Mouse interleukin-2 receptor α gene expression. Interleukin-1 and interleukin-2 control transcription via distinct cis-acting elements

P. Sperisen, Ming Wang San Ming Wang, E. Soldaini, M. Pla, C. Rusterholz, P. Bucher, P. Corthesy, P. Reichenbach, M. Nabholz

Research output: Contribution to journalArticle

59 Scopus citations


We have shown that interleukin-1 (IL-1) and IL-2 control IL-2 receptor α (IL-2Rα) gene transcription in CD4-CD8- murine T lymphocyte precursors. Here we map the cis-acting elements that mediate interleukin responsiveness of the mouse IL-2Rα gene using a thymic lymphoma-derived hybridoma (PC60). The transcriptional response of the IL-2Rα gene to stimulation by IL-1 + IL- 2 is biphasic. IL-1 induces a rapid, protein synthesis-independent appearance of IL-2Rα mRNA that is blocked by inhibitors of NF-κB 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-2Rα transcripts. Transient transfection experiments show that several elements in the promoter-proximal region of the IL-2Rα gene contribute to IL-1 responsiveness, most importantly an NF-κB 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- 2Rα expression has been induced. IL-2 responsiveness requires three distinct elements within the enhancer. Two of these are potential binding sites for STAT proteins.

Original languageEnglish (US)
Pages (from-to)10743-10753
Number of pages11
JournalJournal of Biological Chemistry
Issue number18
Publication statusPublished - Jan 1 1995


ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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