ArticleMolecular and cellular biology1995
The bulk chromatin structure of a murine transgene does not vary with its transcriptional or DNA methylation status.
Article in Molecular and cellular biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- Mutational spectra of aflatoxin BProceedings of the National Academy of Sciences of the United States of America · 2017Article
- DNA methylation precedes chromatin modifications under the influence of the strain-specific modifier Ssm1.Molecular and cellular biology · 2005Article
- A cis-acting element that directs the activity of the murine methylation modifier locus Ssm1.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Constitutively methylated CpG dinucleotides as mutation hot spots in the retinoblastoma gene (RB1).American journal of human genetics · 1997Article
- Epigenetic silencing of a foreign gene in nuclear transformants of Chlamydomonas.The Plant cell · 1997Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The DNA methylation status of HRD, a murine transgene, can be controlled by the genetic background upon which it is carried. We found the transgene to be transcribed in competent tissues only when undermethylated. Chromatin structure over the transgene was assayed by nuclear accessibility with DNase I, MspI, and PstI. While the transgene was up to fivefold more resistant to MspI when methylated than when not methylated, we observed no such difference with DNase I or PstI. We suggest that methyl-CpG-binding proteins are responsible for the difference observed with MspI, but that the chromatin structures are otherwise similarly compacted. Methylation could, therefore, play a regulatory role in gene expression beyond that which can be accomplished by bulk chromatin structure alone.
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