Thayer M J, Weintraub H
Department of Genetics, Hutchinson Cancer Research Center, Howard Hughes Medical Institute, Seattle, Washington 98104.
Cell. 1990 Oct 5;63(1):23-32. doi: 10.1016/0092-8674(90)90285-m.
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.
我们发现，通过微细胞融合将人成纤维细胞11号染色体（含人MyoD基因）从原代细胞转移至10T1/2小鼠成纤维细胞中，可激活转移的人MyoD基因的表达，并将这些细胞转化为成肌细胞。将人11号染色体转移至B78黑色素瘤细胞中也会导致人MyoD的激活。与转移单条11号染色体的结果相反，10T1/2细胞与人皮肤成纤维细胞之间的全细胞杂种不表达生肌表型；然而，当特定的人染色体丢失时，会发生肌生成。这些结果表明，MyoD基因座在原代人成纤维细胞中可能具有功能，但通常会被另一条人成纤维细胞染色体上的一个基因座反式抑制。
