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PLoS genetics2026; 22(5); e1012158; doi: 10.1371/journal.pgen.1012158

An intronic variant in Ferredoxin Reductase (FDXR) creates a cryptic exon in Quarter Horses with Equine Juvenile Spinocerebellar Ataxia.

Abstract: Equine Juvenile Spinocerebellar Ataxia (EJSCA) is a novel autosomal recessive neurologic disease in Quarter Horses. Affected foals display a progressive proprioceptive ataxia by 1-5 weeks of age, leading to recumbency and necessitating euthanasia. Whole genome sequencing was performed on 7 EJSCA cases and unaffected horses that included 4 obligate carriers, 4 unaffected half or full-siblings, and 28 unrelated, unaffected control Quarter Horses. An 82 kb region of association was identified (EquCab3.0, chr11: 6963986-7045999), containing 9 candidate SNPs across four genes (FADS6, FDXR, GRIN2C and TMEM104). Decreased FDXR mRNA expression and a cryptic exon was identified in spinal cord tissue from EJSCA cases via RNA-sequencing. One of the 9 associated SNPs (FDXR-203 c.177 + 1778G > C) was the eighth base pair of this cryptic exon. Affected foals were all homozygous for the variant. Protein concentrations of FDXR were lower in EJSCA cases in spinal cord and liver compared to unaffected controls. The FDXR-203 c.177 + 1778G > C mutation represents the first non-coding neurological genetic variant in horses. Additionally, this is the first genetic cause of a degenerative axonopathy in the horse and a spontaneous disease model to study FDXR pathology in humans.
Copyright: © 2026 Brown et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Publication Date: 2026-05-20 PubMed ID: 42160398PubMed Central: PMC13215600DOI: 10.1371/journal.pgen.1012158Google Scholar: Lookup
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Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

An intronic genetic mutation in the FDXR gene causes an abnormal exon to form, leading to a degenerative neurological disease called Equine Juvenile Spinocerebellar Ataxia (EJSCA) in Quarter Horses. This study identifies the mutation, its effects on gene expression, and its potential as a model for similar human diseases.

Background and Disease Description

  • Equine Juvenile Spinocerebellar Ataxia (EJSCA) is a newly described neurological disorder in Quarter Horses.
  • The disease is autosomal recessive, meaning affected foals inherit two copies of the defective gene.
  • Symptoms start early, within 1-5 weeks after birth, and primarily involve progressive loss of proprioception leading to ataxia (loss of coordination).
  • The condition worsens until affected foals become unable to stand (recumbent) and require euthanasia for humane reasons.

Research Approach

  • Whole genome sequencing was performed on a group of horses including:
    • 7 horses affected with EJSCA,
    • 4 obligate carriers (parents or close relatives carrying one mutant gene),
    • 4 unaffected siblings, and
    • 28 unrelated, unaffected control Quarter Horses.
  • Genome-wide association analysis identified an 82 kb region on chromosome 11 significantly associated with EJSCA.
  • This region contained 9 candidate single nucleotide polymorphisms (SNPs) across four genes: FADS6, FDXR, GRIN2C, and TMEM104.

Key Genetic Finding

  • RNA sequencing of spinal cord tissue from affected horses revealed:
    • Decreased expression of FDXR messenger RNA (mRNA), suggesting reduced gene activity.
    • An abnormal “cryptic” exon created within the FDXR gene that normally does not get spliced into the mRNA.
  • One SNP (FDXR-203 c.177+1778G>C) was found precisely at the eighth base of this cryptic exon, implicating it in abnormal splicing.
  • All affected horses were homozygous (carrying two copies) for this specific intronic variant.

Functional and Protein-Level Effects

  • Protein analysis showed significantly reduced FDXR protein levels in the spinal cord and liver tissues of affected foals compared to unaffected controls.
  • This indicates that the cryptic exon disrupts normal FDXR protein production, likely contributing to disease pathology.

