Jun oncoproteins do not function as primary transcription factors for the mouse major histocompatibility complex class I H-2 genes in fibroblasts.
There are several reports in the literature focusing on regulation of major histocompatibility complex (MHC) class I genes by transcription factors of the jun family. The methods employed in these reports differed in various respects, and their results are inconsistent. In mouse Lewis lung carcinoma, B16-melanoma and F9-teratocarcinoma cell lines, c-jun was characterized as a transcriptional activator of the murine MHC class I H2-Kb gene, while c-jun was identified as a direct transcriptional repressor of the swine class I PD1 gene, and c-jun stably transfected clones of mouse L-fibroblasts markedly reduced their H-2 class I gene expression. In this study, we attempted to reproduce this last effect by means of transient transfection coupled to Northern hybridization, upon transfecting L-fibroblasts with expression vectors for all jun family members as well as with an array of c-jun-derived dominant negative mutants. No change in H-2 class I expression could be identified. Next, we derived two additional fibroblastic cell lines from the fibrosarcoma of the H2-Kk/v-jun transgenic mouse and transfected them with the two most potent c-jun dominant negative mutants, again without eliciting any change in H-2 class I mRNA level. We conclude that the negative regulation of H-2 class I genes by c-jun in cells of the fibroblastic lineage is not a primary effect.
Hatina
J
J
Department of Biology, Faculty of Medicine in Pilsen, Charles University, Czech Republic. jiri.hatina@lfp.cuni.cz
Reischig
J
J
D000818:Animals; D005347:Fibroblasts / Q000378:metabolism*; D006183:H-2 Antigens / Q000096:biosynthesis / Q000235:genetics*; D051379:Mice; D016759:Oncogene Protein p65(gag-jun) / Q000235:genetics / Q000378:metabolism*; D014157:Transcription Factors / Q000378:metabolism*; D014162:Transfection
D006183:H-2 Antigens; D016759:Oncogene Protein p65(gag-jun); D014157:Transcription Factors