<cons sem="G#other_name"><cons sem="G#DNA_domain_or_region">Mouse <cons sem="G#protein_molecule">interleukin-2</cons> receptor alpha gene</cons> expression</cons>. <cons sem="G#protein_molecule">Interleukin-1</cons> and <cons sem="G#protein_molecule">interleukin-2</cons> control transcription via distinct <cons sem="G#DNA_family_or

MEDLINE:95256242 <cons sem="G#other_name"><cons sem="G#DNA_domain_or_region">Mouse <cons sem="G#protein_molecule">interleukin-2</cons> receptor alpha gene</cons> expression</cons>. <cons sem="G#protein_molecule">Interleukin-1</cons> and <cons sem="G#protein_molecule">interleukin-2</cons> control transcription via distinct <cons sem="G#DNA_family_or_group">cis-acting elements</cons>. We have shown that interleukin-1 (IL-1) and IL-2 control IL-2 receptor alpha (IL-2R alpha) gene transcription in CD4-CD8- murine T lymphocyte precursors. Here we map the cis-acting elements that mediate interleukin responsiveness of the mouse IL-2R alpha gene using a thymic lymphoma-derived hybridoma (PC60). The transcriptional response of the IL-2R alpha gene to stimulation by IL-1 + IL-2 is biphasic. IL-1 induces a rapid, protein synthesis-independent appearance of IL-2R alpha mRNA that is blocked by inhibitors of NF-kappa B activation. It also primes cells to become IL-2 responsive and thereby prepares the second phase, in which IL-2 induces a 100-fold further increase in IL- 2R alpha transcripts. Transient transfection experiments show that several elements in the promoter-proximal region of the IL-2R alpha gene contribute to IL-1 responsiveness, most importantly an NF-kappa B site conserved in the human and mouse gene. IL-2 responsiveness, on the other hand, depends on a 78-nucleotide segment 1.3 kilobases upstream of the major transcription start site. This segment functions as an IL- 2-inducible enhancer and lies within a region that becomes DNase I hypersensitive in normal T cells in which IL-2R alpha expression has been induced. IL-2 responsiveness requires three distinct elements within the enhancer. Two of these are potential binding sites for STAT proteins.

MEDLINE:95338146 <cons sem="G#other_name"><cons sem="G#cell_type">Hematopoietic lineage</cons> commitment</cons>: role of <cons sem="G#protein_family_or_group">transcription factors</cons>. This review focuses on the roles of transcription factors in hematopoietic lineage commitment. A brief introduction to lineage commitment and asymmetric cell division is followed by a discussion of several methods used to identify transcription factors important in specifying hematopoietic cell types. Next is presented a discussion of the use of embryonic stem cells in the analysis of hematopoietic gene expression and the use of targeted gene disruption to analyze the role of transcription factors in hematopoiesis. Finally, the status of our current knowledge concerning the roles of transcription factors in the commitment to erythroid, myeloid and lymphoid cell types is summarized.

MEDLINE:95266275 <cons sem="G#other_name"><cons sem="G#virus">Epstein-Barr virus</cons> replicative gene transcription</cons> during <cons sem="G#other_name">de novo infection</cons> of <cons sem="G#cell_type">human thymocytes</cons>: <cons sem="G#other_name">simultaneous early expression</cons> of <cons sem="G#protein_molecule">BZLF-1</cons> and its repressor <cons sem="G#protein_molecule">RAZ</cons>. Epstein-Barr virus (EBV) is known to infect B cells and epithelial cells. We and others have shown that EBV can also infect a subset of thymocytes. Infection of thymocytes was accompanied by the appearance of linear EBV genome within 8 hr of infection. Circularization of the EBV genome was not detected. This is in contrast to the infection in B cells where the genome can circularize within 24 hr of infection. The appearance of the BamHI ZLF-1 gene product, ZEBRA, by RT-PCR, was observed within 8 hr of infection. The appearance of a novel fusion transcript (RAZ), which comprised regions of the BZLF-1 locus and the adjacent BRLF-1 locus, was detected by RT-PCR. ZEBRA protein was also identified in infected thymocytes by immunoprecipitation. In addition, we demonstrated that the EBNA-1 gene in infected thymocytes was transcribed from the Fp promoter, rather than from the Cp/Wp promoter which is used in latently infected B cells. Transcripts encoding gp350/220, the major coat protein of EBV, were identified, but we did not find any evidence of transcription from the LMP-2A or EBER-1 loci in infected thymocytes. These observations suggest that de novo EBV infection of thymocytes differs from infection of B cells. The main difference is that with thymocytes, no evidence could be found that the virus ever circularizes. Rather, EBV remains in a linear configuration from which replicative genes are transcribed.