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Canine Mendelian disease record

Mucopolysaccharidosis, Type IIIA (Discovered in the New Zealand Huntaway; MPS IIIA)

Mucopolysaccharidosis, Type IIIA (Discovered in the New Zealand Huntaway; MPS IIIA). Autosomal recessive. Observed in 0 of 266 breeds tested in the Sniff Atlas, with measured variant frequencies drawn from 242,664 dogs (Donner 2023). Whether a dog carrying this variant is at risk depends on the disease’s inheritance pattern; outcome also depends on penetrance, modifiers, and environment. The frequencies below describe variant prevalence, not confirmed disease incidence.

OMIA identifier
OMIA:001309-9615
Autosomal recessive
Source dataset
Sniff Atlas v1.0.1 / DOI
The human connection

A model of human mucopolysaccharidosis type 3A

This canine condition is studied as a natural model of mucopolysaccharidosis type 3A in people; it is not the same as a human mucopolysaccharidosis type 3A diagnosis. Studying dogs can move medicine forward for everyone; the canine disease remains the subject.

In people, the disease is described as: A rare autosomal recessive lysosomal storage disease caused by deficiency of the enzyme heparan sulfate sulfatase. It is characterized by behavioral changes, sleep disturbances, mental developmental delays and seizures.

In humans it is also called: MPS3A, MPSIIIA, heparan sulfamidase deficiency, heparane sulfamidase deficiency, MPS III A.

Mapped from OMIA via the human disease's OMIM entry to the Mondo Disease Ontology (Monarch Initiative, CC-BY 4.0). Sniff renders this as a model-of link; the canine disease remains the subject of this page.

About this disease

From OMIA's curated record

Documented in OMIA (Online Mendelian Inheritance in Animals). This describes the disease as recorded in the published literature, not a prediction for any individual dog. As of 2026-08-27.

Summary

The only domestic species in which this lysosomal storage disease has been reported is dogs (Fischer et al., 1998).

Molecular genetics

By cloning and sequencing a very likely comparative candidate gene (based on the homologous human disorder), Aronovich et al. (2000) reported a likely causal variant in Dachsunds as "a 3-bp deletion, 737-739delCCA, resulting in the loss of threonine at position 246 in both alleles of the propositus and in one allele of a healthy littermate". Yogalingam et al. (2002) identified a single bp insertion (708-709insC) as a likely causative variant in New Zealand Huntaway dogs.

Human analog

OMIA links this condition to its human counterpart in OMIM (Mendelian Inheritance in Man), the place to read across to the deeper human literature for the same biology.

Source: OMIA (Nicholas, Tammen & the Sydney Informatics Hub), entry OMIA:001309-9615, doi:10.25910/2AMR-PV70 (CC-BY 4.0).

OMIA curates the disease definition, the clinical description and the reference list. The cross-species disease identity is Monarch's. Sniff renders these and adds the breed-level frequencies, the plain-language summary, and a stated reason wherever a number is missing.

Signs & cross-references

How it presents

Catalogued in the Mondo disease ontology (the cross-species disease identity used by the Monarch Initiative) as mucopolysaccharidosis type 3A (MONDO:0009655).

Phenotype terms: Human Phenotype Ontology + Mammalian Phenotype Ontology; disease terms: Mondo (Monarch Initiative). Cross-references curated by OMIA (doi:10.25910/2AMR-PV70, CC-BY 4.0).

The evidence

Published references

The peer-reviewed papers behind this disease, curated by OMIA. Starred entries are OMIA-designated landmark papers. Showing 6 of 21.

References curated by OMIA (Nicholas, Tammen & the Sydney Informatics Hub), doi:10.25910/2AMR-PV70 (CC-BY 4.0). Full list at the OMIA entry.

Your breed

See what Mucopolysaccharidosis, Type IIIA (Discovered in the New Zealand Huntaway; MPS IIIA) looks like in your dog's breed.

Variant frequency by breed

Observed only in small-sample breeds

Maximum variant frequency per breed across variants in the Donner 2023 cohort, with . The list below is split into well-sampled breeds (n ≥ 50 tested) and small-sample breeds (n < 50, where the Wilson CI typically spans more than 20 percentage points and frequencies should not be compared directly to the well-sampled entries). Frequencies are population-level, not per-litter or per-line.

Scope of this record

Scope

This record carries the breed-level carrier frequencies from the Donner 2023 cohort. Penetrance data (the fraction of at-risk dogs that develop the phenotype) is not yet quantified for this disease in the Sniff Atlas v1.0.1. The OMIA entry is the authoritative reference for the clinical phenotype, inheritance pattern, and gene assignment.

Predicted disease relevance at the per-dog level is UNPROVEN. The variant frequency is measured; phenotype outcome depends on penetrance, environment, and modifier loci. Consult a veterinarian for clinical interpretation.

How to cite this record

Citations

If you use this record in published work, cite the Sniff Atlas (the published dataset that carries the breed-level carrier frequencies) and the upstream sources:

  • Sniff Atlas v1.0.1 for the per-breed carrier frequencies:

    Gehring, M. (2026). Sniff Atlas v1.0.1. Zenodo. https://doi.org/10.5281/zenodo.20566358. CC-BY 4.0.

  • OMIA for the disease definition, inheritance, and gene assignment:

    Nicholas, F. W., & Tammen, I. (2024). OMIA. Sydney Informatics Hub, The University of Sydney. https://doi.org/10.25910/2AMR-PV70. Entry: OMIA:001309-9615.

  • Donner et al. 2023 for the breed × variant carrier-frequency cohort:

    Donner, J., Freyer, J., Davison, S., Anderson, H., Blades, M., Honkanen, L., et al. (2023). Genetic prevalence and clinical relevance of canine Mendelian disease variants in over one million dogs. PLOS Genetics, 19(2), e1010651. https://doi.org/10.1371/journal.pgen.1010651.

Full citation formats (BibTeX, RIS, CITATION.cff) at sniff.world/cite.

Related

Related

Last updated
Sources: Sniff Atlas v1.0.1 · OMIA OMIA:001309-9615 · Donner et al. 2023