Fragile X Syndrome (FXS) is a genetic disorder that is a leading cause of autism spectrum disorder. The fmr1 gene encodes an RNA binding protein called Fragile X Mental Retardation protein (FMRP). Loss of gene function results in the loss of this protein. While much research has been done to increase our understanding of the role of FMRP in nervous system development and animal social behavior, less is known about how the loss of FMRP can impact an animal’s ability to locomote and to process sensory information. Our goal in this project was to help close this gap in knowledge by characterizing the effects of fmr1 gene knockdown (KD) in an insect model, the cricket Acheta domesticus. RNA-interference (RNAi) was used to knockdown the expression of the fmr1 gene in the brain of adult crickets on day 1 of adulthood. We observed that crickets with reduced brain fmr1 expression, and thus less FMRP, tend to spend more time in locomotion and travel further distances than do control crickets 9 days after RNAi treatment. Hyperactivity is a common hallmark seen in human and other animal models of FXS. This study will increase our understanding of the effect of reduced levels of FMRP on the ability of an animal to explore its environment. It will provide a foundation for in-depth future study on how FXS may alter sensory processing by the nervous system. It will also provide the investigator with educational development through the mastery of several laboratory techniques, including dsRNA synthesis and RNAi. Such experience will aid the investigator tremendously with his future career goals of pursuing graduate education.
Author: Huy Phạm, Biochemistry and Premedical Studies Major
Faculty Advisor: Kathleen Killian, Department of Biology
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