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THE PLANT CELL, Vol 6, Issue 5 629-643, Copyright © 1994 by American Society of Plant Biologists
Arabidopsis COP8, COP10, and COP11 Genes Are Involved in Repression of Photomorphogenic Development in Darkness
N. Wei, S. F. Kwok, A. G. von Arnim, A. Lee, T. W. McNellis, B. Piekos and X. W. Deng
Department of Biology, Osborn Memorial Laboratories, OML 301, Yale University, 165 Prospect Street, New Haven, Connecticut 06520-8104
Wild-type Arabidopsis seedlings are capable of following two developmental
programs: photomorphogenesis in the light and skotomorphogenesis in
darkness. Screening of Arabidopsis mutants for constitutive
photomorphogenic development in darkness resulted in the identification of
three new loci designated COP8, COP10, and COP11. Detailed examination of
the temporal morphological and cellular differentiation patterns of
wild-type and mutant seedlings revealed that in darkness, seedlings
homozygous for recessive mutations in COP8, COP10, and COP11 failed to
suppress the photomorphogenic developmental pathway and were unable to
initiate skotomorphogenesis. As a consequence, the mutant seedlings grown
in the dark had short hypocotyls and open and expanded cotyledons, with
characteristic photomorphogenic cellular differentiation patterns and
elevated levels of light-inducible gene expression. In addition, plastids
of dark-grown mutants were defective in etioplast differentiation. Similar
to cop1 and cop9, and in contrast to det1 (deetiolated), these new mutants
lacked dark-adaptive change of light-regulated gene expression and retained
normal phytochrome control of seed germination. Epistatic analyses with the
long hypocotyl hy1, hy2, hy3, hy4, and hy5 mutations suggested that these
three loci, similar to COP1 and COP9, act downstream of both phytochromes
and a blue light receptor, and probably HY5 as well. Further, cop8-1,
cop10-1, and cop11-1 mutants accumulated higher levels of COP1, a feature
similar to the cop9-1 mutant. These results suggested that COP8, COP10, and
COP11, together with COP1, COP9, and DET1, function to suppress the
photomorphogenic developmental program and to promote skotomorphogenesis in
darkness. The identical phenotypes resulting from mutations in COP8, COP9,
COP10, and COP11 imply that their encoded products function in close
proximity, possibly with some of them as a complex, in the same signal
transduction pathway.
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