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

Lauren A. Callender, Johannes Schroth, Elizabeth C. Carroll, Conor Garrod-Ketchley, Lisa E. L. Romano, Eleanor Hendy, Audrey Kelly, Paul Lavender, Arne N. Akbar, J. Paul Chapple and Sian M. Henson ()
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Lauren A. Callender: Queen Mary University of London
Johannes Schroth: Queen Mary University of London
Elizabeth C. Carroll: Queen Mary University of London
Conor Garrod-Ketchley: Queen Mary University of London
Lisa E. L. Romano: Queen Mary University of London
Eleanor Hendy: King’s College London
Audrey Kelly: King’s College London
Paul Lavender: King’s College London
Arne N. Akbar: University College London
J. Paul Chapple: Queen Mary University of London
Sian M. Henson: Queen Mary University of London

Nature Communications, 2021, vol. 12, issue 1, 1-11

Abstract: Abstract GATA3 is as a lineage-specific transcription factor that drives the differentiation of CD4+ T helper 2 (Th2) cells, but is also involved in a variety of processes such as immune regulation, proliferation and maintenance in other T cell and non-T cell lineages. Here we show a mechanism utilised by CD4+ T cells to increase mitochondrial mass in response to DNA damage through the actions of GATA3 and AMPK. Activated AMPK increases expression of PPARG coactivator 1 alpha (PPARGC1A or PGC1α protein) at the level of transcription and GATA3 at the level of translation, while DNA damage enhances expression of nuclear factor erythroid 2-related factor 2 (NFE2L2 or NRF2). PGC1α, GATA3 and NRF2 complex together with the ATR to promote mitochondrial biogenesis. These findings extend the pleotropic interactions of GATA3 and highlight the potential for GATA3-targeted cell manipulation for intervention in CD4+ T cell viability and function after DNA damage.

Date: 2021
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DOI: 10.1038/s41467-021-23715-7

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