To investigate the regulatory mechanisms controlling expression of the
vimentin-encoding gene (Vim) during mouse myeloid leukemia M1 cell di
fferentiation, mouse Vim was cloned and the transcriptional activity o
f its 5' promoter region was analysed by chloramphenicol acetyltransfe
rase (CAT) assay. Analyses of various deletion mutants revealed that a
188-bp fragment of the proximal Vim promoter (pVim) was sufficient fo
r 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. De
tailed 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.