Format

Send to

Choose Destination
See comment in PubMed Commons below
Mol Cell Biol. 1990 Aug;10(8):3934-44.

Differential trans activation associated with the muscle regulatory factors MyoD1, myogenin, and MRF4.

Author information

1
Department of Biological Sciences, Purdue University, West Lafayette, Indiana 47907.

Abstract

Expression of the mammalian muscle regulatory factors MyoD1, myogenin, and MRF4 will convert C3H10T1/2 fibroblasts to stable muscle cell lineages. Recent studies have shown that MyoD1 and myogenin also trans-activate expression of a number of cotransfected contractile protein genes, suggesting that these muscle regulatory factors are involved in controlling terminal differentiation events. The extent and specificity of trans activation by the muscle regulatory factors, however, have not been compared directly. In this study, we found that MyoD1, myogenin, and MRF4 exhibited different trans-activation capacities. In contrast to MyoD1 and myogenin, MRF4 was inefficient in trans-activating most of the genes tested, although conversion of C3H10T1/2 fibroblasts to a myogenic lineage was observed at similar frequencies with all three factors. Addition of basic fibroblast growth factor to cells expressing exogenous muscle regulatory factors inhibited the transcriptional activation of cotransfected genes, demonstrating that MyoD1, myogenin, or MRF4 proteins alone are not sufficient to produce a terminally differentiated phenotype. In all cases, trans activation was dependent on signal transduction pathways that are regulated by fibroblast growth factor. Our observations, coupled with previous studies showing differences in the temporal expression and protein structure of MyoD1, myogenin, and MRF4, suggest that the individual members of the muscle regulatory factor family have distinct biological roles in controlling skeletal muscle development.

PMID:
1695319
PMCID:
PMC360904
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Support Center