Previously, the underlying genetic mechanisms behind these fractures had remained elusive. However, these new findings have enabled the RVC to identify a novel DNA variant associated with fractures, impacting the expression of collagen type III.
Bone fractures are common in Thoroughbred racehorses, due to the forces the bones can experience, and are a leading cause of euthanasia. Approximately 60 horses each year are euthanised on UK racecourses as a result. However, fracture is a complex condition, with both environmental and genetic risk factors affecting a horse’s susceptibility.
Led by Dr. Debbie Guest, Senior Research Fellow at RVC, the team developed a polygenic risk score to gauge disease susceptibility based on various genes. They were then able to use this information to select cells from horses whose risk placed them at the extreme ends of the population with either very low or very high risk. These cells were then used in laboratory studies to establish a cell model and investigate the genetic factors involved in fracture risk.
The research team’s findings indicate that bone cells from horses predisposed to fractures express collagen type III at reduced levels due to alterations in their DNA sequence in the region which controls how much collagen III is produced.
This discovery provides a crucial step forward in identifying genetically high-risk horses. By understanding the genetic causes of fractures,, this research can help identify, diagnose, and manage high-risk horses, improving the health and welfare of Thoroughbreds in the racing industry.
Ongoing research aims to validate the risk-scoring system across different horse populations and further explore genetic factors using the established cell model.
For more details, see:
Palomino Lago, E.; Baird, A.; Blott, S.C.; McPhail, R.E.; Ross, A.C.; Durward-Akhurst, S.A.; Guest, D.J.
A Functional Single-Nucleotide Polymorphism Upstream of the Collagen Type III Gene Is Associated with Catastrophic Fracture Risk in Thoroughbred Horses.
Animals 2024, 14, 116.
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