Functional Conservation of Electric Fish Myogenic Regulatory Factors


Meeting Abstract

P2.23  Jan. 5  Functional Conservation of Electric Fish Myogenic Regulatory Factors KIM, H. J.; GUETH, R.*; UNGUEZ, G. A.; New Mexico State University; New Mexico State University; New Mexico State University rgueth09@hotmail.com

The myogenic regulatory factors (MRFs) belonging to the MyoD family are pivotal in the differentiation and commitment of cells to the skeletal muscle lineage, and the transcriptional activation of muscle-specific genes (reviewed in Rudnicki and Jaenisch, BioEssays, 17: 203-209, 1995). However, the role of MRFs in maintaining the muscle phenotype are less well understood. We have been using the myogenically derived electric organ (EO) of the electric fish S. macrurus as a model system to address these questions because the mature cells of the EO are not contractile but retain some muscle proteins. Expression studies reveal that EO cells transcribe the MRF genes MyoD, myogenin, myf5 and MRF4 despite their incomplete muscle phenotype. Also, sequence analyses show that the functional domains observed in mammalian MRFs are highly conserved in S. macrurus MRF homologs (Kim et al, Dev Genes Evol, 214:380-392; Kim and Unguez, ASCB Abst. 2005). In the present study, we explore the conservation of S. macrurus MRFs at the functional level by testing for their ability to convert 10T1/2 mouse embryonic cells into muscle cells in vitro. Transfection of cells with each S. macrurus MRF resulted in the detection of sarcomeric myosin heavy chain (MHC) in 10T1/2 cells with no apparent differences in conversion by different MRFs. Further, the MHC expression in cells induced by S. macrurus MRFs was comparable to that obtained with mouse MRFs. These preliminary data demonstrate that S. macrurus MRFs can function in a heterologous system and underscore the contribution of an MRF transcriptional program in maintaining the muscle-like phenotype of EO cells that is distinct from MRF-dependent myogenesis in other vertebrates. Supported by NIH grants RR16480 and S06-GMO8136.

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