Transcriptional regulation of the vimentin-encoding gene in mouse myeloid leukemia M1 cells.
To investigate the regulatory mechanisms controlling expression of the vimentin-encoding gene (Vim) during mouse myeloid leukemia M1 cell differentiation, mouse Vim was cloned and the transcriptional activity of its 5' promoter region was analysed by chloramphenicol acetyltransferase (CAT) assay. Analyses of various deletion mutants revealed that a 188-bp fragment of the proximal Vim promoter (pVim) was sufficient for effective transcription in M1 cells. This 188-bp sequence is highly conserved between mouse, hamster and human. Further deletion analyses revealed that a minimum promoter element (-44 to +26) is essential for basic promoter function and could respond to cell differentiation. Detailed analyses of mutant and chimeric pVim constructs defined a CCAAT box at -89 to -84 to be an essential positive regulatory element. A G+C-rich element between the CCAAT and TATA boxes was found to act as a strong negative regulatory element in Vim transcription.
Department of Cell Biology, Kyoto University, Japan.
N
N
Nakamura
M
M
Shida
K
K
Hirayoshi
K
K
Nagata
D000818:Animals; D001483:Base Sequence; D002454:Cell Differentiation; D003001:Cloning, Molecular; D018507:Gene Expression Regulation, Developmental; D015972:Gene Expression Regulation, Neoplastic; D007951:Leukemia, Myeloid / Q000235:genetics*; D051379:Mice; D008969:Molecular Sequence Data; D011401:Promoter Regions, Genetic; D012333:RNA, Messenger / Q000235:genetics; D012334:RNA, Neoplasm / Q000235:genetics; D014407:Tumor Cells, Cultured; D014746:Vimentin / Q000235:genetics*
D012333:RNA, Messenger; D012334:RNA, Neoplasm; D014746:Vimentin