Paper Type

Master's Thesis


College of Arts and Sciences

Degree Name

Master of Science in Biology (MS)



NACO controlled Corporate Body

University of North Florida. Department of Biology

First Advisor

Dr. David Waddell

Second Advisor

Dr. Frank Smith

Third Advisor

Dr. Wolfdieter Springer

Department Chair

Dr. Cliff Ross

College Dean

Dr. George Rainbolt


Skeletal muscle atrophy can result from a range of physiological conditions, including denervation, immobilization, hindlimb unweighting, and aging. To better characterize the molecular genetic events of atrophy, a microarray was performed using skeletal muscle isolated from mice after 3 and 14 days of denervation and compared to control muscle to identify novel atrophy-induced genes. The microarray revealed that FGGY carbohydrate kinase domain containing (Fggy) is expressed in skeletal muscle and is induced in response to denervation. Bioinformatic analysis of the Fggy gene locus revealed two validated alternative isoforms, that we have termed Fggy-L-552 and Fggy-S-387, which have distinct transcription initiation sites. In order to confirm that Fggy is expressed in muscle, the cDNAs of the two validated alternative variants were cloned from myoblast cells. Interestingly, two novel alternative splice variants, designated Fggy-L-482 and Fggy-S-344, were also cloned, suggesting that at least four Fggy splice variants are expressed in skeletal muscle. Quantitative RT-PCR (RT-qPCR) was performed using RNA isolated from muscle cells and primers designed to distinguish the four alternative Fggy transcripts. The RT-qPCR data reveals that the Fggy-L transcripts are more highly expressed during myoblast differentiation, while the Fggy-S transcripts show relatively stable expression in proliferating myoblasts and differentiated myotubes. Confocal fluorescent microscopy revealed that the Fggy-L variants appear to localize evenly throughout the cytoplasm, while the Fggy-S variants produce a more punctuate localization pattern throughout the cytoplasm of proliferating muscle cells. Finally, ectopic expression of Fggy-L-552 and Fggy-S-387 resulted in inhibition of muscle cell differentiation and attenuation of the MAP kinase and AKT signaling pathways. The characterization of novel genes induced during neurogenic atrophy helps improve our understanding of the molecular and cellular events that lead to muscle atrophy and may eventually lead to new therapeutic targets for the treatment of muscle wasting.