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Placental genomics mediates genetic associations with complex health traits and disease

Author

Listed:
  • Arjun Bhattacharya

    (University of California
    University of California)

  • Anastasia N. Freedman

    (University of North Carolina)

  • Vennela Avula

    (University of North Carolina)

  • Rebeca Harris

    (University of North Carolina)

  • Weifang Liu

    (University of North Carolina)

  • Calvin Pan

    (University of California)

  • Aldons J. Lusis

    (University of California
    University of California
    University of California)

  • Robert M. Joseph

    (Boston University School of Medicine)

  • Lisa Smeester

    (University of North Carolina
    University of North Carolina
    University of North Carolina)

  • Hadley J. Hartwell

    (University of North Carolina)

  • Karl C. K. Kuban

    (Boston University Medical Center)

  • Carmen J. Marsit

    (Rollins School of Public Health Emory University)

  • Yun Li

    (University of North Carolina
    University of North Carolina
    University of North Carolina)

  • T. Michael O’Shea

    (University of North Carolina)

  • Rebecca C. Fry

    (University of North Carolina
    University of North Carolina
    University of North Carolina)

  • Hudson P. Santos

    (University of North Carolina
    University of North Carolina)

Abstract

As the master regulator in utero, the placenta is core to the Developmental Origins of Health and Disease (DOHaD) hypothesis but is historically understudied. To identify placental gene-trait associations (GTAs) across the life course, we perform distal mediator-enriched transcriptome-wide association studies (TWAS) for 40 traits, integrating placental multi-omics from the Extremely Low Gestational Age Newborn Study. At $$P \;

Suggested Citation

  • Arjun Bhattacharya & Anastasia N. Freedman & Vennela Avula & Rebeca Harris & Weifang Liu & Calvin Pan & Aldons J. Lusis & Robert M. Joseph & Lisa Smeester & Hadley J. Hartwell & Karl C. K. Kuban & Car, 2022. "Placental genomics mediates genetic associations with complex health traits and disease," Nature Communications, Nature, vol. 13(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-28365-x
    DOI: 10.1038/s41467-022-28365-x
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    References listed on IDEAS

    as
    1. Nicholas Mancuso & Simon Gayther & Alexander Gusev & Wei Zheng & Kathryn L. Penney & Zsofia Kote-Jarai & Rosalind Eeles & Matthew Freedman & Christopher Haiman & Bogdan Pasaniuc, 2018. "Large-scale transcriptome-wide association study identifies new prostate cancer risk regions," Nature Communications, Nature, vol. 9(1), pages 1-11, December.
    2. Jeffrey T Leek & John D Storey, 2007. "Capturing Heterogeneity in Gene Expression Studies by Surrogate Variable Analysis," PLOS Genetics, Public Library of Science, vol. 3(9), pages 1-12, September.
    3. Chen Cao & Bowei Ding & Qing Li & Devin Kwok & Jingjing Wu & Quan Long, 2021. "Power analysis of transcriptome-wide association study: Implications for practical protocol choice," PLOS Genetics, Public Library of Science, vol. 17(2), pages 1-20, February.
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    Cited by:

    1. Gianluca Ursini & Pasquale Di Carlo & Sreya Mukherjee & Qiang Chen & Shizhong Han & Jiyoung Kim & Maya Deyssenroth & Carmen J. Marsit & Jia Chen & Ke Hao & Giovanna Punzi & Daniel R. Weinberger, 2023. "Prioritization of potential causative genes for schizophrenia in placenta," Nature Communications, Nature, vol. 14(1), pages 1-17, December.
    2. Jennifer P. Nguyen & Timothy D. Arthur & Kyohei Fujita & Bianca M. Salgado & Margaret K. R. Donovan & Hiroko Matsui & Ji Hyun Kim & Agnieszka D’Antonio-Chronowska & Matteo D’Antonio & Kelly A. Frazer, 2023. "eQTL mapping in fetal-like pancreatic progenitor cells reveals early developmental insights into diabetes risk," Nature Communications, Nature, vol. 14(1), pages 1-22, December.

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