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Volume 272, Number 25, Issue of June 20, 1997 pp. 15993-16001
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.

Activation Transcription Factor 1 Involvement in the Regulation of Murine H-2D^d Expression

(Received for publication, April 23, 1996, and in revised form, March 12, 1997)

From the Department of Pathology and the Kaplan Cancer Center, New York University Medical Center, New York, New York 10016

Resistance to radiation leukemia virus-induced leukemia is correlated with an increase in H-2D expression on the thymocyte surface. Recently, it has been shown that elevated H-2D^d expression on the infected thymocyte is a result of elevated mRNA transcription and that the transcriptional increase is correlated with elevated levels of a DNA binding activity, H-2 binding factor 1 (H-2 BF1), which recognizes the 5-flanking sequences (5-TGACGCG-3) of the H-2D^d gene. This target for transcription factor binding has been found to be identical in the 5-regulatory region of 12 rodent class I genes, nine of which have been shown to be functional genes. Furthermore, this cis-element is found 5 of 20 primate class I genes (15 human genes), seven of which are known to be functional. Here, we demonstrate that activation transcription factor 1 (ATF-1) is one component of H-2 BF1. In addition, the levels of ATF-1 mRNA in uninfected and radiation leukemia virus-infected thymocytes parallel those of H-2D^d mRNA, and therefore, it is suggested that ATF-1 up-regulates the transcription of the H-2D^d gene after radiation leukemia virus infection of thymocytes. Transfection experiments also demonstrate that ATF-1 activates a reporter plasmid that contains the H-2 BF1 motif, but not a reporter lacking this motif. This is the first demonstration of the interaction of ATF-1 with 5-regulatory sequences of major histocompatibility complex class I genes.

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