ArticlePloS one2011
MU2 and HP1a regulate the recognition of double strand breaks in Drosophila melanogaster.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 20 citations in OpenAlex.
- Expanding the HP1a-binding consensus and molecular grammar for heterochromatin assembly.Nucleic acids research · 2025Article
- Review
- Insights into HP1a-Chromatin Interactions.Cells · 2020Review
- Arp2/3 and Unc45 maintain heterochromatin stability inExperimental biology and medicine (Maywood, N.J.) · 2019Article
- Nuclear actin filaments in DNA repair dynamics.Nature cell biology · 2019Review
- High MYC Levels Favour Multifocal Carcinogenesis.Frontiers in genetics · 2018Article
- And yet, it moves: nuclear and chromatin dynamics of a heterochromatic double-strand break.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Nuclear Dynamics of Heterochromatin Repair.Trends in genetics : TIG · 2017Review
- Cervantes and Quijote protect heterochromatin from aberrant recombination and lead the way to the nuclear periphery.Nucleus (Austin, Tex.) · 2016Article
- Heterochromatic breaks move to the nuclear periphery to continue recombinational repair.Nature cell biology · 2015Article
- Loss of Pol32 in Drosophila melanogaster causes chromosome instability and suppresses variegation.PloS one · 2015Article
- Nuclear dynamics of radiation-induced foci in euchromatin and heterochromatin.Mutation research · 2013Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Chromatin structure regulates the dynamics of the recognition and repair of DNA double strand breaks; open chromatin enhances the recruitment of DNA damage response factors, while compact chromatin is refractory to the assembly of radiation-induced repair foci. MU2, an orthologue of human MDC1, a scaffold for ionizing radiation-induced repair foci, is a widely distributed chromosomal protein in Drosophila melanogaster that moves to DNA repair foci after irradiation. Here we show using yeast 2 hybrid screens and co-immunoprecipitation that MU2 binds the chromoshadow domain of the heterochromatin protein HP1 in untreated cells. We asked what role HP1 plays in the formation of repair foci and cell cycle control in response to DNA damage. After irradiation repair foci form in heterochromatin but are shunted to the edge of heterochromatic regions an HP1-dependent manner, suggesting compartmentalized repair. Hydroxyurea-induced repair foci that form at collapsed replication forks, however, remain in the heterochromatic compartment. HP1a depletion in irradiated imaginal disc cells increases apoptosis and disrupts G2/M arrest. Further, cells irradiated in mitosis produced more and brighter repair foci than to cells irradiated during interphase. Thus, the interplay between MU2 and HP1a is dynamic and may be different in euchromatin and heterochromatin during DNA break recognition and repair.
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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.