摘要
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.
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 oligo- dendrocytes. Taken together, our new data demonstrate an important function of TRPC3 with regards to the survival, plur- ipotency and neural differentiation of mESCs.
基金
supported by the Hong Kong Research Grants Council(RGC)General Research Fund awards(662113,16101714,16100115)
the ANR/RGC joint research scheme award(AHKUST601/13)
the Hong Kong Theme-based Research Scheme award(T13-706/11-1)
the Hong Kong Innovation and Technology Commission(ITCPD/17-9)
