HS1,2 Enhancer Regulation of Germline ε and γ2b Promoters in Murine B Lymphocytes: Evidence for Specific Promoter-Enhancer Interactions

DOI PDF 被引用文献2件
  • Jurga Laurencikiene
    Department of Cell and Molecular Biology, Karolinska Institutet , Stockholm ,
  • Vilma Deveikaite
    Department of Cell and Molecular Biology, Karolinska Institutet , Stockholm ,
  • Eva Severinson
    Department of Cell and Molecular Biology, Karolinska Institutet , Stockholm ,

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公開日
2001-09
権利情報
  • https://academic.oup.com/pages/standard-publication-reuse-rights
DOI
  • 10.4049/jimmunol.167.6.3257
公開者
Oxford University Press (OUP)

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<jats:title>Abstract</jats:title> <jats:p>During an immune response, activated B cells develop into high rate Ig-secreting plasma cells. They also switch from production of IgM to IgG, IgA, or IgE. This process requires a DNA recombination event, which is regulated at the transcriptional level by the production of isotype-specific, sterile germline (GL) transcripts. Induction of these transcripts is controlled by GL promoters and, possibly, by IgH 3′ enhancers. We investigated the interaction of the GL ε and γ2b promoters with the HS1,2 enhancer using transiently transfected mouse primary B cells and cell lines. The constructs used for the transfections contained a GL promoter upstream and HS1,2 downstream of a luciferase reporter gene. Both GL ε and γ2b promoters synergized strongly with the HS1,2 enhancer in activated primary B cells, a mature B cell line, and a plasma cell line. We show that the major activity of HS1,2 in activated primary B cells occurs within a 310-bp fragment that includes NF-κB, OCT, and NF of activated B cells (Ets/AP-1) sites. By mutating the consensus sequences for various transcription factors, we have determined which sites in HS1,2 are important for synergy with the GL ε and γ2b promoters. Our findings indicate that different sites in HS1,2 might selectively interact with the GL ε and γ2b promoters. We also provide evidence that B cell-specific activator protein is not an absolute suppressor of HS1,2 activity.</jats:p>

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