Transcription of MyoD and myogenin in the non-contractile electrogenic cells of the weakly electric fish, Sternopygus macrurus.

Abstract

The MyoD family of basic helix-loop-helix (bHLH) myogenic regulatory factors (MRFs) are transcriptional activators of skeletal muscle gene expression and are pivotal in inducing the full myogenic program. The expression of these factors after muscle differentiation is complete and the mechanism by which they modulate (or maintain) the muscle phenotype is less well understood. The myogenically derived electric organ (EO) of the electric fish Sternopygus macrurus is an excellent model to address this question. The electrocytes, i.e., the electrogenic cells of the EO, are not contractile but they do retain some muscle proteins. In order to examine the molecular regulatory pathways that control the muscle-to-electrocyte cell conversion, we have cloned the MyoD and myogenin cDNAs from S. macrurus. Clustal-based alignments showed that the functional domains observed in mammalian MyoD and myogenin are highly conserved in these MRF homologs. Expression analyses revealed that mature electrocytes, which retain the muscle proteins dystrophin, desmin, acetylcholine receptors (AChRs), alpha-actin, and alpha-actinin, also transcribe the MyoD and myogenin genes. RT-PCR studies confirmed that expression of these MRFs is confined to the myogenic lineage. Surprisingly, the levels of MyoD and myogenin transcripts in skeletal muscle and EO could not be used to predict the level to which a cell manifests the muscle program. We conclude that expression of multiple MRFs is not sufficient to induce non-contractile cells to fully express the skeletal muscle program. These data also suggest that the MRF transcriptional program in S. macrurus may be distinct from MRF-dependent myogenesis in other vertebrate systems.