IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v9y2018i1d10.1038_s41467-018-05856-4.html
   My bibliography  Save this article

FOXD1-dependent MICU1 expression regulates mitochondrial activity and cell differentiation

Author

Listed:
  • Santhanam Shanmughapriya

    (Lewis Katz School of Medicine at Temple University
    Lewis Katz School of Medicine at Temple University)

  • Dhanendra Tomar

    (Lewis Katz School of Medicine at Temple University
    Lewis Katz School of Medicine at Temple University)

  • Zhiwei Dong

    (Lewis Katz School of Medicine at Temple University
    Lewis Katz School of Medicine at Temple University)

  • Katherine J. Slovik

    (University of Pennsylvania)

  • Neeharika Nemani

    (Lewis Katz School of Medicine at Temple University
    Lewis Katz School of Medicine at Temple University)

  • Kalimuthusamy Natarajaseenivasan

    (Lewis Katz School of Medicine at Temple University
    Lewis Katz School of Medicine at Temple University)

  • Edmund Carvalho

    (Lewis Katz School of Medicine at Temple University
    Lewis Katz School of Medicine at Temple University)

  • Christy Lu

    (Lewis Katz School of Medicine at Temple University
    Lewis Katz School of Medicine at Temple University)

  • Kaitlyn Corrigan

    (Lewis Katz School of Medicine at Temple University
    Lewis Katz School of Medicine at Temple University)

  • Venkata Naga Srikanth Garikipati

    (Lewis Katz School of Medicine at Temple University)

  • Jessica Ibetti

    (Lewis Katz School of Medicine at Temple University)

  • Sudarsan Rajan

    (Lewis Katz School of Medicine at Temple University
    Lewis Katz School of Medicine at Temple University)

  • Carlos Barrero

    (Temple University)

  • Kurt Chuprun

    (Lewis Katz School of Medicine at Temple University)

  • Raj Kishore

    (Lewis Katz School of Medicine at Temple University
    Lewis Katz School of Medicine at Temple University)

  • Salim Merali

    (Temple University)

  • Ying Tian

    (Lewis Katz School of Medicine at Temple University)

  • Wenli Yang

    (University of Pennsylvania)

  • Muniswamy Madesh

    (Lewis Katz School of Medicine at Temple University
    Lewis Katz School of Medicine at Temple University
    University of Texas Health San Antonio)

Abstract

Although many factors contribute to cellular differentiation, the role of mitochondria Ca2+ dynamics during development remains unexplored. Because mammalian embryonic epiblasts reside in a hypoxic environment, we intended to understand whether mCa2+ and its transport machineries are regulated during hypoxia. Tissues from multiple organs of developing mouse embryo evidenced a suppression of MICU1 expression with nominal changes on other MCU complex components. As surrogate models, we here utilized human embryonic stem cells (hESCs)/induced pluripotent stem cells (hiPSCs) and primary neonatal myocytes to delineate the mechanisms that control mCa2+ and bioenergetics during development. Analysis of MICU1 expression in hESCs/hiPSCs showed low abundance of MICU1 due to its direct repression by Foxd1. Experimentally, restoration of MICU1 established the periodic cCa2+ oscillations and promoted cellular differentiation and maturation. These findings establish a role of mCa2+ dynamics in regulation of cellular differentiation and reveal a molecular mechanism underlying this contribution through differential regulation of MICU1.

Suggested Citation

  • Santhanam Shanmughapriya & Dhanendra Tomar & Zhiwei Dong & Katherine J. Slovik & Neeharika Nemani & Kalimuthusamy Natarajaseenivasan & Edmund Carvalho & Christy Lu & Kaitlyn Corrigan & Venkata Naga Sr, 2018. "FOXD1-dependent MICU1 expression regulates mitochondrial activity and cell differentiation," Nature Communications, Nature, vol. 9(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-05856-4
    DOI: 10.1038/s41467-018-05856-4
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/s41467-018-05856-4
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/s41467-018-05856-4?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-05856-4. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.