TRPC3 is required for the survival, pluripotency and neural differentiation of mouse embryonic stem cells (mESCs)

Research output: Journal Publications and Reviews (RGC: 21, 22, 62)21_Publication in refereed journal

2 Scopus Citations
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Author(s)

  • Helen Baixia Hao
  • Sarah E. Webb
  • Marc Moreau
  • Catherine Leclerc
  • Andrew L. Miller

Related Research Unit(s)

Detail(s)

Original languageEnglish
Pages (from-to)253-265
Journal / PublicationScience China Life Sciences
Volume61
Issue number3
Online published31 Jan 2018
Publication statusPublished - Mar 2018

Abstract

Transient receptor potential canonical subfamily member 3 (TRPC3) is known to be important for neural development and the formation of neuronal networks. Here, we investigated the role of TRPC3 in undifferentiated mouse embryonic stem cells (mESCs) and during the differentiation of mESCs into neurons. CRISPR/Cas9-mediated knockout (KO) of TRPC3 induced apoptosis and the disruption of mitochondrial membrane potential both in undifferentiated mESCs and in those undergoing neural differentiation. In addition, TRPC3 KO impaired the pluripotency of mESCs. TRPC3 KO also dramatically repressed the neural differentiation of mESCs by inhibiting the expression of markers for neural progenitors, neurons, astrocytes and oligodendrocytes. Taken together, our new data demonstrate an important function of TRPC3 with regards to the survival, pluripotency and neural differentiation of mESCs.

Research Area(s)

  • apoptosis, CRISPR/Cas9, mitochondrial membrane potential, mouse embryonic stem cells (mESCs), neuron differentiation, pluripotency, transient receptor potential canonical subfamily member 3 (TRPC3)

Citation Format(s)

TRPC3 is required for the survival, pluripotency and neural differentiation of mouse embryonic stem cells (mESCs). / Hao, Helen Baixia; Webb, Sarah E.; Yue, Jianbo; Moreau, Marc; Leclerc, Catherine; Miller, Andrew L.

In: Science China Life Sciences, Vol. 61, No. 3, 03.2018, p. 253-265.

Research output: Journal Publications and Reviews (RGC: 21, 22, 62)21_Publication in refereed journal