This article is part of a series of Cure SMA grant announcements being shared throughout the winter/spring.
Cure SMA has awarded a $150,000 grant to Timra Gilson, Ph.D., of Indiana University, for her project titled, “αCOP complex dependent axonal transport of RNA.” Dr. Gilson is a post-doctoral researcher working in the laboratory of Dr. Elliot Androphy.
Dr. Gilson is one of three 2020 recipients of the Audrey Lewis Young Investigator Award, periodically given to younger researchers working in the SMA field. Audrey Lewis founded Families of SMA, now Cure SMA, and the goal of this legacy award is to make a positive impact on the early phase of a talented researcher’s career, enabling them to focus on the SMA field and efforts to develop treatments and a cure for SMA.
Dr. Gilson will study the role of αCOP, a cellular component that aids in protein transport between different parts of the cell. She has previously shown that motor neurons unable to extend a neurite—or projection from the body of the cell—due to SMN depletion, are rescued for neurite length by over expression of αCO protein. Similarly, in the zebrafish model of SMA, over-expression of αCOP restores normal neurite outgrowth. In this project, Dr. Gilson seeks to understand how the over-expression of αCOP rescues neurite outgrowth in SMN motor neurons.
Meet Dr. Gilson
Tell us about your work?
I was an undergraduate at Purdue University and completed my Ph.D. in Biochemistry at Johns Hopkins University. I currently am a post-doctoral fellow at Indiana University. In previous labs, my area of focus was on Adenovirus, which is responsible for the common cold, swimmer’s diarrhea, and pink eye. I was interested in examining the differences between infected and normal cells, as well as evolution of the virus.
How did you first become involved with SMA research?
After I returned to Indiana University and joined the lab of Dr. Elliot Androphy, I was introduced to the field of SMA research. In general, I am curious how normal cells can be altered under different conditions, and this gave me the opportunity to transition from studying the effects of viral infection to the effects of disease caused by presence or absence of proteins in cells.
What is your current role in SMA research?
Our lab is focused on discovering the mechanism behind how the addition of an extra transport protein (known as αCOP) to SMA cells makes them behave normally. We have examined this phenomenon in cells grown in the lab, as well as in mouse and zebrafish models of SMA. We also use biochemical techniques to examine changes in amounts and location of RNAs and proteins within neurons.
What do you hope to learn from this research project?
The life expectancy of SMA mice is drastically shorter than normal mice. We aim to understand how over-expression of αCOP promotes a longer lifespan in SMA mice.
How will this project work?
αCOP is known as a transport protein, meaning that it moves other proteins and molecules within cell. We will investigate how these molecules are selected and moved by αCOP, and how this influences SMA severity in cells and SMA mice.
What is the significance of your study?
Understanding how over-expression of αCOP is increasing transport of select molecules to the axons of motor neurons could lead to new insights about SMA pathology.
About Cure SMA’s Basic Research Funding
This grant to Dr. Gilson is part of $1,100,000 in new basic research funding that we’re currently announcing. Basic research is the first step in our comprehensive research model. We fund basic research to investigate the biology and cause of SMA, in order to identify the most effective strategies for drug discovery. We also use this funding to develop tools that facilitate SMA research.