The DMRT3 gene, or Doublesex and Mab-3 Related Transcription Factor 3, provides instructions for creating a protein that functions as a transcription factor. This molecule controls the activity of other genes by binding to their DNA. Its primary role is the formation of neurons responsible for coordinating physical movement. During embryonic development, DMRT3 directs the development of these neurons within the brain and spinal cord, ensuring that the resulting neural circuits are assembled correctly.
The “Gait-Keeper” Gene in Horses
In horses, a variation of the DMRT3 gene known as the “gait-keeper” mutation visibly affects how some animals move. This variation involves a single change in the gene’s DNA sequence, which introduces an early “stop” signal during protein construction. This results in a shorter, altered DMRT3 protein that modifies the neural circuits controlling limb movement.
This genetic alteration is linked to the ability of certain horse breeds to perform alternative gaits beyond the standard walk, trot, and canter. For instance, Standardbreds in harness racing often carry this mutation, which enables them to pace—a gait where both legs on the same side move forward together. This is distinct from the trot, a diagonal gait, and allows for higher speeds without breaking into a canter.
Similarly, the Icelandic horse is known for its additional gaits, including the tölt, a smooth, four-beat ambling gait. The presence of the DMRT3 mutation is widespread in this breed and is necessary for performing these unique patterns of movement. The altered gene function provides a smoother ride or enables greater speed in a non-cantering gait, traits that have been selectively bred for.
Neurological Role in Limb Coordination
The DMRT3 gene influences movement by shaping the development of interneurons within the spinal cord. Specifically, DMRT3 is active in a class of interneurons designated as dI6. These nerve cells act as links in the complex wiring that makes up the central nervous system.
The primary function of these interneurons is to form circuits that synchronize movement between the body’s left and right sides, as well as between the forelimbs and hindlimbs. These neural pathways create a network that dictates the pattern and timing of limb movements for a coordinated gait. The standard DMRT3 protein helps establish the cross-body coordination seen in a trot.
When the “gait-keeper” mutation occurs, the resulting truncated protein alters the function of these dI6 interneurons. This disruption changes the established neural circuits that enforce the diagonal pairing of limbs. The modified signaling pathways allow for different limb-timing combinations, such as the lateral pairing seen in pacing or the unique footfall sequence of the tölt.
Function in Other Species
The DMRT3 gene is not exclusive to horses and is a highly conserved gene found across many vertebrate species, including fish, mice, and humans. Its widespread existence indicates its role in the biology of movement and nervous system development over millions of years of evolution.
In other species, DMRT3 performs a similar task in coordinating locomotion. In mice, for example, the gene is involved in establishing the neural circuits that control stride and limb coordination, much like in horses. Studies have confirmed its role in specifying the spinal cord neurons necessary for generating rhythmic movement.
While the “gait-keeper” mutation’s effect on ambling gaits is most documented in horses, the gene is also a component of human biology. In humans, DMRT3 is involved in developing the spinal cord neurons that manage locomotion. Although the equine mutation is not a factor in human movement, the gene’s basic function in building the neural framework for coordinated motion is a shared biological principle.