det1, cop1, and cop9 mutations cause inappropriate expression of several gene sets.
Author(s) -
Raphael Mayer,
Dorotea Raventós,
N H Chua
Publication year - 1996
Publication title -
the plant cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.324
H-Index - 341
eISSN - 1532-298X
pISSN - 1040-4651
DOI - 10.1105/tpc.8.11.1951
Subject(s) - biology , mutant , gene , genetics , arabidopsis , phenotype , gene expression , cop9 signalosome , signal transduction , mutation , microbiology and biotechnology , biochemistry , protease , peptide hydrolases , enzyme
Genetic studies using Arabidopsis offer a promising approach to investigate the mechanisms of light signal transduction during seedling development. Several mutants, called det/cop, have been isolated based on their deetiolated/constitutive photomorphogenic phenotypes in the dark. This study examines the specificity of the det/cop mutations with respect to their effects on genes regulated by other signal transduction pathways. Steady state mRNA levels of a number of differently regulated gene sets were compared between mutants and the wild type. We found that det2, cop2, cop3, and cop4 mutants displayed a gene expression pattern similar to that of the wild type. By contrast, det1, cop1, and cop9 mutations exhibited pleiotropic effects. In addition to light-responsive genes, genes normally inducible by plant pathogens, hypoxia, and developmental programs were inappropriately expressed in these mutants. Our data provide evidence that DET1, COP1, and COP9 most likely act as negative regulators of several sets of genes, not just those involved in light-regulated seedling development.
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