Scientific article

Silencing and trans-activation of the mouse IL-2 gene in Xenopus oocytes by proteins from resting and mitogen-induced primary T-lymphocytes

Published inEMBO Journal, vol. 10, no. 6, p. 1399-1406
Publication date1991

The Xenopus oocyte system was used to test functionally, putative trans‐active elements involved in the transcriptional control of the mouse interleukin‐2 (IL‐2) gene in resting and mitogen‐induced primary T‐lymphocytes. The IL‐2 gene injected into the oocyte is active over a wide range of DNA concentrations. This basal activity is silenced by the addition of protein extracts from G0‐arrested spleen cells. Extracts from 8 h‐stimulated spleen cells do not silence but moderately increase transcription over basal level. When IL‐2 transcription is silenced first by an injection of extract from resting spleen cells, the addition of proteins from stimulated cells results in a strong increase in transcription (derepression). Use of proteins from purified splenic T‐lymphocytes shows that both silencer(s) and activator(s) are contributed by these cells. Extracts from control tissues have neither a silencing nor stimulatory effect. None of the proteins tested affects the activities of co‐injected control genes. Injections with IL‐2 promoter mutants indicate that the main target sequence of the silencing and activating factors is a purine region (Pu‐box) lying between positions −261 and −292 upstream of the IL‐2 gene. Bandshift assays show differential binding of the Pu‐box with proteins from resting or activated T‐cells. Previous Article Next Article

  • Gene regulation
  • Growth factors
  • Microinjection
  • Repressor
  • Trans-activation
  • Swiss National Science Foundation - 3.298-0.87, 3.586-0.87 & 3.128654.90
Citation (ISO format)
MOUZAKI, Athanasia et al. Silencing and trans-activation of the mouse IL-2 gene in <i>Xenopus</i> oocytes by proteins from resting and mitogen-induced primary T-lymphocytes. In: EMBO Journal, 1991, vol. 10, n° 6, p. 1399–1406. doi: 10.1002/j.1460-2075.1991.tb07660.x
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Article (Published version)
ISSN of the journal0261-4189

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