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Blood, 1 May 2002, Vol. 99, No. 9, pp. 3404-3410
NEOPLASIA
Interactions of GATA-2 with the promyelocytic leukemia zinc
finger (PLZF) protein, its homologue FAZF, and the t(11;17)-generated
PLZF-retinoic acid receptor alpha oncoprotein
Shinobu Tsuzuki and
Tariq Enver
From the Section of Gene Function and Regulation,
Institute of Cancer Research, Chester Beatty Laboratories, London,
United Kingdom.
Transcription factor GATA-2 is implicated in the survival and
growth of multipotential progenitors. Here we report that the promyelocytic leukemia zinc finger (PLZF) protein can interact with
GATA-2 and can modify its transactivation capacity. Fanconi anemia zinc
finger (FAZF), a PLZF-homologous protein that has been variously
described as ROG (repressor of GATA), and TZFP (testis zinc finger
protein) also interact with GATA-2. The zinc finger region of GATA-2 is
required for binding to PLZF and FAZF, but distinct interfaces on the
PLZF and FAZF molecules mediate the interaction, suggesting that GATA-2
activity is controlled by these 2 homologous proteins through distinct
mechanisms. GATA-2 can also physically associate with the PLZF-RAR
fusion protein generated by the t(11;17) chromosomal translocation
associated with acute promyelocytic leukemia (APL). Functional
experiments showed that this interaction has the capacity to render
GATA-dependent transcription responsive to treatment with a combination
of all-trans retinoic acid and the histone deacetylase
inhibitor trichostatin A (TSA). This combination of drugs has been
shown to stimulate the terminal differentiation of leukemic
t(11;17)-associated APL blasts, raising the possibility that GATA
target genes may be involved in the molecular pathogenesis of APL.
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