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Molecular and Cellular Biology, November 2005, p. 9773-9783, Vol. 25, No. 22
0270-7306/05/$08.00+0 doi:10.1128/MCB.25.22.9773-9783.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Département de Microbiologie et d'Infectiologie, Faculté de Médecine, Université de Sherbrooke, Sherbrooke, QC J1H 5N4, Canada,1 Biochemistry and Biophysics, School of Molecular Biosciences, Washington State University, Pullman, Washington 99164-46602
Received 5 January 2005/ Returned for modification 7 February 2005/ Accepted 25 August 2005
Chromatin rearrangements occur during repair of cyclobutane pyrimidine dimers (CPDs) by nucleotide excision repair (NER). Thereafter, the original structure must be restored to retain normal genomic functions. How NER proceeds through nonnucleosomal chromatin and how open chromatin is reestablished after repair are unknown. We analyzed NER in ribosomal genes (rDNA), which are present in multiple copies but only a fraction are actively transcribed and nonnucleosomal. We show that removal of CPDs is fast in the active rDNA and that chromatin reorganization occurs during NER. Furthermore, chromatin assembles on nonnucleosomal rDNA during the early events of NER but in the absence of DNA repair. The resumption of transcription after removal of CPDs correlates with the reappearance of nonnucleosomal chromatin. To date, only the passage of replication machinery was thought to package ribosomal genes in nucleosomes. In this report, we show that early events after formation of UV photoproducts in DNA also promote chromatin assembly.
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