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A conserved IL-2 responsive enhancer in the IL-2R alpha gene
P Bucher1, P Corthésy, J Imbert
1Swiss Institute for Experimental Cancer Research (ISREC), Epalinges, Switzerland.
IL-2 stimulates expression of the alpha subunit of the high affinity IL-2 receptor (IL-2R alpha) in antigen-activated T lymphocytes, by increasing IL-2R alpha gene transcription. This response is mediated by a 52 nt IL-2 responsive enhancer (IL-2rE) that is conserved between mouse and man. The mouse enhancer is 1.3 kb upstream of the transcription start site and co-localizes with an inducible DNasel hypersensitive site, whereas the human homologue maps to -4 kb. The human IL-2rE is functional in rodent cells. Both enhancers contain two potential STAT binding sites and an Ets consensus motif. One of the STAT motifs overlaps with a binding site for GATA factors. Functional analysis of the mouse and human enhancers indicates that IL-2-activated STAT5 and the constitutively active Ets protein Elf-1 play a predominant role in controlling IL-2rE activity.
IL-2 stimulates expression of the alpha subunit of the high affinity IL-2 receptor (IL-2R alpha) in antigen-activated T lymphocytes, by increasing IL-2R alpha gene transcription. This response is mediated by a 52 nt IL-2 responsive enhancer (IL-2rE) that is conserved between mouse and man. The mouse enhancer is 1.3 kb upstream of the transcription start site and co-localizes with an inducible DNasel hypersensitive site, whereas the human homologue maps to -4 kb. The human IL-2rE is functional in rodent cells. Both enhancers contain two potential STAT binding sites and an Ets consensus motif. One of the STAT motifs overlaps with a binding site for GATA factors. Functional analysis of the mouse and human enhancers indicates that IL-2-activated STAT5 and the constitutively active Ets protein Elf-1 play a predominant role in controlling IL-2rE activity.