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In-vitro Mutagenesis

In-vitro Mutagenesis

To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.

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Related Experiment Video

Updated: Dec 13, 2025

Generating CRISPR/Cas9 Mediated Monoallelic Deletions to Study Enhancer Function in Mouse Embryonic Stem Cells

Generating CRISPR/Cas9 Mediated Monoallelic Deletions to Study Enhancer Function in Mouse Embryonic Stem Cells

Published on: April 2, 2016

Brain transcriptome study through CRISPR/Cas9 mediated mouse Dip2c gene knock-out.

Zin Mar Oo¹, Salah Adlat¹, Rajiv Kumar Sah¹

¹Transgenic Research Center, School of Life Sciences, Northeast Normal University, Changchun, Jilin 130024, China.

|July 25, 2020

Summary

Researchers used CRISPR/Cas9 gene editing to create Dip2C knockout mice. This study reveals Dip2C regulates key genes involved in brain functions like memory and neural signaling.

Keywords:

CRISPR/Cas9 Dip2C knockout Transcriptome

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Last Updated: Dec 13, 2025

Generating CRISPR/Cas9 Mediated Monoallelic Deletions to Study Enhancer Function in Mouse Embryonic Stem Cells

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Published on: April 2, 2016

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Published on: June 24, 2022

Efficient Genome Editing of Mice by CRISPR Electroporation of Zygotes

Efficient Genome Editing of Mice by CRISPR Electroporation of Zygotes

Published on: December 16, 2022

Area of Science:

Neuroscience
Genetics
Molecular Biology

Background:

The biological functions of Dip2C, highly expressed in the brain, remain largely unknown.
Genes regulated by Dip2C in the brain have not been previously studied.

Purpose of the Study:

To generate targeted gene deletions of Dip2c in mice using the CRISPR/Cas9 system.
To investigate the brain transcriptome regulated by Dip2C.

Main Methods:

Utilized CRISPR/Cas9 technology for targeted large fragment deletion (Dip2C^Δ160kb) and small deletion (Dip2c^Δ2bp) in mice.
Confirmed gene expression loss via quantitative real-time PCR (qPCR).
Analyzed brain transcriptome changes using RNA sequencing (RNAseq) in Dip2c^Δ2bp mice.

Main Results:

Achieved efficient targeted large fragment deletions of the Dip2c gene with an average efficiency of 26.7%.
Identified 838 differentially expressed genes (DEGs) in the brain of Dip2c^Δ2bp mice (252 upregulated, 586 downregulated).
Gene Ontology and KEGG pathway analyses revealed enrichment in neurological functions, including 'memory', 'neuropeptide signaling pathway', and 'neuroactive ligand-receptor interaction pathway'.

Conclusions:

Dip2C plays a significant role in regulating genes associated with brain development and function.
Key Dip2C-regulated genes include Grid2ip, Grin2a, Grin2c, Grm4, and various GABA and glutamate receptor subunits.
This research provides novel insights into the molecular mechanisms underlying Dip2C's function in the brain.