorimetrically, on single apical cells. Dark-grown tissue contained about 100 times less chlorophyll than tissue grown under standard white light conditions. Red light given for 24 h to dark adapted filaments induced an increase in the chlorophyll content in the wildtype, but not in ptr116. Blue light induced an increase in chlorophyll both in wildtype and in ptr116. The red light effect on the wildtype was partially reversible with far-red. If ptr116 was grown on phycocyanobilin, an increase in chlorophyll was also found when cells were irradiated with red light. The results indicate that phytochrome as well as a blue light photoreceptor regulate chlorophyll accumulation in C. purpureus protonemata. It can be assumed that in ptr116, the synthesis of the phytochrome chromophore is blocked specifically beyond the synthesis common to chlorophyll and the phytoehrome chromophore and affects an enzymatic step between protoporphyrin and biliverdin.
CITATION STYLE
Lamparter, T., Esch, H., Cove, D., & Hartmann, E. (1997). Phytochrome control of phototropism and chlorophyll accumulation in the apical cells of protonemal filaments of wildtype and an aphototropic mutant of the moss Ceratodon purpureus. Plant and Cell Physiology, 38(1), 51–58. https://doi.org/10.1093/oxfordjournals.pcp.a029084
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