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  High-Affinity Sites Form an Interaction Network to Facilitate Spreading of the MSL Complex across the X Chromosome in Drosophila

Ramirez, F., Lingg, T., Toscano, S., Lam, K.-C., Georgiev, P., Chung, H.-R., et al. (2015). High-Affinity Sites Form an Interaction Network to Facilitate Spreading of the MSL Complex across the X Chromosome in Drosophila. Molecular Cell, 60, 146-162. doi:doi: 10.1016/j.molcel.2015.08.024.

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Ramirez, Fidel1, Author
Lingg, Thomas1, 2, Author
Toscano, S.3, Author              
Lam, Kin-Chung2, 3, Author              
Georgiev, P.3, Author              
Chung, Ho-Ryun4, Author
Lajoie, Bryan R.5, Author
de Wit, Elzo6, Author
Zhan, Ye5, Author
de laat, Wouter6, Author
Dekker, Job5, 7, Author
Manke, T.8, Author              
Akhtar, Asifa3, Author              
Affiliations:
1Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, 79108 Freiburg, DE, ou_2243640              
2Faculty of Biology, University of Freiburg, Freiburg, Germany, ou_persistent22              
3Department of Chromatin Regulation, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243643              
4Max Planck Institute for Molecular Genetics, Berlin, Germany, ou_persistent22              
5Programm in Systems Biology, Department of Biochemistry and Molecular Pharmacology, University of massachusetts Medical School, Worcester, MA, USA, ou_persistent22              
6Hubrecht Institute, Royal netherlands Academy of Arts and Sciences and University Medical Center Utrecht, Utrecht, The Netherlands, ou_persistent22              
7Howard Hughes Medical Center , New York, USA, ou_persistent22              
8Department of Epigenetics, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243644              

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 Abstract: Dosage compensation mechanisms provide a paradigm to study the contribution of chromosomal conformation toward targeting and spreading of epigenetic regulators over a specific chromosome. By using Hi-C and 4C analyses, we show that high-affinity sites (HAS), landing platforms of the male-specific lethal (MSL) complex, are enriched around topologically associating domain (TAD) boundaries on the X chromosome and harbor more long-range contacts in a sex-independent manner. Ectopically expressed roX1 and roX2 RNAs target HAS on the X chromosome in trans and, via spatial proximity, induce spreading of the MSL complex in cis, leading to increased expression of neighboring autosomal genes. We show that the MSL complex regulates nucleosome positioning at HAS, therefore acting locally rather than influencing the overall chromosomal architecture. We propose that the sex-independent, three-dimensional conformation of the X chromosome poises it for exploitation by the MSL complex, thereby facilitating spreading in males.

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Language(s): eng - English
 Dates: 2015-10-01
 Publication Status: Published in print
 Pages: 17
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: DOI: doi: 10.1016/j.molcel.2015.08.024
 Degree: -

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Title: Molecular Cell
Source Genre: Journal
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Publ. Info: Cambridge, Mass. : Cell Press
Pages: 17 Volume / Issue: 60 Sequence Number: - Start / End Page: 146 - 162 Identifier: Other: 954925610929
ISSN: 1097-2765
CoNE: https://pure.mpg.de/cone/journals/resource/954925610929