Open AccessRegulation of a human cardiac actin gene introduced into rat L6 myoblasts suggests a defect in their myogenic program.
Author(s) -
Robert J. Hickey,
Arthur I. Skoultchi,
Peter W. Gunning,
Larry Kedes
Publication year - 1986
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.6.9.3287
Subject(s) - myogenesis , biology , myocyte , actin , skeletal muscle , gene expression , microbiology and biotechnology , cardiac muscle , gene , regulation of gene expression , genetics , endocrinology
The rat myogenic cell line L6E9 induces skeletal but not cardiac alpha-actin mRNA upon fusion to form myotubes. However, when a human cardiac alpha-actin gene was introduced into L6E9 myoblasts, differentiation of the cells led to the accumulation of human gene transcripts in parallel with those derived from the endogenous skeletal alpha-actin gene. This result demonstrates that factors which direct rat myogenesis can regulate a muscle gene from another species and that the L6E9 cells may have a defect in their ability to activate endogenous cardiac actin gene expression.