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(Received for publication, April 30, 1997, and in revised form, June 17, 1997)
From the Chromosomal translocation t(11;17)(q23;21) is
associated with a retinoic acid-resistant form of acute promyelocytic
leukemia. The translocation fuses the RAR
Volume 272, Number 36,
Issue of September 5, 1997
pp. 22447-22455
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
,
,
,
,§
Brookdale Center for Developmental and
Molecular Biology, Mount Sinai School of Medicine, New York,
New York 10029 and the § Department of Medicine, Mount
Sinai School of Medicine, New York, New York 10029
gene to the
PLZF gene, resulting in the formation of reciprocal fusion
proteins, hypothesized to play prominent roles in leukemogenesis.
Promyelocytic leukemia zinc finger (PLZF) encodes a transcription
factor with nine Krüppel-like zinc fingers, seven of which are
retained in the t(11;17) fusion protein RAR-PLZF. We identified a
specific DNA-binding site for the PLZF protein and showed that PLZF
binds to this site through its most carboxyl seven zinc fingers. In
co-transfection experiments, PLZF repressed transcription through its
cognate binding site. This repression function of PLZF was mapped to
two regions on the protein, including the evolutionarily conserved POZ
domain. In contrast, the RAR-PLZF protein activated transcription of a promoter containing a PLZF response element. These results suggest that RAR-PLZF, generated in acute promyelocytic leukemia, is an
aberrant transcription factor that can deregulate the expression of
PLZF target genes and contribute to leukemogenesis.
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