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J. Biol. Chem., Vol. 277, Issue 7, 4918-4924, February 15, 2002
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From the CNRS UMR8532, Institut Gustave-Roussy, PR2, 39 rue Camille
Desmoulins, 94805 Villejuif, France
Ku has been implicated in nuclear processes,
including DNA break repair, transcription, V(D)J recombination, and
telomere maintenance. Its mode of action involves two distinct
mechanisms: one in which a nonspecific binding occurs to DNA ends and a
second that involves a specific binding to negative regulatory elements involved in transcription repression. Such elements were identified in
mouse mammary tumor virus and human T cell leukemia virus retroviruses. The purpose of this study was to investigate a role for Ku in the
regulation of human immunodeficiency virus (HIV)-1 transcription. First, HIV-1 LTR activity was studied in CHO-K1 cells and in
CH0-derived xrs-6 cells, which are devoid of Ku80. LTR-driven
expression of a reporter gene was significantly increased in xrs-6
cells. This enhancement was suppressed after re-expression of Ku80.
Second, transcription of HIV-1 was followed in U1 human cells that were depleted in Ku by using a Ku80 antisense RNA. Ku depletion led to a
increase of both HIV-1 mRNA synthesis and viral production compared
with the parent cells. These results demonstrate that Ku acts as a
transcriptional repressor of HIV-1 expression. Finally, a putative
Ku-specific binding site was identified within the negative regulatory
region of the HIV-1 long terminal repeat, which may account for this
repression of transcription.
Ku Represses the HIV-1 Transcription
IDENTIFICATION OF A PUTATIVE Ku BINDING SITE HOMOLOGOUS TO THE
MOUSE MAMMARY TUMOR VIRUS NRE1 SEQUENCE IN THE HIV-1 LONG TERMINAL
REPEAT*
*
This work was supported by grants from Ensemble contre le
Sida and the Agence Nationale de Recherche sur le SIDA.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: CNRS UMR8532, Institut
Gustave Roussy, PR2, 39 rue Camille Desmoulins, 94805 Villejuif, France. Tel.: 33-1-42-11-50-43; Fax: 33-1-42-11-52-76; E-mail: jfm@igr.fr.
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