Skip to main content
Disease Variant Modeling

Point Mutation Mouse Models

Since 1998, ingenious targeting laboratory has generated hundreds of point mutation mouse models for researchers studying disease mechanisms, protein function, and therapeutic development. Our mouse models have supported research published in more than 800 peer reviewed articles, including in Science, Nature, and Cell.

Point mutation mice carry specific nucleotide changes at endogenous genomic loci, expressing variant proteins under normal regulatory control. Unlike overexpression systems, point mutation knockin models maintain physiological expression levels and tissue distribution.

2,500+
Projects Completed
800+
Publications
26+
Years Experience
100%
Success Rate

Applications of Point Mutation Models

Disease Variant Modeling

Human genetic studies identify disease associated variants, but understanding how these variants cause disease requires functional models:

GWAS variants:Model SNPs identified in genome wide association studies
Mendelian disease mutations:Reproduce mutations causing inherited disorders
Cancer driver mutations:Express oncogenic point mutations at endogenous loci
Pharmacogenomic variants:Model variants affecting drug response

Point mutation knockin provides definitive evidence linking specific variants to phenotypic outcomes.

Protein Function Studies

Point mutations enable precise dissection of protein function:

Catalytic site mutations:Abolish enzymatic activity while preserving protein expression
Phosphorylation site mutations:Block or mimic phosphorylation to study signaling
Binding site mutations:Disrupt specific protein-protein or protein-ligand interactions
Domain function:Identify essential residues within functional domains

Drug Target Modeling

Point mutation models support therapeutic development:

Resistance mutations:Model drug resistance variants for next generation compound development
Humanized binding sites:Enable testing of human specific therapeutics
Gain of function variants:Model activating mutations as therapeutic targets

Types of Point Mutations

Missense Mutations

Single nucleotide changes that alter the encoded amino acid:

  • Most common type of disease associated coding variant
  • May affect protein folding, stability, or function
  • Phenotypic severity varies from silent to lethal

Nonsense Mutations

Single nucleotide changes that create premature stop codons:

  • Typically result in truncated, non functional proteins
  • May trigger nonsense mediated decay
  • Model loss of function alleles

Silent Mutations

Nucleotide changes that do not alter the encoded amino acid:

  • Create restriction sites for genotyping
  • Serve as linked markers for allele tracking
  • Control for targeting procedure effects

Regulatory Mutations

Changes in non coding regulatory sequences:

  • Promoter or enhancer variants affecting expression level
  • Splice site variants affecting transcript processing
  • UTR variants affecting mRNA stability or translation

Common Point Mutation Applications

Phosphorylation Site Mutations

Mutation TypeEffectApplication
Serine to Alanine (S→A)Blocks phosphorylationLoss of phospho regulation
Threonine to Alanine (T→A)Blocks phosphorylationLoss of phospho regulation
Tyrosine to Phenylalanine (Y→F)Blocks phosphorylationLoss of phospho regulation
Serine to Aspartate (S→D)Mimics phosphorylationConstitutive activation
Serine to Glutamate (S→E)Mimics phosphorylationConstitutive activation

Common Disease Mutations

GeneMutationDiseaseApplication
APPSwedish (K670N/M671L)Alzheimer diseaseAmyloid pathology
KRASG12D, G12V, G12CCancerOncogenic signaling
BRAFV600EMelanomaTargeted therapy studies
SOD1G93AALSMotor neuron disease
CFTRF508delCystic fibrosisProtein folding

Technical Approach

Allele Design Options

Point mutation alleles can be designed with varying complexity:

Simple knockin

Point mutation only

Conditional point mutation

LoxP flanked wildtype exon enables Cre mediated conversion to mutant

Inducible point mutation

Combine with inducible Cre for temporal control

Dual reporter

Fluorescent markers distinguish wildtype from mutant expressing cells

Experimental Considerations

Homozygous vs Heterozygous Analysis

Consider the genetics of your disease or question:

