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Cohesin interacts with a panoply of splicing factors required for cell cycle progression and genomic organization

Jung-Sik Kim, Xiaoyuan He, Jie Liu, Zhijun Duan, Taeyeon Kim, Julia Gerard, Brian Kim, William S. Lane, William S. Noble, Bogdan Budnik, Todd Waldman
doi: https://doi.org/10.1101/325209
Jung-Sik Kim
1Lombardi Comprehensive Cancer Center, Georgetown University School of Medicine, Washington, DC 20057, USA.
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Xiaoyuan He
1Lombardi Comprehensive Cancer Center, Georgetown University School of Medicine, Washington, DC 20057, USA.
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Jie Liu
2Department of Genome Sciences, University of Washington, Seattle, WA 98195, USA.
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Zhijun Duan
3Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, WA 98195, USA.
4Division of Hematology, University of Washington, Seattle, WA 98195, USA.
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Taeyeon Kim
1Lombardi Comprehensive Cancer Center, Georgetown University School of Medicine, Washington, DC 20057, USA.
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Julia Gerard
1Lombardi Comprehensive Cancer Center, Georgetown University School of Medicine, Washington, DC 20057, USA.
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Brian Kim
1Lombardi Comprehensive Cancer Center, Georgetown University School of Medicine, Washington, DC 20057, USA.
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William S. Lane
5Mass Spectrometry and Proteomics Resource Laboratory, Harvard University, Cambridge, MA 02138, USA.
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William S. Noble
2Department of Genome Sciences, University of Washington, Seattle, WA 98195, USA.
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Bogdan Budnik
5Mass Spectrometry and Proteomics Resource Laboratory, Harvard University, Cambridge, MA 02138, USA.
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Todd Waldman
1Lombardi Comprehensive Cancer Center, Georgetown University School of Medicine, Washington, DC 20057, USA.
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  • For correspondence: waldmant@georgetown.edu
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Abstract

The cohesin complex regulates sister chromatid cohesion, chromosome organization, gene expression, and DNA repair. Here we report that endogenous human cohesin interacts with a panoply of splicing factors and RNA binding proteins, including diverse components of the U4/U6.U5 tri-snRNP complex and several splicing factors that are commonly mutated in cancer. The interactions are enhanced during mitosis, and the interacting splicing factors and RNA binding proteins follow the cohesin cycle and prophase pathway of regulated interactions with chromatin. Depletion of cohesin-interacting splicing factors results in stereotyped cell cycle arrests and alterations in genomic organization. These data support the hypothesis that splicing factors and RNA binding proteins control cell cycle progression and genomic organization via regulated interactions with cohesin and chromatin.

One Sentence Summary Endogenous tagging reveals that cohesin interacts with diverse chromatin-bound splicing factors that regulate cell cycle progression and genomic organization in human cells.

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Posted May 17, 2018.
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Cohesin interacts with a panoply of splicing factors required for cell cycle progression and genomic organization
Jung-Sik Kim, Xiaoyuan He, Jie Liu, Zhijun Duan, Taeyeon Kim, Julia Gerard, Brian Kim, William S. Lane, William S. Noble, Bogdan Budnik, Todd Waldman
bioRxiv 325209; doi: https://doi.org/10.1101/325209
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Cohesin interacts with a panoply of splicing factors required for cell cycle progression and genomic organization
Jung-Sik Kim, Xiaoyuan He, Jie Liu, Zhijun Duan, Taeyeon Kim, Julia Gerard, Brian Kim, William S. Lane, William S. Noble, Bogdan Budnik, Todd Waldman
bioRxiv 325209; doi: https://doi.org/10.1101/325209

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