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Overexpression of PU.1 induces growth and differentiation inhibition and
apoptotic cell death in murine erythroleukemia cells
T Yamada, N Kondoh, M Matsumoto, M Yoshida, A Maekawa and T Oikawa
Department of Cell Genetics, Sasaki Institute, Tokyo, Japan.
PU.1 is a member of the ets family of transcription factors and is
expressed in Friend virus-induced murine erythroleukemia (MEL) cells as a
consequence of proviral integration into the PU.1/Spi-1 locus. After
induction of MEL cell differentiation by treatment with dimethylsulfoxide
(DMSO), expression of the PU.1/Spi-1 gene decreased before induction of
beta-globin gene expression. Overexpression of PU.1 by using a
zinc-inducible expression plasmid in MEL cells resulted in unexpected
growth inhibition of the transfectants. When PU.1- overexpressing
transfectants were treated with DMSO, growth inhibition became much
pronounced and apoptosis was induced. Expression of the beta-globin gene
was not induced under this condition. Neither growth inhibition nor
apoptosis was induced in MEL cells after expression of mutant PU.1 proteins
with a deletion of the activation domain or the DNA-binding Ets domain
irrespective of the presence of DMSO. Interestingly, beta-globin gene
expression was not induced in the transfectants expressing the former
mutant, whereas it was induced in those expressing the latter one in the
presence of DMSO. These results indicate that overexpression of PU.1 in MEL
cells results in growth and differentiation inhibition and, in conjunction
with DMSO treatment, apoptotic cell death. These results also suggest that
the activation domain and the Ets domain of PU.1 contribute differently to
induction of these effects.
Volume 89,
Issue 4,
pp. 1383-1393,
02/15/1997
Copyright © 1997 by The American Society of Hematology
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