Spleen-specific Expression of the Malaria-inducible Intronless Mouse Gene imap38

• Published in: The Journal of biological chemistry Vol. 274; no. 34; pp. 24383 - 24391
• Main Authors: Krücken, Jürgen, Stamm, Olaf, Schmitt-Wrede, Hans-Peter, Wunderlich, Frank, Mincheva, Antoaneta, Lichter, Peter
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 20.08.1999; American Society for Biochemistry and Molecular Biology
• Subjects: 5' Untranslated Regions - physiology; Amino Acid Sequence; Animals; Base Sequence; Cell Line; Chromosome Mapping; Female; GTP-Binding Proteins; H-2 Antigens - genetics; Malaria - genetics; Malaria - immunology; Membrane Proteins - genetics; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Inbred DBA; Molecular Sequence Data; Organ Specificity; Plasmodium chabaudi; Plasmodium chabaudi - physiology; Promoter Regions, Genetic; Protein Biosynthesis; Spleen - metabolism
• ISSN: 0021-9258; 1083-351X
• DOI: 10.1074/jbc.274.34.24383

We characterize the mouse gene imap38 and its inducibility by Plasmodium chabaudi malaria among different lymphoid tissues and mouse strains of different H-2 complex and non-H-2 background.Imap38 is a single copy gene assigned to chromosome 6B. It consists of only one exon of 1900 base pairs encoding a highly basic 25.8-kDa protein. Confocal laser scanning microscopy localizes differently tagged IMAP38 proteins in nuclei of transfected cells. Reporter gene assays reveal that the 1730-base pair 5′-flanking region, containing an RSINE1 repeat immediately adjacent to initiation site +1, exhibits promoter activity in nonmurine cells, while it is largely repressed in diverse mouse cell lines, which corresponds to the situation in mouse tissues. P. chabaudi malaria induces imap38 expression almost exclusively in the spleen but not in other lymphoid organs. Parasite lysates are able to induce imap38 in the spleen, but not in spleen cells ex vivo. Activation of spleen cells by LPS and other stimuli is not sufficient to induce imap38. Inducibility of imap38 requires signals from both parasites and the intact spleen, and it is controlled by genes of that non-H-2 background, which also controls development of protective immunity against P. chabaudi malaria.