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GATA3 controls mitochondrial biogenesis in primary human CD4+ T cells during DNA damage

Lauren A. Callender,Johannes Schroth,Elizabeth C. Carroll,Elizabeth C. Carroll,Lisa E. L. Romano,E. Hendy,Audrey Kelly,P. Lavender,A. Akbar,J. Chapple,S. Henson

Published 2019 in bioRxiv

ABSTRACT

GATA binding protein 3 (GATA3) has conventionally been regarded as a lineage-specific transcription factor that drives the differentiation of CD4+ T helper (Th) 2 cells. However, increasing evidence shows that in addition to regulating T cell development, GATA3 is also involved in a myriad of processes such as immune regulation, proliferation and maintenance in other T cell and non-T cell lineages. Here we identify a previously unknown function for this molecule whereby in the presence of DNA damage GATA3 can induce mitochondrial biogenesis and promote mitochondrial fitness through the transcriptional coactivator peroxisome-proliferator-activated receptor γ co-activator-1α (PGC1α) in CD4+ T cells. These findings extend the pleotropic nature of GATA3 and highlight the potential for GATA3-targeted cell manipulation for clinical interventions.

PUBLICATION RECORD

  • Publication year

    2019

  • Venue

    bioRxiv

  • Publication date

    2019-08-06

  • Fields of study

    Biology, Medicine, Chemistry

  • Identifiers
    DOI 10.1101/727479
  • External record

    Open on Semantic Scholar

  • Source metadata

    Semantic Scholar

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