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A role for YY1 in sex-biased transcription revealed through X-linked promoter activity and allelic binding analyses

View ORCID ProfileChih-yu Chen, Wenqiang Shi, Allison M. Matthews, Yifeng Li, David J. Arenillas, Anthony Mathelier, Masayoshi Itoh, Hideya Kawaji, Timo Lassmann, FANTOM Consortium, Yoshihide Hayashizaki, Piero Carninci, Alistair R. R. Forrest, Carolyn J. Brown, View ORCID ProfileWyeth W. Wasserman
doi: https://doi.org/10.1101/044172
Chih-yu Chen
1Centre for Molecular Medicine and Therapeutics, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada
2Graduate Program in Bioinformatics, University of British Columbia, Vancouver,British Columbia, Canada
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  • ORCID record for Chih-yu Chen
Wenqiang Shi
1Centre for Molecular Medicine and Therapeutics, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada
2Graduate Program in Bioinformatics, University of British Columbia, Vancouver,British Columbia, Canada
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Allison M. Matthews
1Centre for Molecular Medicine and Therapeutics, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada
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Yifeng Li
1Centre for Molecular Medicine and Therapeutics, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada
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David J. Arenillas
1Centre for Molecular Medicine and Therapeutics, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada
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Anthony Mathelier
1Centre for Molecular Medicine and Therapeutics, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada
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Masayoshi Itoh
3RIKEN Omics Science Center, Yokohama, Japan
4RIKEN Center for Life Science Technologies, Division of Genomic Technologies,Yokohama, Japan
5RIKEN Preventive Medicine and Diagnosis Innovation Program, Wako, Saitama, Japan
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Hideya Kawaji
3RIKEN Omics Science Center, Yokohama, Japan
4RIKEN Center for Life Science Technologies, Division of Genomic Technologies,Yokohama, Japan
5RIKEN Preventive Medicine and Diagnosis Innovation Program, Wako, Saitama, Japan
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Timo Lassmann
3RIKEN Omics Science Center, Yokohama, Japan
4RIKEN Center for Life Science Technologies, Division of Genomic Technologies,Yokohama, Japan
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Yoshihide Hayashizaki
3RIKEN Omics Science Center, Yokohama, Japan
5RIKEN Preventive Medicine and Diagnosis Innovation Program, Wako, Saitama, Japan
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Piero Carninci
3RIKEN Omics Science Center, Yokohama, Japan
4RIKEN Center for Life Science Technologies, Division of Genomic Technologies,Yokohama, Japan
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Alistair R. R. Forrest
3RIKEN Omics Science Center, Yokohama, Japan
4RIKEN Center for Life Science Technologies, Division of Genomic Technologies,Yokohama, Japan
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Carolyn J. Brown
6Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada
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  • For correspondence: wyeth@cmmt.ubc.ca carolyn.brown@ubc.ca
Wyeth W. Wasserman
1Centre for Molecular Medicine and Therapeutics, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada
6Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada
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  • ORCID record for Wyeth W. Wasserman
  • For correspondence: wyeth@cmmt.ubc.ca carolyn.brown@ubc.ca
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Abstract

Sex differences in susceptibility and progression have been reported in numerous diseases. Female cells have two copies of the X chromosome with X-chromosome inactivation imparting mono-allelic gene silencing for dosage compensation. However, a subset of genes, named escapees, escape silencing and are transcribed bi-allelically resulting in sexual dimorphism. Here we conducted analyses of the sexes using human datasets to gain perspectives in such regulation. We identified transcription start sites of escapees (escTSSs) based on higher transcription levels in female cells using FANTOM5 CAGE data. Significant over-representations of YY1 transcription factor binding motif and ChIP-seq peaks around escTSSs highlighted its positive association with escapees. Furthermore, YY1 occupancy is significantly biased towards the inactive X (Xi) at long non-coding RNA loci that are frequent contacts of Xi-specific superloops. Our study elucidated the importance of YY1 on transcriptional activity on Xi in general through sequence-specific binding, and its involvement at superloop anchors.

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Posted March 21, 2016.
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A role for YY1 in sex-biased transcription revealed through X-linked promoter activity and allelic binding analyses
Chih-yu Chen, Wenqiang Shi, Allison M. Matthews, Yifeng Li, David J. Arenillas, Anthony Mathelier, Masayoshi Itoh, Hideya Kawaji, Timo Lassmann, FANTOM Consortium, Yoshihide Hayashizaki, Piero Carninci, Alistair R. R. Forrest, Carolyn J. Brown, Wyeth W. Wasserman
bioRxiv 044172; doi: https://doi.org/10.1101/044172
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A role for YY1 in sex-biased transcription revealed through X-linked promoter activity and allelic binding analyses
Chih-yu Chen, Wenqiang Shi, Allison M. Matthews, Yifeng Li, David J. Arenillas, Anthony Mathelier, Masayoshi Itoh, Hideya Kawaji, Timo Lassmann, FANTOM Consortium, Yoshihide Hayashizaki, Piero Carninci, Alistair R. R. Forrest, Carolyn J. Brown, Wyeth W. Wasserman
bioRxiv 044172; doi: https://doi.org/10.1101/044172

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