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Mouse Classroom | Introduction to the Genotypes of Transgenic Mice and ApoE Knockout Mice

Recently, many researchers have been puzzled by the genotypes of certain mouse strains. To address this, we’ve launched a new column—“Mouse Classroom”—to provide a concise overview of mouse genotypes and phenotypes. In this installment, we’ll introduce the APP/Ps1/tau triple-transgenic mice and the (B6) ApoE knockout mice.

 

APP/Ps1/tau (three-transgenic) mice

The full name of the triple-transgenic mouse is: B6;129-Tg(APPSwe,tauP301L)1Lfa Psen1 tm1Mpm /Mmj. We often refer to it as the APP/Ps1/tau mouse or the triple-transgenic mouse. The strain’s genetic background is B6129SF2/J, which corresponds to an F2 cross between C57BL/6 and 129S mice; the construction process is illustrated in the figure.

Figure 1: Workflow for generating triple-transgenic mice

(Image sourced from the internet)

The three‑turn mouse is characterized by two alleles. Psen1tm1Mpm It is composed of Tg(APPSwe,tauP301L)1Lfa; these two alleles harbor multiple variants in related genes. Transgene expression is driven by the Thy1 (Thy1.2) regulatory element.

 

Detailed genotype information:

Psen1tm1Mpm

Name: presenilin 1; targeted mutation 1, Mark P Mattson

Alias: PS1M146VKI -  ;PS1M146V ;PS-1 M146V KI ;PS1KI

Type: Allele

Chromosome location: Chromosome 12

Site alteration: targeted mutation

MGI ID: MGI:1930937

Psen1

Name: presenilin 1

Alias: S182; presenilin-1; PS-1; Ad3h; PS1

Type: Gene

Chromosome location: Chromosome 12

Site alteration: targeted mutation

MGI ID: MGI:1202717

NCBI accession number: 19164

Thy1

Name: thymus cell antigen 1; theta

Alternative names: T25; Thy1.1; Thy1.2; Thy-1.2; CD90; Thy-1; Thy1.2

Type: Gene

Chromosomal location: Chromosome 9

Site alteration: targeted mutation

MGI Number: 98747

NCBI accession number: 21838

MATP

Name: microtubule-associated protein tau

Type: Gene

Chromosomal location: Chromosome 17

Site alteration: targeted mutation

APP

Name: amyloid beta precursor protein

Type: Gene

Chromosome location: Chromosome 21

Site alteration: targeted mutation

Tg(APPSwe,tauP301L)1Lfa

Name: transgene insertion 1; Frank M LaFerla

Alias: Tg(APP*Swe,MAPT*P301L)1Lfa

Type: Genetically Modified

Chromosomal location: unknown

MGI Number: 2672831

 

The influence of genotype on phenotype:

Homozygote:

Homozygous mice carrying the three transgenes are viable and fertile.

This mouse begins to exhibit cognitive deficits at 4 months of age.

Amyloid‑β peptide deposition can be observed at 6 months of age (it may begin as early as 3–4 months, though it is not yet detectable), followed by the appearance of neurofibrillary tangles in the hippocampus and cortex, and senile plaques in the frontal cortex.

Between 12 and 15 months, conformational changes and aggregates of hyperphosphorylated tau protein were detected in the hippocampus.

Heterozygote : The heterozygous transgenic phenotype is similar to that of the homozygous genotype.

Heterozygote : The heterozygous knockout phenotype is similar to that of the wild type.

Note: A hemizygote refers to a male carrying a mutation on the X chromosome, or to a mouse of either sex that carries an inserted transgene without a homologous allele on the other chromosome.

 

(B6) ApoE mice

ApoE mouse, full name: B6.129P2- Apoe tm1Unc /J. We often refer to these mice simply as ApoE mice, which are used to study cardiovascular diseases, atherosclerosis, lipid metabolism–related disorders, and the role of ApoE in Alzheimer’s disease, among other topics.

Detailed genotype information:

Apoe tm1Unc

Name: Apolipoprotein E; Target Mutation 1

Alternative names: EKO; ApoE-KO; APOE KO; apoE0; Apoe tm1Un; AopE(-); mEKO; mE -,

Type: Allele

Chromosomal location: Chromosome 7

Site alteration: knockout

MGI Number: 1857129

APOE

Name: Apolipoprotein E

Alias: Apoe

Type: Gene

Chromosomal location: Chromosome 7

Gene modification method: knockout

MGI Number: 88057

NCBI accession number: 11816

 

Mouse phenotype:

This mouse strain exhibits markedly elevated plasma lipid levels, with arterial lipid deposition observable as early as 3 months of age. With advancing age, extensive lesions resembling the early stages of atherosclerosis develop. Cholesterol levels are significantly increased and remain unaffected by age or sex. By 17 months, lipomatous fibromas appear in the brain, accompanied by lipid droplets and foam cells. Recent studies have further demonstrated that these gene‑knockout mice display impairments in learning and memory, along with synaptic damage.

 

Breeding method: Homozygous × Homozygous

 

Data reference: The images are sourced from the internet; please contact us for removal if there is any infringement.

 

 

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