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A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer

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A mouse model engineered to conditionally express the progesterone receptor-B isoform.

Lan Hai¹, Maria M Szwarc¹, Margeaux Wetendorf²

¹Department of Molecular & Cellular Biology, Baylor College of Medicine, Houston, Texas.

Genesis (New York, N.Y. : 2000)

|July 14, 2018

Summary

A new transgenic mouse model allows conditional expression of progesterone receptor-B (PGR-B). Overexpression in mammary glands caused abnormal development and lactation failure, demonstrating PGR-B

Keywords:

differentiation isoform lactation mammary gland mouse progesterone receptor-B proliferation transgenic

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Published on: August 12, 2014

Area of Science:

Reproductive biology
Developmental biology
Genetics

Background:

The progesterone receptor (PR) is crucial for reproductive functions.
The progesterone receptor-B (PGR-B) isoform plays a key role in mammary gland development and function.
Understanding PGR-B's specific roles requires precise genetic tools.

Purpose of the Study:

To generate and validate a novel transgenic mouse model for conditional PGR-B expression.
To investigate the functional consequences of PGR-B overexpression in the mammary gland.

Main Methods:

Utilized Rosa26 gene targeting in mouse embryonic stem cells to create the Pgr-B^LSL mouse.
Crossed Pgr-B^LSL mice with MMTV-CREA mice to generate PR-B:OE bigenic mice.
Analyzed mammary gland morphology, proliferation, and lactation in PR-B:OE mice.

Main Results:

Transgene-derived PGR-B protein was specifically targeted to the virgin mammary gland epithelium.
PR-B:OE mice exhibited abnormal mammary morphogenesis, including dilated ducts and precocious branching.
Mammary glands in PR-B:OE mice failed terminal differentiation and lactation, leading to neonatal death.

Conclusions:

The Pgr-B^LSL mouse is a valuable tool for studying PGR-B function in various progesterone-responsive systems.
PGR-B overexpression disrupts normal mammary gland development and lactation.
This model facilitates research into the physiological and pathophysiological roles of PGR-B.