FOXD1-dependent MICU1 expression regulates mitochondrial activity and cell differentiation

Santhanam Shanmughapriya (), Dhanendra Tomar, Zhiwei Dong, Katherine J. Slovik, Neeharika Nemani, Kalimuthusamy Natarajaseenivasan, Edmund Carvalho, Christy Lu, Kaitlyn Corrigan, Venkata Naga Srikanth Garikipati, Jessica Ibetti, Sudarsan Rajan, Carlos Barrero, Kurt Chuprun, Raj Kishore, Salim Merali, Ying Tian, Wenli Yang () and Muniswamy Madesh ()
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Santhanam Shanmughapriya: Lewis Katz School of Medicine at Temple University
Dhanendra Tomar: Lewis Katz School of Medicine at Temple University
Zhiwei Dong: Lewis Katz School of Medicine at Temple University
Katherine J. Slovik: University of Pennsylvania
Neeharika Nemani: Lewis Katz School of Medicine at Temple University
Kalimuthusamy Natarajaseenivasan: Lewis Katz School of Medicine at Temple University
Edmund Carvalho: Lewis Katz School of Medicine at Temple University
Christy Lu: Lewis Katz School of Medicine at Temple University
Kaitlyn Corrigan: 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
Carlos Barrero: Temple University
Kurt Chuprun: Lewis Katz School of Medicine at Temple University
Raj Kishore: 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

Nature Communications, 2018, vol. 9, issue 1, 1-12

Abstract: 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.

Date: 2018
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DOI: 10.1038/s41467-018-05856-4

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