Activation and repression of myogenesis in somatic cell hybrids: evidence for trans-negative regulation of MyoD in primary fibroblasts.
We show that transfer of human fibroblast chromosome 11 (containing the human MyoD gene) from primary cells into 10T1/2 mouse fibroblasts by microcell fusion activates expression of the transferred human MyoD gene and converts these cells to myoblasts. Transfer of human chromosome 11 into B78 melanoma cells also leads to the activation of human MyoD. In contrast to the results where a single chromosome 11 is transferred, whole-cell hybrids between 10T1/2 cells and human skin fibroblasts do not express the myogenic phenotype; however, when specific human chromosomes are lost, myogenesis occurs. These results suggest that the MyoD locus is potentially functional in primary human fibroblasts, but is normally repressed in trans by a locus on a different human fibroblast chromosome.
Department of Genetics, Hutchinson Cancer Research Center, Howard Hughes Medical Institute, Seattle, Washington 98104.
M J
MJ
Thayer
H
H
Weintraub
D000818:Animals; D015139:Blotting, Southern; D002454:Cell Differentiation; D002460:Cell Line; D002880:Chromosomes, Human, Pair 11; D004247:DNA / Q000235:genetics / Q000302:isolation & purification; D005347:Fibroblasts; D005786:Gene Expression Regulation; D006801:Humans; D006822:Hybrid Cells / Q000166:cytology*; D008546:Melanoma, Experimental; D051379:Mice; D009132:Muscles / Q000166:cytology*; D017570:MyoD Protein; D009687:Nuclear Proteins / Q000235:genetics; D010750:Phosphoproteins / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics; D014162:Transfection
D017570:MyoD Protein; C057363:MyoD1 myogenic differentiation protein; D009687:Nuclear Proteins; D010750:Phosphoproteins; D012333:RNA, Messenger; D004247:DNA