Search Results
You are looking at 1 - 1 of 1 items for
- Author: Blair Walker x
- Refine by access: Content accessible to me x
Department of Sciences, University of British Columbia, Vancouver, Canada
Search for other papers by Celia Siu in
Google Scholar
PubMed
Search for other papers by Sam Wiseman in
Google Scholar
PubMed
Search for other papers by Sitanshu Gakkhar in
Google Scholar
PubMed
Search for other papers by Alireza Heravi-Moussavi in
Google Scholar
PubMed
Search for other papers by Misha Bilenky in
Google Scholar
PubMed
Search for other papers by Annaick Carles in
Google Scholar
PubMed
Search for other papers by Thomas Sierocinski in
Google Scholar
PubMed
Search for other papers by Angela Tam in
Google Scholar
PubMed
Search for other papers by Eric Zhao in
Google Scholar
PubMed
Search for other papers by Katayoon Kasaian in
Google Scholar
PubMed
Search for other papers by Richard A Moore in
Google Scholar
PubMed
Search for other papers by Andrew J Mungall in
Google Scholar
PubMed
Search for other papers by Blair Walker in
Google Scholar
PubMed
Search for other papers by Thomas Thomson in
Google Scholar
PubMed
Department of Medical Genetics, University of British Columbia, Vancouver, Canada
Search for other papers by Marco A Marra in
Google Scholar
PubMed
Department of Microbiology & Immunology, Michael Smith Laboratories, University of British Columbia, Vancouver, Canada
Search for other papers by Martin Hirst in
Google Scholar
PubMed
Department of Medical Genetics, University of British Columbia, Vancouver, Canada
Department of Molecular Biology & Biochemistry, Simon Fraser University, Burnaby, Canada
Search for other papers by Steven J M Jones in
Google Scholar
PubMed
The thyroid gland, necessary for normal human growth and development, functions as an essential regulator of metabolism by the production and secretion of appropriate levels of thyroid hormone. However, assessment of abnormal thyroid function may be challenging suggesting a more fundamental understanding of normal function is needed. One way to characterize normal gland function is to study the epigenome and resulting transcriptome within its constituent cells. This study generates the first published reference epigenomes for human thyroid from four individuals using ChIP-seq and RNA-seq. We profiled six histone modifications (H3K4me1, H3K4me3, H3K27ac, H3K36me3, H3K9me3, H3K27me3), identified chromatin states using a hidden Markov model, produced a novel quantitative metric for model selection and established epigenomic maps of 19 chromatin states. We found that epigenetic features characterizing promoters and transcription elongation tend to be more consistent than regions characterizing enhancers or Polycomb-repressed regions and that epigenetically active genes consistent across all epigenomes tend to have higher expression than those not marked as epigenetically active in all epigenomes. We also identified a set of 18 genes epigenetically active and consistently expressed in the thyroid that are likely highly relevant to thyroid function. Altogether, these epigenomes represent a powerful resource to develop a deeper understanding of the underlying molecular biology of thyroid function and provide contextual information of thyroid and human epigenomic data for comparison and integration into future studies.