Significance and Implications

  • This mutation is the first identified non-coding (intronic) neurological variant in horses, expanding understanding of genetic causes beyond coding regions.
  • It represents the inaugural genetic cause identified for a degenerative axonopathy (a disease involving nerve fiber degeneration) in horses.
  • The spontaneous disease model in Quarter Horses can be used to study FDXR-related pathology, which may provide insights into similar human neurodegenerative disorders involving this gene.

Cite This Article

APA
Brown BN, Dahlgren AR, Ghosh S, Durbin-Johnson B, Willis A, Olivas C, York D, Grahn R, Bellone RR, Cortopassi GA, Miller AD, Brown CT, Woolard K, Finno CJ. (2026). An intronic variant in Ferredoxin Reductase (FDXR) creates a cryptic exon in Quarter Horses with Equine Juvenile Spinocerebellar Ataxia. PLoS Genet, 22(5), e1012158. https://doi.org/10.1371/journal.pgen.1012158

Publication

PLoS genetics
ISSN: 1553-7404
NlmUniqueID: 101239074
Country: United States
Language: English
Volume: 22
Issue: 5
Pages: e1012158
PII: e1012158

Researcher Affiliations

Brown, Briana N
  • Department of Population Health and Reproduction, School of Veterinary Medicine, University of California-Davis, Davis, California, United States of America.
Dahlgren, Anna R
  • Department of Population Health and Reproduction, School of Veterinary Medicine, University of California-Davis, Davis, California, United States of America.
Ghosh, Sharmila
  • Department of Population Health and Reproduction, School of Veterinary Medicine, University of California-Davis, Davis, California, United States of America.
Durbin-Johnson, Blythe
  • Bioinformatics Core Facility, Genome Center, University of California-Davis, Davis, California, United States of America.
Willis, Andrew
  • Weatherford Equine Medical Center, Weatherford, Texas, United States of America.
Olivas, Cassandra
  • Department of Population Health and Reproduction, School of Veterinary Medicine, University of California-Davis, Davis, California, United States of America.
York, Daniel
  • Department of Surgical and Radiological Sciences, School of Veterinary Medicine, University of California-Davis, Davis, California, United States of America.
Grahn, Robert
  • Veterinary Genetics Laboratory, School of Veterinary Medicine, University of California-Davis, Davis, California, United States of America.
Bellone, Rebecca R
  • Department of Population Health and Reproduction, School of Veterinary Medicine, University of California-Davis, Davis, California, United States of America.
  • Veterinary Genetics Laboratory, School of Veterinary Medicine, University of California-Davis, Davis, California, United States of America.
Cortopassi, Gino A
  • Department of Molecular Biosciences, School of Veterinary Medicine, University of California-Davis, Davis, California, United States of America.
Miller, Andrew D
  • Department of Biomedical Sciences, Section of Anatomic Pathology, College of Veterinary Medicine, Cornell University, Ithaca, New York, United States of America.
Brown, C Titus
  • Department of Population Health and Reproduction, School of Veterinary Medicine, University of California-Davis, Davis, California, United States of America.
Woolard, Kevin
  • Department of Anatomic Pathology, School of Veterinary Medicine, University of California-Davis, Davis, California, United States of America.
Finno, Carrie J
  • Department of Population Health and Reproduction, School of Veterinary Medicine, University of California-Davis, Davis, California, United States of America.

MeSH Terms

  • Animals
  • Horses / genetics
  • Polymorphism, Single Nucleotide
  • Exons / genetics
  • Horse Diseases / genetics
  • Spinocerebellar Ataxias / genetics
  • Spinocerebellar Ataxias / veterinary
  • Introns / genetics
  • Whole Genome Sequencing
  • Spinal Cord / metabolism
  • Spinal Cord / pathology
  • Female
  • Male

Conflict of Interest Statement

I have read the journal’s policy, and the authors of this manuscript have the following competing interests: A portion of the revenue generated by UC Davis Veterinary Genetics Lab (UCD-VGL) for tests discovered in the Finno Laboratory (MYHM and EJSCA) provides funding for additional research conducted in the Finno Laboratory. RRB and RG are affiliated with the UC Davis Veterinary Genetics Laboratory offering commercial diagnostics testing for horses and other species.

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