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(Received for publication, January 18, 1996, and in revised form, March 8, 1996)
,
,
and
From the We have previously defined the lipopolysaccharide
(LPS)-responsive element (LRE) in the promoters of murine RANTES
(regulated on activation normal T-cell expressed) (MuRantes) and murine
IP-10/crg-2, chemokines which have potent chemotactic
properties for inflammatory cells including monocytes and T
lymphocytes. In the present work, we studied the transcriptional
mechanism of MuRantes gene induction by virus and compared it with that
of LPS in an effort to understand the host responses to virus and
bacterial toxins at the molecular level. MuRantes mRNA expression
is induced by Newcastle disease virus (NDV) and LPS in the RAW 264.7 macrophage cell line and peritoneal macrophages of LPS-responsive
C3HeB/FeJ mice. In LPS-hyporesponsive C3H/HeJ mice, only NDV induces
this chemokine gene, indicating that the pathways of transcriptional
activation by NDV and LPS are not identical. Using a transient
transfection assay, the minimal virus-responsive element (VRE) was
localized between nt
Department of Pathology, University of
Maryland, School of Medicine, Baltimore, Maryland 21201 and the
¶ Department of Molecular Biology and Genetics, The Johns Hopkins
University, School of Medicine, Baltimore, Maryland 21205
175 and
116. The VRE contains previously
defined LRE motif 1 (TCAYRCTT) and motif 3 ((T/A)GRTTTCA(G/C)TTT), which were shown to
also be important for initiation of transcription by virus.
NDV-stimulated nuclear extracts were tested for
trans-activating factors able to bind the VRE. The
chromosomal protein HMG-I(C) was shown to bind the 3
-A·T-rich
domains of the VRE, and the presence of HMG-I(C) was demonstrated in
the VRE-protein complex formed with nuclear extracts from
NDV-stimulated, but not unstimulated cells. These findings demonstrate
the role of HMG-I(C) in activation of MuRantes promoter by NDV.
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