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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.

Mouse Models of Cancer Study

Mouse Models of Cancer Study

Mice have long served as models for studying human biology and pathology because of their phylogenetic and physiological similarity with humans. They are also easy to maintain and breed in the laboratory, and hence, many inbred strains are now available for research. Studies on mice have contributed immeasurably to our understanding of cancer biology.
The development of transgenic, knockout, and knock-in mice has led to an exponential increase in their use as model organisms in research,...

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Related Experiment Video

Updated: Sep 18, 2025

Quantitative Analysis of Protein Expression to Study Lineage Specification in Mouse Preimplantation Embryos

Quantitative Analysis of Protein Expression to Study Lineage Specification in Mouse Preimplantation Embryos

Published on: February 22, 2016

Conditional knockout mouse model demonstrates that Copa expression is required for viability in development and

Timra Gilson¹, Jacob W Astroski¹, Wang Qun²

¹Indiana University School of Medicine, Department of Dermatology, 545 Barnhill Drive, Emerson Hall 139, Indianapolis, IN, 46202, United States.

Biochemical and Biophysical Research Communications

|June 24, 2025

Summary

This summary is machine-generated.

The COPI coatomer protein alpha subunit (Copa) is essential for cell survival, as its absence causes embryonic lethality in mice. Conditional knockout models reveal its critical role in maintaining neuronal health and preventing autoimmune-related endoplasmic reticulum stress.

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Evaluation of Planar-Cell-Polarity Phenotypes in Ciliopathy Mouse Mutant Cochlea

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Published on: February 21, 2016

Area of Science:

Cell Biology
Genetics
Immunology

Background:

The COPI coatomer complex regulates intracellular transport between the Golgi apparatus and Endoplasmic Reticulum (ER).
Mutations in the COPA gene, encoding the alpha subunit of COPI, are linked to an autoimmune disorder affecting multiple organs.
Understanding the function of Copa is crucial for elucidating its role in cellular homeostasis and disease pathogenesis.

Purpose of the Study:

To characterize a conditional-ready Copa knockout mouse model.
To investigate the in vivo consequences of Copa deletion in different cell types and developmental stages.
To explore the cellular mechanisms underlying COPA syndrome.

Main Methods:

Generation and characterization of conditional-ready Copa knockout mice.
Systemic and cell-specific deletion of Copa using Cre-lox technology.
In vitro culture of lung fibroblasts and Dorsal Root Ganglion neurons from knockout mice.
Analysis of STING signaling, ER stress, and neuronal viability.

Main Results:

Systemic homozygous deletion of Copa resulted in embryonic lethality.
Conditional deletion of Copa under the Mnx1 promoter allowed for viable adult mice with mild glucose intolerance.
Deletion of Copa in lung fibroblasts recapitulated COPA syndrome phenotypes, including STING hyperactivation and ER stress.
Copa expression is required for axonal arbor maintenance and survival of Dorsal Root Ganglion neurons.

Conclusions:

Copa is essential for embryonic development and cellular viability.
Conditional knockout models provide insights into tissue-specific functions of Copa.
Copa deficiency leads to STING pathway activation and ER stress, contributing to COPA syndrome.
Copa plays a vital role in neuronal maintenance and survival.