Live Cell Imaging Reveals Marked Variability in Myoblast Proliferation and Fate

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SAT 88-108-GHRH, GH & IGF Biology & Signaling
Basic/Translational
Saturday, June 15, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SAT-99
Sean Gross*1 and Peter S Rotwein2
1OHSU, 2Oregon Health & Science University, Portland, OR
During the process of muscle regeneration, activated stem cells termed satellite cells proliferate, and then differentiate to form new myofibers that restore the injured area. Yet not all satellite cells contribute to muscle repair. Some continue to proliferate, others die, and others become quiescent. The mechanisms that regulate the adoption of different cell fates in a muscle cell precursor population remain unclear. Here we used live cell imaging and lineage tracing to study cell fate in the C2 myoblast line. Analyzing the behavior of individual myoblasts revealed marked variability in both cell cycle duration and viability, but similarities between cells derived from the same parental lineage. As a consequence, lineage sizes and outcomes differed dramatically, and individual lineages made uneven contributions toward the terminally differentiated population. Thus, the cohort of myoblasts undergoing differentiation at the end of an experiment differed dramatically from the lineages present at the beginning. Treatment with IGF-I increased myoblast number by maintaining viability and by stimulating a fraction of cells to complete one additional cell cycle in differentiation medium, and as a consequence reduced the variability of the terminal population compared with controls. Overall, our results reveal that heterogeneity is an intrinsic property of cultured myoblasts, and demonstrate the power of live cell imaging for understanding how muscle differentiation is regulated.

Nothing to Disclose: SG, PSR

*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm

Sources of Research Support: This work was supported by NIH research grant 5R01 DK042748 (to P. R.) and NIH Training Grant T32 CA106195 (S.M.G).