De-etiolated 1 and damaged DNA binding protein 1 interact to regulate Arabidopsis photomorphogenesis.
BACKGROUND: Plant development is exquisitely sensitive to light. Seedlings grown in the dark have a developmentally arrested etiolated phenotype, whereas in the light they develop leaves and complete their life cycle. Arabidopsis de-etiolated 1 (det1) mutants develop like light-grown seedlings even when grown in the dark. DET1 encodes a nuclear protein that appears to act downstream from multiple photoreceptors to regulate morphogenesis and gene expression in response to light. However, its function has remained unknown.RESULTS: We used microarrays to examine defects in transcription in dark-grown det1 seedlings. We found extensive changes in gene expression, including many of the transcriptional responses observed in light-treated wild-type seedlings. We used an epitope-tagging approach to determine the basis of DET1 function. GFP-DET1 rescues the det1 phenotype, is localized to the nucleus, and forms an approximately 350 kDa complex, which is required for full DET1 activity. We affinity-purified the DET1 complex and identified an approximately 120 kDa copurifying protein that is the plant homolog of UV-Damaged DNA Binding Protein 1 (DDB1), a protein implicated in the human disease xeroderma pigmentosa. A null mutation in Arabidopsis DDB1A results in no obvious phenotype on its own, yet it enhances the phenotype of a weak det1 allele.CONCLUSIONS: DET1 and DDB1 interact both biochemically and genetically. In animal cells, DDB1 interacts with histone acetyltransferase complexes. The DET1/DDB1 complex may regulate gene expression in response to light via recruitment of HAT activity. Thus, DET1, whose sequence is conserved in both animals and plants, may play a direct role in the regulation of many genes.[1]References
- De-etiolated 1 and damaged DNA binding protein 1 interact to regulate Arabidopsis photomorphogenesis. Schroeder, D.F., Gahrtz, M., Maxwell, B.B., Cook, R.K., Kan, J.M., Alonso, J.M., Ecker, J.R., Chory, J. Curr. Biol. (2002) [Pubmed]
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