ArticleDNA research : an international journal for rapid publication of reports on genes and genomes2011
Polycomb group-dependent, heterochromatin protein 1-independent, chromatin structures silence retrotransposons in somatic tissues outside ovaries.
Article in DNA research : an international journal for rapid publication of reports on genes and genomes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Components from the Human c-myb Transcriptional Regulation System Reactivate Epigenetically Repressed Transgenes.International journal of molecular sciences · 2020Article
- Key role of piRNAs in telomeric chromatin maintenance and telomere nuclear positioning in Drosophila germline.Epigenetics & chromatin · 2018Article
- MicroRNA-Dependent Transcriptional Silencing of Transposable Elements in Drosophila Follicle Cells.PLoS genetics · 2015Article
- Spatio-temporal requirements for transposable element piRNA-mediated silencing during Drosophila oogenesis.Nucleic acids research · 2014Article
- During a short window of Drosophila oogenesis, piRNA biogenesis may be boosted and mobilization of transposable elements allowed.Frontiers in genetics · 2014Article
- Maternal depletion of Piwi, a component of the RNAi system, impacts heterochromatin formation in Drosophila.PLoS genetics · 2013Article
- Article
- Homology-dependent silencing by an exogenous sequence in the Drosophila germline.G3 (Bethesda, Md.) · 2012Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Somatic cells are equipped with different silencing mechanisms that protect the genome against retrotransposons. In Drosophila melanogaster, a silencing pathway implicating the argonaute protein PIWI represses retrotransposons in cells surrounding the oocyte, whereas a PIWI-independent pathway is involved in other somatic tissues. Here, we show that these two silencing mechanisms result in distinct chromatin structures. Using sensor transgenes, we found that, in somatic tissues outside of the ovaries, these transgenes adopt a heterochromatic configuration implicating hypermethylation of H3K9 and K27. We identified the Polycomb repressive complexes (PRC1 and 2), but not heterochromatin protein 1 to be necessary factors for silencing. Once established, the compact structure is stably maintained through cell divisions. By contrast, in cells where the silencing is PIWI-dependent, the transgenes display an open and labile chromatin structure. Our data suggest that a post-transcriptional gene silencing (PTGS) mechanism is responsible for the repression in the ovarian somatic cells, whereas a mechanism that couples PTGS to transcriptional gene silencing operates to silence retrotransposons in the other somatic tissues.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.