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

Ramirez, Fidel; Lingg, Thomas; Toscano, S.; Lam, Kin-Chung; Georgiev, P.; Chung, Ho-Ryun; Lajoie, Bryan R.; de Wit, Elzo; Zhan, Ye; de laat, Wouter; Dekker, Job; Manke, T.; Akhtar, Asifa

doi:doi: 10.1016/j.molcel.2015.08.024

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

MPG-Autoren

Ramirez, Fidel
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Lingg, Thomas
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;
Faculty of Biology, University of Freiburg;

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Toscano, S.
Department of Chromatin Regulation, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Lam, Kin-Chung
Faculty of Biology, University of Freiburg;
Department of Chromatin Regulation, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Georgiev, P.
Department of Chromatin Regulation, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Manke, T.
Department of Epigenetics, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Akhtar, Asifa
Department of Chromatin Regulation, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Zitation

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.

Zitierlink: https://hdl.handle.net/someHandle/test/escidoc:902583

Zusammenfassung

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.