Blockage of RNA polymerase II at a cyclobutane pyrimidine dimer and 6–4 photoproduct

The blockage of transcription elongation by RNA polymerase II (pol II) at a DNA damage site on the transcribed strand triggers a transcription-coupled DNA repair (TCR), which rapidly removes DNA damage on the transcribed strand of the expressed gene and allows the resumption of transcription. To ana...

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Bibliographic Details
Published in:	Biochemical and biophysical research communications Vol. 320; no. 4; pp. 1133 - 1138
Main Authors:	Mei Kwei, Joan Seah, Kuraoka, Isao, Horibata, Katsuyoshi, Ubukata, Manabu, Kobatake, Eiry, Iwai, Shigenori, Handa, Hiroshi, Tanaka, Kiyoji
Format:	Journal Article
Language:	English
Published:	United States Elsevier Inc 06-08-2004
Subjects:	6–4 Photoproduct Cyclobutane pyrimidine dimer DNA - chemistry DNA - genetics DNA - radiation effects DNA - ultrastructure DNA Damage - genetics DNA Repair - genetics Gene Expression Regulation - radiation effects Gene Silencing - radiation effects Humans Pyrimidine Dimers - genetics RNA polymerase II RNA Polymerase II - genetics RNA Polymerase II - radiation effects Transcription elongation Transcription-coupled DNA repair Transcriptional Elongation Factors - genetics Ultraviolet Rays Transcription elongation 6–4 Photoproduct RNA polymerase II Transcription-coupled DNA repair Cyclobutane pyrimidine dimer
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Summary:	The blockage of transcription elongation by RNA polymerase II (pol II) at a DNA damage site on the transcribed strand triggers a transcription-coupled DNA repair (TCR), which rapidly removes DNA damage on the transcribed strand of the expressed gene and allows the resumption of transcription. To analyze the effect of UV-induced DNA damage on transcription elongation, an in vitro transcription elongation system using pol II and oligo(dC)-tailed templates containing a cyclobutane pyrimidine dimer (CPD) or 6–4 photoproduct (6–4PP) at a specific site was employed. The results showed that pol II incorporated nucleotides opposite the CPD and 6–4PP and then stalled. Pol II formed a stable ternary complex consisting of pol II, the DNA damage template, and the nascent transcript. Furthermore, atomic force microscopy imaging revealed that pol II stalled at the damaged region. These findings may provide the basis for analysis of the initiation step of TCR.
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2
ISSN:	0006-291X 1090-2104
DOI:	10.1016/j.bbrc.2004.06.066