CONTROL OF TYPE-I AND TYPE-II COLLAGEN AND FIBRONECTIN GENE-EXPRESSION IN CHONDROCYTES DELINEATED BY VIRAL TRANSFORMATION

被引:49
作者
ALLEBACH, ES
BOETTIGER, D
PACIFICI, M
ADAMS, SL
机构
[1] UNIV PENN, SCH MED, DEPT HUMAN GENET, PHILADELPHIA, PA 19104 USA
[2] UNIV PENN, SCH MED, DEPT MICROBIOL, PHILADELPHIA, PA 19104 USA
[3] UNIV PENN, SCH MED, DEPT ANAT, PHILADELPHIA, PA 19104 USA
关键词
D O I
10.1128/MCB.5.5.1002
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The effects of transformation by Rous sarcoma virus on expression of types I and II collagen and fibronectin genes were analyzed in vertebral chondrocytes and compared with expression of these genes in skin fibroblasts. Transformed chondrocytes display a dramatically decreased amount of type II collagen RNA, which can account fully for the decreased synthetic rate of this protein. These cells also display greatly increased amounts of type I collagen RNA species, which are translated efficiently in vitro, but not in the intact cells. The type I collagen RNA species in transformed chondrocytes are shown to be nearly indistinguishable from those found in skin fibroblasts, and they clearly differ from the type I collagen RNA species found in normal chondrocytes. Transformed chondrocytes also display an increased amount of fibronectin RNA, which can account fully for the increased synthetic rate of this protein. Thus, the effects of transformation by Rous sarcoma virus on type I collagen and fibronectin RNA species in chondrocytes are the opposite of those observed in fibroblasts, which display decreased amounts of these 3 RNA species. These data indicate that the effects of transformation on the genes encoding type I collagen and fibronectin must be modulated by host cell-specific factors. They also imply that the types I and II collagen genes may be regulated by different mechanisms, the type I genes being controlled at both transcriptional and postranscriptional levels, and the type II gene being controlled primarily at the transcriptional level.
引用
收藏
页码:1002 / 1008
页数:7
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