MU Researchers Identify Coding Gene Responsible for Locomotion and Central Nervous System Development
Studies could shed light on paralysis, stroke and other disorders, including Alzheimer’s disease
Waters identified a coding gene that has profound effects on central nervous system development and locomotion that could shed light on paralysis, stroke and other disorders of the central nervous system.
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Story posted: April 02, 2014
By: Jeff Sossamon
COLUMBIA, Mo. – Coding genes contain DNA sequences that are used to assign functions required for development and maintenance within a cell. These coding genes articulate how a fingernail grows, help develop nerve cells responsible for chewing, and are vital in helping the spinal cord facilitate movement in arms or legs. Recently, University of Missouri researchers identified a coding gene that has profound effects on central nervous system development and locomotion that could shed light on paralysis, stroke and other disorders of the central nervous system, including Alzheimer’s disease.
“Understanding the genes that enable us to walk normally and have motor control assists researchers in developing strategies for repairing neural circuits and therapies,” said Samuel T. Waters, assistant professor of biological sciences in the College of Arts and Science and a researcher in the Bond Life Sciences Center at MU. “We work extensively with two very important coding genes called Gbx1 and Gbx2. We’re finding that these genes are essential for development of the central nervous system. Our work is taking us to the point where we’re getting a bird’s eye view of what’s regulating the body’s ability to have locomotive control.”
Waters and his researchers, including graduate student Desiré Buckley, investigated the function of the Gbx1 coding gene by deactivating it in mouse embryos and observing their development over an 18.5-day period. Genes can be isolated, targeted and then inactivated throughout the tissue.
Waters found that when Gbx1 is inactivated, neural circuit development in the spinal cord—the portion of the cord that allows the mice to walk normally—is compromised, Waters said.
“The difference between walking and being paralyzed could be as simple as turning a light switch on and off,” Waters said. “Isolating this gene could eventually contribute to developing gene therapies for paralysis in humans that occurs from abnormal development or from a direct injury, including central nervous system damage through a stroke or blunt trauma, like a car accident.”
Waters’ research has led to the investigation of other coding genes and their responsibilities and roles in development. The study, “Characterization of the Gbx1 mouse mutant: a requirement for Gbx1 in normal locomotion and sensorimotor circuit development,” was published in PLoSOne.
Editor’s Note: For an extended version of this article, please visit: “ MU researchers find key gene in spinal locomotion, yield insight on paralysis .”