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Updated: Jul 4, 2025
Differentiation and Characterization of Neural Progenitors and Neurons from Mouse Embryonic Stem Cells
Published on: May 15, 2020
Transcriptomic profiling of Dip2a in the neural differentiation of mouse embryonic stem cells
Mingze Yao1, Lei Zhang1,2, Xiaojuan Teng3
1Institutes of Biomedical Sciences, Shanxi Provincial Key Laboratory for Medical Molecular Cell Biology, Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education, Shanxi University, Taiyuan 030006, China.
Introduction:
The disconnected-interacting protein 2 homolog A (DIP2A), a member of disconnected-interacting 2 protein family, has been shown to be involved in human nervous system-related mental illness. This protein is highly expressed in the nervous system of mouse. Mutation of mouse DIP2A causes defects in spine morphology and synaptic transmission, autism-like behaviors, and defective social novelty [5], [27], indicating that DIP2A is critical to the maintenance of neural development. However, the role of DIP2A in neural differentiation has yet to be investigated.
Objective:
To determine the role of DIP2A in neural differentiation, a neural differentiation model was established using mouse embryonic stem cells (mESCs) and studied by using gene-knockout technology and RNA-sequencing-based transcriptome analysis.
Results:
We found that DIP2A is not required for mESCs pluripotency maintenance, but loss of DIP2A causes the neural differentiation abnormalities in both N2B27 and KSR medium. Functional knockout of Dip2a gene also decreased proliferation of mESCs by perturbation of the cell cycle and profoundly inhibited the expression of a large number of neural development-associated genes which mainly enriched in spinal cord development and postsynapse assembly.
Conclusions:
The results of this report demonstrate that DIP2A plays an essential role in regulating differentiation of mESCs towards the neural fate.