Dominant mutations:Heterozygotes may show phenotype; homozygotes may be more severe or lethal
Recessive mutations:Homozygotes required for phenotype
Haploinsufficiency:Heterozygotes show partial phenotype
Gain of function:One copy may suffice for full effect

Strain Background

Strain background can modify point mutation phenotypes:

C57BL/6:Generate for consistency with most published literature
Disease backgrounds:Consider strain specific modifiers for disease relevant backgrounds
Consistency:Maintain consistent background for comparisons
Learn more

Controls

Appropriate controls for point mutation studies:

Wildtype littermates:Same genetic background without mutation
Heterozygous carriers:Intermediate genotype for dosage studies
Parallel knockouts:Compare point mutation to complete loss of function

Selected Publications

Point mutation models generated by ingenious targeting laboratory:

Navarro HI, Daly AE, Rodriguez B, Wu S, Ngo KA, Fraser A, Schiffman A, Liu Y, Smale ST, Chia JJ, Hoffmann A. (2025).

NF-κB RelB suppresses the inflammatory gene expression programs of dendritic cells by competing with RelA for binding to target gene promoters

Cell Discov 11(1): 13

Mohassel P, Hearn H, Rooney J, Zou Y, Johnson K, Norato G, Nalls MA, Yun P, Ogata T, Silverstein S, Sleboda DA, Roberts TJ, Rifkin DB, Bönnemann CG. (2025).

Collagen type VI regulates TGF-β bioavailability in skeletal muscle in mice

J Clin Invest 9(135): e173354

Hockemeyer K, Sakellaropoulos T, Chen X, Ivashkiv O, Sirenko M, Zhou H, Gambi G, Battistello E, Avrampou K, Sun Z, Guillamot M, Chiriboga L, Jour G, Dolgalev I, Corrigan, K, Bhatt, Osman I, Tsirigos A, Kourtis N, Aifantis I. (2024).

The stress response regulator HSF1 modulates natural killer cell anti-tumour immunity

Nat Cell Bio 26(10): 1734-1744

What Researchers Say

The people at InGenious are friendly, professional, and extremely good at what they do. I have made 5 Knockin mice with them and everything has gone like clockwork.

David B. Roth, MD, PhD

Perelman School of Medicine, University of Pennsylvania

Start Your Point Mutation Project

Our scientific consultants are ready to discuss your point mutation requirements and optimal allele design for your research goals. Initial consultation is provided at no charge and includes mutation strategy, allele design options, timeline and price estimate.

✦ New for 2026

Breeding Scheme Architect

Plan complex multi-allele breeding strategies, calculate expected genotype ratios, and estimate time to experimental cohorts—all before starting your project.

Visualize multi-generation breeding paths
Calculate Mendelian ratios automatically
Estimate timeline to study ready cohorts

Free Research Tool

No account required

Allele 1Gene-flox (conditional)
Allele 2Cre-driver (tissue-specific)
TargetHomozygous knockout

→ 3 generations to target genotype

Lab Signals

Point Mutation Design Expertise

Subscribe to Lab Signals for expert insights on disease variant modeling, allele design strategies, and point mutation mouse generation.

Subscribe Free

Frequently Asked Questions

Yes. Point mutation knockins change specific nucleotides while preserving all other gene sequences.

Any single or multiple nucleotide change can be modeled, including disease-associated variants, catalytic site mutations (kinase dead, protease dead), phosphorylation site mutations, and regulatory element mutations. Point mutations enable precise study of how specific amino acid changes affect protein function and disease phenotypes.

Yes. Point mutations can be designed as conditional alleles using LoxP-flanked wildtype exons. Cre-mediated recombination converts wildtype to mutant sequence, enabling temporal or tissue-specific control over mutation expression. This is valuable for modeling mutations that would be lethal if expressed globally from conception.

Heterozygous models are used for dominant mutations or haploinsufficiency studies. Homozygous models are required for recessive mutations. Some mutations show dose-dependent effects where heterozygotes show partial phenotypes and homozygotes show more severe or lethal phenotypes. Genetic analysis determines whether heterozygotes or homozygotes are appropriate.