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PMID: 2208280 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Activation and repression of myogenesis in somatic cell hybrids: evidence for trans-negative regulation of MyoD in primary fibroblasts.

Cell ·Vol. 63 ·No. 1 ·1990-10-05 ·Pages 23-32

Thayer MJ, Weintraub H

Abstract

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.

Related Genes
MeSH Terms
Animals Blotting, Southern Cell Differentiation Cell Line Chromosomes, Human, Pair 11 DNA/genetics,isolation & purification Fibroblasts Gene Expression Regulation Humans Hybrid Cells/cytology Melanoma, Experimental Mice Muscles/cytology MyoD Protein Nuclear Proteins/genetics Phosphoproteins/genetics RNA, Messenger/genetics Transfection
Chemicals
MyoD Protein MyoD1 myogenic differentiation protein Nuclear Proteins Phosphoproteins RNA, Messenger DNA
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Thayer M J
Department of Genetics, Hutchinson Cancer Research Center, Howard Hughes Medical Institute, Seattle, Washington 98104.
Weintraub H
Article Info
Journal
Cell
Abbr.
Cell
ISSN
0092-8674
Published
1990-10-05
Pages
23-32
Language
English
Region
United States
NLM ID
0413066
Subset
IM
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