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THE PLANT CELL, Vol 3, Issue 11 1177-1186, Copyright © 1991 by American Society of Plant Biologists
Phytochrome-Deficient hy1 and hy2 Long Hypocotyl Mutants of Arabidopsis Are Defective in Phytochrome Chromophore Biosynthesis
B. M. Parks and P. H. Quail
University of California-Berkeley/United States Department of Agriculture Plant Gene Expression Center, 800 Buchanan Street, Albany, California 94710
The hy1 and hy2 long hypocotyl mutants of Arabidopsis contain normal levels
of immunochemically detectable phytochrome A, but the molecule is
photochemically nonfunctional. We have investigated the biochemical basis
for this lack of function. When the hy1 and hy2 mutants were grown in white
light on a medium containing biliverdin IX[alpha], a direct precursor to
phytochromobilin, the phytochrome chromophore, the seedlings developed with
a morphological phenotype indistinguishable from the light-grown wild-type
control. Restoration of a light-grown phenotype in the hy1 mutant was also
accomplished by using phycocyanobilin, a tetrapyrrole analog of
phytochromobilin. Spectrophotometric and immunochemical analyses of the
rescued hy1 and hy2 mutants demonstrated that they possessed wild-type
levels of photochemically functional phytochrome that displayed
light-induced conformational changes in the holoprotein indistinguishable
from the wild type. Moreover, phytochrome A levels declined in vivo in
response to white light in rescued hy1 and hy2 seedlings, indicative of
biliverdin-dependent formation of photochemically functional phytochrome A
that was then subject to normal selective turnover in the
far-red-light-absorbing form. Combined, these data suggest that the hy1 and
hy2 mutants are inhibited in chromophore biosynthesis at steps prior to the
formation of biliverdin IX[alpha], thus potentially causing a global
functional deficiency in all members of the phytochrome photoreceptor
family.
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