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Mouse Models of Cancer Study

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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.
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A Non-random Mouse Model for Pharmacological Reactivation of Mecp2 on the Inactive X Chromosome

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A mouse model for Meckel syndrome type 3.

Susan A Cook¹, Gayle B Collin, Roderick T Bronson

¹The Jackson Laboratory, Bar Harbor, Maine 04609, USA.

Journal of the American Society of Nephrology : JASN

|February 13, 2009

Summary

This summary is machine-generated.

A new mouse model with a Tmem67 gene deletion mimics Meckel-Gruber syndrome type 3 (MKS3), exhibiting polycystic kidney disease and hydrocephalus. This discovery aids research into primary cilia

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Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

Published on: July 3, 2020

Area of Science:

Genetics
Developmental Biology
Nephrology

Background:

Meckel-Gruber syndrome type 3 (MKS3) is a severe autosomal recessive disorder.
MKS3 is characterized by polycystic kidney disease, liver cysts, polydactyly, and brain abnormalities.
Defects in primary cilia are hypothesized to cause MKS3.

Purpose of the Study:

To describe a novel mouse model for Meckel-Gruber syndrome type 3.
To investigate the role of the Tmem67 gene in kidney development and primary cilia function.

Main Methods:

Spontaneous deletion of the mouse ortholog Tmem67.
Phenotypic characterization using microcomputed tomography, histology, scanning electron microscopy, and immunohistochemistry.
Transgenic rescue to verify the mutated gene.

Main Results:

The Tmem67 deletion mouse model exhibits polycystic kidney disease and premature death.
Hydrocephalus was observed in some Tmem67 mutant mice.
The study confirmed Tmem67 as the mutated gene responsible for the observed phenotype.

Conclusions:

The Tmem67 deletion mouse provides a valuable model for studying MKS3.
This model will advance understanding of the primary cilium's role in kidney development and disease.
Further research can explore therapeutic strategies for MKS3 and related ciliopathies.