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Free Content The phytochrome-deficient pcd2 mutant of pea is unable to convert biliverdin IXα to 3(Z)-phytochromobilin

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During screening of ethylmethane sulphonate-mutagenized pea (Pisum sativum L.) seedlings under far-red light a mutant line, AF130, was isolated which showed a reduction in both red and far-red light-induced de-etiolation responses. The photomorphogenic phenotype of AF130 results from a single recessive mutation which is not allelic with the previously described phytochrome chromophore biosynthesis mutant pcd1. This new mutant has been designated pcd2, for p hytochrome c hromophore d eficient 2. Like pcd1, etiolated pcd2 seedlings are severely deficient in spectrally active phytochrome and contain wild-type levels of phytochrome A apoprotein which is not substantially depleted by red light treatment. Etioplast preparations from pcd2 seedlings can metabolize heme to biliverdin (BV) IXα, but are unable to convert BV IXα to the phytochrome chromophore, phytochromobilin. The PCD1 and PCD2 genes therefore control consecutive steps in phytochromobilin synthesis. Despite a similarly severe impairment of photomorphogenic responses, pcd2 mutant seedlings do not display the strongly chlorotic phenotype of pcd1, suggesting that this characteristic of pcd1 does not result from phytochrome deficiency per se, but is a specific effect of the pcd1 mutation. A double mutant between pcd1 and pcd2 was constructed. This mutant is paler than pcd1 and less responsive to red light than either single mutant, but retains a strong response to blue light.
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Document Type: Research Article

Affiliations: 1: Department of Plant Science, University of Tasmania, GPO Box 252-55 Hobart, Tasmania 7001, Australia, 2: Laboratory for Photoperception and Signal Transduction, Frontier Research Program, Institute of Physical and Chemical Research (RIKEN), Hirosawa 2-1, Wako-shi, Saitama-ken 351-01, Japan, and

Publication date: June 1, 1997

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