ArticleGenetics2008
Analysis of chromatin structure of genes silenced by heterochromatin in trans.
Article in Genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed.
- Effects of Chromatin Structure Modifiers on the trans-Acting Heterochromatin Position Effect in Drosophila melanogaster.Doklady. Biochemistry and biophysics · 2023Article
- Triple-Helical DNA inCells · 2018Article
- Article
- The Differences Between Cis- and Trans-Gene Inactivation Caused by Heterochromatin in Drosophila.Genetics · 2016Article
- Epigenetic control of embryonic stem cell differentiation.Stem cell reviews and reports · 2012Review
- The molecular basis for stability of heterochromatin-mediated silencing in mammals.Epigenetics & chromatin · 2009Article
- Genetic and molecular analysis of gene trans-inactivation caused by homologous eu-heterochromatic chromosome rearrangement in Drosophila melanogaster.Doklady. Biochemistry and biophysicsArticle
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While heterochromatic gene silencing in cis is often accompanied by nucleosomal compaction, characteristic histone modifications, and recruitment of heterochromatin proteins, little is known concerning genes silenced by heterochromatin in trans. An insertion of heterochromatic satellite DNA in the euchromatic brown (bw) gene of Drosophila melanogaster results in bwDominant (bwD), which can inactivate loci on the homolog by relocation near the centric heterochromatin (trans-inactivation). Nucleosomal compaction was found to accompany trans-inactivation, but stereotypical heterochromatic histone modifications were mostly absent on silenced reporter genes. HP1 was enriched on trans-inactivated reporter constructs and this enrichment was more pronounced on adult chromatin than on larval chromatin. Interestingly, this HP1 enrichment in trans was unaccompanied by an increase in the 2MeH3K9 mark, which is generally thought to be the docking site for HP1 in heterochromatin. However, a substantial increase in the 2MeH3K9 mark was found on or near the bwD satellite insertion in cis, but did not spread further. These observations suggest that the interaction of HP1 with chromatin in cis is fundamentally different from that in trans. Our molecular data agree well with the differential phenotypic effect on bwD trans-inactivation of various genes known to be involved in histone modification and cis gene silencing.
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