Gene variant linked to reduced performance in Arabian racehorses

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Built for speed? Researchers have linked variants of gene in Arabian horses to race success.
Built for speed? Researchers have linked variants of a gene in Arabian horses to the likelihood of race success.

A study conducted on Arabian horses found that those with a particular variant of a gene which plays an important role in a process called apoptosis were less likely to win galloping races.

The authors, writing in the journal BMC Veterinary Research, suggest that testing for different variants of the gene might be employed to selectively improve the racing performance of Arabian horses.

Apoptosis involves the death of cells which occur as a normal and controlled part of an organism’s growth or development.

The process plays an important role in the regulation of healthy tissue, as well as in the maintenance of exercising muscles.

During an intensive physical effort, the regulation of cell deaths by apoptosis results in the replacement of unaccustomed muscle cells by new cells that are better suited to exercise.

Katarzyna Ropka-Moli and her colleagues set out in their Arabian horse study to learn more about the expression of two genes, SH3FR1 and SH3RF2, that control apoptosis in muscle during training periods characterized by different intensities.

Skeletal muscle biopsies were collected from 15 Arabian horses in an untrained state, after an intense gallop phase, and at the end of the racing season.

An association study was also performed on 250 Arabian horses, using blood or hair follicle samples, to assess the effect of a particular missense variant, known as SH3RF2:c.796 T > C (p.Ser266Pro), on race performance traits in flat gallop racing.

The study team’s gene expression analysis confirmed a significant decrease in the anti-apoptotic SH3RF2 (POSHER) gene during training periods that differed in intensity.

The highest SH3RF2 expression level was detected in the muscles of untrained horses, whereas the lowest expression was identified at the end of the racing season in horses that were fully adapted to the exercise. A non-significant decrease in SH3RF1 gene expression following the training periods was observed.

They also found that horses carrying the previously mentioned missense variant gene, in which the substitution of serine by proline occurs at amino acid position 266 (the CC genotype), were less likely to win and competed in fewer races.

Analysis of the SH3RF2:c.796 T > C genotype frequencies showed that the most frequent were horses with CC (47.7%), followed by TC (43.7%), then TT at 8.6%.

Horses with the TT genotype achieved the highest financial benefits, both for total winnings and for winnings per race.

The researchers said their work showed the supposed regulation mechanism of exercise-induced apoptosis in horses at the molecular level in Arabian horses.

“It is assumed that exercise-induced apoptosis is promoted by the up-regulation of pro-apoptotic genes and/or the down-regulation of anti-apoptotic genes.

“The decrease in SH3RF2 gene expression observed in the present study supports this thesis and suggests which molecular pathway might be involved in the regulation of apoptosis following exercise.”

They continued: “The identified SH3RF2: c.796 T > C missense variant was associated with selected racing performance traits, which is important information during the evaluation of horses’ exercise predisposition.

“The association results and frequencies of the CT and TT genotypes suggest the possibility of using SH3RF2 variant in selection to improve the racing performance of Arabian horses.”

The five-strong research team was affiliated with a range of institutions in Kraków, Poland.

Molecular characterization of the apoptosis-related SH3RF1 and SH3RF2 genes and their association with exercise performance in Arabian horses
K. Ropka-Molik, M. Stefaniuk-Szmukier, K. Piórkowska, T. Szmatoła and M. Bugno-Poniewierska
BMC Veterinary Research 2018 14:237 https://doi.org/10.1186/s12917-018-1567-0

The study, published under a Creative Commons License, can be read here

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