RUNX1-dependent RAG1 deposition instigates human TCR-δ locus rearrangement

نویسندگان

  • Agata Cieslak
  • Sandrine Le Noir
  • Amélie Trinquand
  • Ludovic Lhermitte
  • Don-Marc Franchini
  • Patrick Villarese
  • Stéphanie Gon
  • Jonathan Bond
  • Mathieu Simonin
  • Laurent Vanhille
  • Christian Reimann
  • Els Verhoeyen
  • Jerome Larghero
  • Emmanuelle Six
  • Salvatore Spicuglia
  • Isabelle André-Schmutz
  • Anton Langerak
  • Bertrand Nadel
  • Elizabeth Macintyre
  • Dominique Payet-Bornet
  • Vahid Asnafi
چکیده

V(D)J recombination of TCR loci is regulated by chromatin accessibility to RAG1/2 proteins, rendering RAG1/2 targeting a potentially important regulator of lymphoid differentiation. We show that within the human TCR-α/δ locus, Dδ2-Dδ3 rearrangements occur at a very immature thymic, CD34(+)/CD1a(-)/CD7(+dim) stage, before Dδ2(Dδ3)-Jδ1 rearrangements. These strictly ordered rearrangements are regulated by mechanisms acting beyond chromatin accessibility. Importantly, direct Dδ2-Jδ1 rearrangements are prohibited by a B12/23 restriction and ordered human TCR-δ gene assembly requires RUNX1 protein, which binds to the Dδ2-23RSS, interacts with RAG1, and enhances RAG1 deposition at this site. This RUNX1-mediated V(D)J recombinase targeting imposes the use of two Dδ gene segments in human TCR-δ chains. Absence of this RUNX1 binding site in the homologous mouse Dδ1-23RSS provides a molecular explanation for the lack of ordered TCR-δ gene assembly in mice and may underlie differences in early lymphoid differentiation between these species.

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عنوان ژورنال:

دوره 211  شماره 

صفحات  -

تاریخ انتشار 2014