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Survival motor neuron (SMN) plays important roles in snRNP assembly and mRNA splicing. Deficiency of SMN causes spinal muscular atrophy (SMA), a leading genetic disease causing childhood mortality. Previous studies have shown that SMN regulates stem cell self-renewal and pluripotency in Drosophila and mouse and is abundantly expressed in mouse embryonic stem cells. However, whether SMN is required for establishment of pluripotency is unclear. In this study, we show that SMN is gradually upregulated in preimplantation mouse embryos and cultured cells undergoing cell reprogramming. Ectopic expression of SMN increased cell reprogramming efficiency, whereas knockdown of SMN impeded induced pluripotent stem cell (iPSC) colony formation. iPSCs could be derived from SMA model mice, but impairment in differentiation capacity may be present. The ectopic overexpression of SMN in iPSCs can upregulate the expression levels of some pluripotent genes and restore the neuronal differentiation capacity of SMA-iPSCs. Taken together, our findings not only demonstrate the functional relevance of SMN in establishment of cell pluripotency but also propose its potential application in facilitating iPSC derivation.

Original publication

DOI

10.1089/scd.2022.0091

Type

Journal article

Journal

Stem Cells Dev

Publication Date

11/2022

Volume

31

Pages

696 - 705

Keywords

induced pluripotent stem cells, neuronal differentiation, somatic cell reprogramming, spinal muscular atrophy, survival motor neuron, Animals, Mice, Cellular Reprogramming, Motor Neurons, Muscular Atrophy, Spinal, Induced Pluripotent Stem Cells, Gene Expression