Analysis of the rearrangements associated with carcinogen-induced activation of the hamster thymidine kinase gene

Frederic G. Barr, Sridharan Rajagopalan, Michael W. Lieberman

Research output: Contribution to journalArticle

2 Scopus citations

Abstract

We have previously shown that chemical carcinogen treatment of RJK92 hamster cells activates the quiescent thymidine kinase (TK) gene and that 20% of the TK+ variants have a rearrangement in the region 5′ to the TK gene (Barr et al. (1986) Mol. Cell. Biol. 6, 3023-3033). After cloning the wild type 5′ region to obtain detailed mapping data and hybridization probes, we localized the rearrangement breakpoints by Southern blot analysis to a 1.5 kb region 6 kb 5′ to the origin of transcription. This analysis also demonstrated that the rearrangements consist at least partly of a deletion of wild type sequences 5′ to this breakpoint region. The region near the transcription origin in the rearranged TK genes has a DNase I-sensitive chromatin conformation and a DNase I hypersensitive site as well as the previously described domain of demethylation (Ibid.). Though this domain of demethylation extends into the breakpoint region, the rearranged region is not associated with DNase I sensitivity nor hypersensitive sites. The rearrangement also does not detectably alter the growth-related regulation of TK activity in these cells.

Original languageEnglish (US)
Pages (from-to)129-135
Number of pages7
JournalNucleic Acids Research
Volume18
Issue number1
DOIs
StatePublished - Jan 11 1990

ASJC Scopus subject areas

  • Genetics

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