ArticleExperimental cell research2011
Mammalian ChlR1 has a role in heterochromatin organization.
Article in Experimental cell research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 26 citations in OpenAlex.
- Chl1 coordinates with H3K9 methyltransferase Clr4 to reduce the accumulation of RNA-DNA hybrids and maintain genome stability.iScience · 2022Article
- The budding yeast protein Chl1p is required for delaying progression through G1/S phase after DNA damage.Cell division · 2021Article
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- Review
- The repair geneOncology reviews · 2021Article
- Role of the DDX11 DNA Helicase in Warsaw Breakage Syndrome Etiology.International journal of molecular sciences · 2021Review
- Article
- Spotlight on Warsaw Breakage Syndrome.The application of clinical genetics · 2019Review
- Review
- Interaction of the Warsaw breakage syndrome DNA helicase DDX11 with the replication fork-protection factor Timeless promotes sister chromatid cohesion.PLoS genetics · 2018Article
- Epigenetic features of human telomeres.Nucleic acids research · 2018Article
- The Cellular DNA Helicase ChlR1 Regulates Chromatin and Nuclear Matrix Attachment of the Human Papillomavirus 16 E2 Protein and High-Copy-Number Viral Genome Establishment.Journal of virology · 2017Article
- Molecular functions and cellular roles of the ChlR1 (DDX11) helicase defective in the rare cohesinopathy Warsaw breakage syndrome.Cellular and molecular life sciences : CMLS · 2014Review
- Roles of ChlR1 DNA helicase in replication recovery from DNA damage.Experimental cell research · 2013Article
- Chl1 DNA helicase regulates Scc2 deposition specifically during DNA-replication in Saccharomyces cerevisiae.PloS one · 2013Article
- Cohesin codes - interpreting chromatin architecture and the many facets of cohesin function.Journal of cell science · 2013Review
- DNA helicases associated with genetic instability, cancer, and aging.Advances in experimental medicine and biology · 2013Article
- The DEAD/DEAH box helicase, DDX11, is essential for the survival of advanced melanomas.Molecular cancer · 2012Article
- DNA helicase and helicase-nuclease enzymes with a conserved iron-sulfur cluster.Nucleic acids research · 2012Review
- Expanding the Genetic Blueprint of Wilms Tumor: An Account of 71 Novel Variants across 16 Genes with Novel Implications for Wilms Tumor Pathogenesis.Journal of Indian Association of Pediatric SurgeonsArticle
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
The ChlR1 DNA helicase, encoded by DDX11 gene, which is responsible for Warsaw breakage syndrome (WABS), has a role in sister-chromatid cohesion. In this study, we show that human ChlR1 deficient cells exhibit abnormal heterochromatin organization. While constitutive heterochromatin is discretely localized at perinuclear and perinucleolar regions in control HeLa cells, ChlR1-depleted cells showed dispersed localization of constitutive heterochromatin accompanied by disrupted centromere clustering. Cells isolated from Ddx11(-/-) embryos also exhibited diffuse localization of centromeres and heterochromatin foci. Similar abnormalities were found in HeLa cells depleted of combinations of HP1α and HP1β. Immunofluorescence and chromatin immunoprecipitation showed a decreased level of HP1α at pericentric regions in ChlR1-depleted cells. Trimethyl-histone H3 at lysine 9 (H3K9-me3) was also modestly decreased at pericentric sequences. The abnormality in pericentric heterochromatin was further supported by decreased DNA methylation within major satellite repeats of Ddx11(-/-) embryos. Furthermore, micrococcal nuclease (MNase) assay revealed a decreased chromatin density at the telomeres. These data suggest that in addition to a role in sister-chromatid cohesion, ChlR1 is also involved in the proper formation of heterochromatin, which in turn contributes to global nuclear organization and pleiotropic effects.
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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.