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In this issue |
DAXX is an essential, highly conserved protein that is associated with PML
nuclear bodies and might function as a transcriptional repressor. Knockout
work seems to indicate that it has an anti-apoptotic role; however, a variety
of overexpression studies in cultured cells suggest that the protein instead
promotes apoptosis. So which is it? Jennifer Michaelson and Philip Leder have
settled this question by using RNA interference to knock down DAXX synthesis
in the very cell lines used in the overexpression experiments (see
p. 345). They demonstrate that
apoptosis is increased in DAXX-depleted cells and that transfection of the
anti-apoptotic protein Bcl-2 can rescue this phenotype. These findings
indicate that DAXX does indeed protect cells from apoptosis, casting
significant doubt on the overexpression work. The authors do, however, observe
derepression of transcription in the DAXX-depleted cells, confirming that the
protein functions as a repressor. Interestingly, they also identify the
transcription factors NF-
B and E2F1 as novel DAXX targets. Since both
are implicated in control of apoptosis, inhibition of NF-B- and
E2F1-dependent transcription could underlie the anti-apoptotic activity of
DAXX.
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