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A Regulatory Sequence of Simian Virus 40 is Inactivated by UV-Induced Damage

  • T. C. Brown
  • P. A. Cerutti
Part of the NATO ASI Series book series (NSSA, volume 124)

Abstract

Damage in the DNA of eurocaryotic cells can modulate gene expression by several independent mechanisms. Lesions can block RNA synthesis by posing obstacles to RNA polymerase II. In general, bulky lesions are effective (1, 2), if temporary (3), blocks to transcription while damage introduced by alkylating agents is less potent (4). Damage can also affect gene expression by altering the pattern of methylated cytosine residues in DNA, either by inhibiting the activity of eucaryotic maintenance methyl transferase (5) or because DNA synthesized during excision repair is incompletely methylated (6). The ability of damage to alter methylation patterns may lead to heritable changes in gene expression (7). Chromosomal proteins close to the sites of damage in DNA (8) may be modified by the addition of poly ADP-ribose (9). Such modification may change the conformation of the chromatin in a way that alters gene expression (10). Finally, damage may block protein-DNA interactions required for transcription by distorting the DNA sequences that ordinarily serve as protein binding sites (11–13).

Keywords

Bulky Lesion Transcriptional Control Region SV40 Genome Alter Methylation Pattern Methylated Cytosine Residue 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1986

Authors and Affiliations

  • T. C. Brown
    • 1
  • P. A. Cerutti
    • 1
  1. 1.Department of CarcinogenesisSwiss Institute for Experimental Cancer ResearchEpalinges/LausanneSwitzerland

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