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Naming Genetically Engineered Mice (Part II): From Being Understandable to Being Written Correctly

2026-10-29

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2026 CKM Guidelines Released: Chronic Diseases Enter the Era of Integrated Cardiorenal-Metabolic Management—It’s Time to Rethink Animal Models

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A Guide to Safe Mouse Handling | Manual on Mouse Transport Protocols and Troubleshooting

[Mouse Strain Analysis] Why do APP/PS1 transgenic mice “change color”? Decoding strain origins through coat color.

　　In the field of Alzheimer’s disease (AD) research, APP/PS1 double-transgenic mice are indispensable “model warriors” for scientists. They have been engineered to express mutant genes associated with familial AD in humans—namely, the amyloid precursor protein (APP) and presenilin 1 (PS1)—thereby accelerating the formation of β‑amyloid (Aβ) plaques in the brain and mimicking the core pathological hallmarks of the disease.

　　For more detailed information, please refer to previous introductions.

　　Key Insights | APP/PS1 Double-Transgenic Mice: Cognitive Function, Hippocampal β‑Aβ, and Telomere Length—Everything You Want to Know Is Right Here!

　　If you’ve worked with this strain, you’ll notice that even among APP/PS1 mice, there is indeed a distinction between black and…

　　Mouse gray (Agouti) in two colors.

　　To begin with the conclusion: the coat color differences (black versus gray) observed in APP/PS1 transgenic mice arise from the hybrid nature of their genetic background strains, but the coat color itself does not directly influence the core pathological processes of Alzheimer’s disease (AD).

　　| Coat Color Characteristics of the Base Strain

　　The ASIP gene is a key genetic factor in the determination of animal coat color, primarily influencing hair coloration by regulating the synthesis and distribution of melanin.

　　Image source: [1]

　　C57BL/6 (B6):

　　C57BL/6 (B6) inbred mice have a standard black coat color. Their coat color is primarily determined by the following genotypes:

　　Image source: Aniphe BioLab

　　A Locus (ASIP gene): Typically a/a (homozygous recessive), allowing eumelanin (black/brown pigment) to be expressed throughout the body.

　　B Locus (TYRP1 gene): Typically B/B (homozygous dominant), resulting in black eumelanin.

　　C Locus (TYR gene): Typically C/C (homozygous dominant), with normal tyrosinase function and sufficient melanin synthesis.

　　Therefore, B6 is the standard black mouse (a/a, B/B, C/C).

　　C3H/HeJ (C3H):

　　C3H/HeJ (C3H) inbred mice have a standard coat color of agouti gray. Their key coat-color genotype is:

　　Image source: Aniphe BioLab

　　A Locus (ASIP gene): A/A or A/a (dominant). The ASIP protein inhibits eumelanin synthesis, resulting in a “banded” appearance of the hair shaft—black at the tip, yellow/brown along the midshaft, and gray at the root—characteristic of the “mouse‑gray” phenotype.

　　Therefore, C3H is the standard mouse gray color (A/A or A/a).

　　| The Root Cause of Coat Color Segregation

　　In the “C57BL/6;C3H” hybrid background, the key genes determining coat color—particularly the A locus and the B locus—are not fixed homozygous in the population.

　　A Locus (ASIP gene) is key:

　　B6 contributes the a allele (recessive, permitting black coloration throughout the body).

　　C3H contributes the A allele (dominant, resulting in mouse gray color).

　　In breeding populations with mixed backgrounds:

　　Image source: Aniphe BioLab

　　If a mouse inherits the a allele from both parents (a/a), the ASIP protein is either not expressed or nonfunctional, allowing eumelanin to be expressed throughout the body (with coat color determined by the B locus).

　　If a mouse inherits at least one A allele (A/A or A/a), the ASIP protein becomes active, inhibiting eumelanin synthesis and resulting in yellow/brown bands along the hair shaft, giving rise to the agouti phenotype.

　　| Impact on research—coat color is unrelated to AD pathology

　　The coat color gene (A or a allele) is located on a different chromosome and is independent of the integration sites of the APP and PS1 transgenes.

　　Black or mouse‑gray APP/PS1 mice, so long as they carry the transgene, will develop the expected Aβ plaque pathology and associated cognitive deficits. Fur color is merely a visible, randomly segregating marker within the background genome.

　　Both coat-color variants of mice serve as valid AD models, and the difference in coat color itself does not compromise their core utility in recapitulating Aβ pathology.

　　Summary

　　Aniphe BioLab has established a comprehensive and systematic library of AD mouse models, including APP/Ps1 mice, 3×Tg‑AD mice, 5×FAD mice, Tau P301S mice, APOE4 mice, and more. Models are available in stock across all age groups. Please feel free to inquire.

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　　References:

　　[1] Zheng Linan, Yu Ruwang. Epigenetic Molecular Mechanisms of Mouse Coat Color [J]. Biology Teaching, 2024, 49(11): 2–4.

　　[2] He Xiaodan. Analysis of the Association Between the Agouti Gene and Coat Color Phenotype in Mice, and Investigation of Its Genetic Variations [D]. Donghua University, 2014.

Multivariate Modeling Platform for Recurrent Psoriasis: Recreating Lesional Pathological Features to Accelerate Dermatological Drug Validation

J Exp Med (5): Combined CRISPR Perturbation Screening—When Multiple Genes Are Altered Simultaneously, How Do We Unravel the True Causal Networks of Living Systems?