THE PHYTOCHROME-DEFICIENT PCD2 MUTANT OF PEA IS UNABLE TO CONVERT BILIVERDIN IX-ALPHA TO 3(Z)-PHYTOCHROMOBILIN

During screening of ethylmethane sulphonate-mutagenized pea (Pisum sat ivum L.) seedlings under far-red light a mutant line, AF130, was isola ted which showed a reduction in both red and far-red light-induced dee tiolation responses. The photomorphogenic phenotype of AF130 results f rom a single recessive mutation which is not allelic with the previous ly described phytochrome chromophore biosynthesis mutant pcd1. This ne w mutant has been designated pcd2, for phytochrome chromophore deficie nt 2. Like pcd1, etiolated pcd2 seedlings are severely deficient in sp ectrally active phytochrome and contain wild-type levels of phytochrom e A apoprotein which is not substantially depleted by red light treatm ent. Etioplast preparations from pcd2 seedlings can metabolize heme to biliverdin (BV) IX alpha, but are unable to convert BV IX alpha to th e phytochrome chromophore, phytochromobilin. The PCD1 and PCD2 genes t herefore control consecutive steps in phytochromobilin synthesis. Desp ite a similarly severe impairment of photomorphogenic responses, pcd2 mutant seedlings do not display the strongly chlorotic phenotype of pc d1, suggesting that this characteristic of pcd1 does not result from p hytochrome deficiency per se, but is a specific effect of the pcd1 mut ation. A double mutant between pcd1 and pcd2 was constructed. This mut ant is paler than pcd1 and less responsive to red light than either si ngle mutant, but retains a strong response to blue light.