Interleukin-2 (IL-2)-mediated induction of the IL-2 receptor alpha chain gene. Critical role of two functionally redundant tyrosine residues in the IL-2 receptor beta chain cytoplasmic domain and suggestion that these residues mediate more than Stat5 activation

J Biol Chem. 1997 Mar 28;272(13):8704-9. doi: 10.1074/jbc.272.13.8704.

Abstract

The interleukin-2 receptor alpha chain (IL-2Ralpha) is potently induced by antigens, mitogens, and certain cytokines that include IL-2 itself. This induction leads to the formation of high affinity IL-2 receptors when IL-2Ralpha is co-expressed with the beta (IL-2Rbeta) and gamma (gammac) chains of this receptor. We investigated the signaling pathways mediating IL-2-induced IL-2Ralpha mRNA expression using 32D myeloid progenitor cells stably transfected with either wild type IL-2Rbeta or mutants of IL-2Rbeta containing tyrosine to phenylalanine substitutions. Of the six cytoplasmic tyrosines in IL-2Rbeta, we have found that only the two tyrosines that mediate Stat5 activation (Tyr-392 and Tyr-510) contribute to IL-2-induced IL-2Ralpha gene expression and that either tyrosine alone is sufficient for this process. Interestingly, the IL-7 receptor contains a tyrosine (Tyr-429)-based sequence resembling the motifs encompassing Tyr-392 and Tyr-510 of IL-2Rbeta. Further paralleling the IL-2 system, IL-7 could activate Stat5 and drive expression of IL-2Ralpha mRNA in 32D cells transfected with the human IL-7R. However, IL-3 could not induce IL-2Ralpha mRNA in 32D cells, despite its ability to activate Stat5 via the endogenous IL-3 receptor. Moreover, the combination of IL-3 and IL-2 could not "rescue" IL-2Ralpha mRNA expression in cells containing an IL-2Rbeta mutant with phenylalanine substitutions at Tyr-392 and Tyr-510. These data suggest that Tyr-392 and Tyr-510 couple to an additional signaling pathway beyond STAT protein activation in IL-2-mediated induction of the IL-2Ralpha gene.

MeSH terms

  • Antigens, CD / chemistry
  • Antigens, CD / metabolism
  • DNA-Binding Proteins / biosynthesis
  • DNA-Binding Proteins / metabolism*
  • Humans
  • Interleukin-2 / metabolism
  • Interleukin-3 / metabolism
  • Interleukin-7 / metabolism
  • Milk Proteins*
  • RNA, Messenger / metabolism
  • Receptors, Interleukin / chemistry
  • Receptors, Interleukin / metabolism
  • Receptors, Interleukin-2 / chemistry
  • Receptors, Interleukin-2 / genetics*
  • Receptors, Interleukin-7
  • STAT5 Transcription Factor
  • Trans-Activators / biosynthesis
  • Trans-Activators / metabolism*
  • Transcription, Genetic
  • Transfection
  • Tyrosine*

Substances

  • Antigens, CD
  • DNA-Binding Proteins
  • Interleukin-2
  • Interleukin-3
  • Interleukin-7
  • Milk Proteins
  • RNA, Messenger
  • Receptors, Interleukin
  • Receptors, Interleukin-2
  • Receptors, Interleukin-7
  • STAT5 Transcription Factor
  • Trans-Activators
  • Tyrosine