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Related Experiment Video

Updated: Dec 11, 2025

Forward Genetic Approach to Uncover Stress Resistance Genes in Mice — A High-throughput Screen in ES Cells

Forward Genetic Approach to Uncover Stress Resistance Genes in Mice — A High-throughput Screen in ES Cells

Published on: November 11, 2015

Dominant atopy risk mutations identified by mouse forward genetic analysis.

Jeffrey A SoRelle^1,2, Zhe Chen¹, Jianhui Wang¹

¹Center for the Genetics of Host Defense, University of Texas Southwestern Medical Center, Dallas, TX, USA.

|August 19, 2020

Summary

Genetic mutations can cause atopy, a tendency to develop allergies. Researchers identified genes that regulate immunoglobulin E (IgE) production in mice, finding that up to 37% of people may carry risk mutations.

Keywords:

IgE IgG1 allergy atopy papain

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Last Updated: Dec 11, 2025

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A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging

A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging

Published on: July 14, 2016

Area of Science:

Immunology
Genetics
Allergy Research

Background:

Atopy, the tendency to develop allergic sensitization, is heritable but rarely linked to specific gene mutations.
Atopic individuals exhibit elevated immunoglobulin E (IgE) responses to allergens.
Understanding the genetic basis of atopy is crucial for developing targeted therapies.

Purpose of the Study:

To identify genes contributing to atopy through a forward genetic screen in mice.
To investigate the genetic factors influencing aberrant IgE and IgG1 production in response to allergens.

Main Methods:

Conducted a forward genetic screen using N-ethyl-N-nitrosourea (ENU)-induced mutations in mice.
Assessed antigen-specific IgE and IgG1 production following papain immunization.
Validated candidate genes through independent mutation analysis.

Main Results:

Verified the effects of mutations in 23 out of 31 candidate genes on IgE or IgG1 responses.
Identified 20 genes influencing IgE response, with 8 being necessary and 12 repressing IgE.
Discovered nine novel genes involved in the IgE response, with five genes' roles (Flcn, Map1lc3b, Me2, Prkd2, Scarb2) requiring further investigation.
Found that loss-of-function mutations in nine IgE-limiting genes were dominant or semi-dominant, without causing immunodeficiency in heterozygotes.

Conclusions:

Up to 37% of the human population may be heterozygous carriers of at least one dominant atopy risk mutation.
This study provides significant insights into the genetic architecture of atopy.
Identified novel genetic factors that could be targets for future allergy treatments.