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Chronic activation of JNK JAK/STAT and oxidative stress signalling causes the loser cell status

Author

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  • Iwo Kucinski

    (University of Cambridge
    University of Cambridge)

  • Michael Dinan

    (University of Cambridge)

  • Golnar Kolahgar

    (University of Cambridge)

  • Eugenia Piddini

    (University of Cambridge
    University of Bristol)

Abstract

Cell competition is a form of cell interaction that causes the elimination of less fit cells, or losers, by wild-type (WT) cells, influencing overall tissue health. Several mutations can cause cells to become losers; however, it is not known how. Here we show that Drosophila wing disc cells carrying functionally unrelated loser mutations (Minute and mahjong) display the common activation of multiple stress signalling pathways before cell competition and find that these pathways collectively account for the loser status. We find that JNK signalling inhibits the growth of losers, while JAK/STAT signalling promotes competition-induced winner cell proliferation. Furthermore, we show that losers display oxidative stress response activation and, strikingly, that activation of this pathway alone, by Nrf2 overexpression, is sufficient to prime cells for their elimination by WT neighbours. Since oxidative stress and Nrf2 are linked to several diseases, cell competition may occur in a number of pathological conditions.

Suggested Citation

  • Iwo Kucinski & Michael Dinan & Golnar Kolahgar & Eugenia Piddini, 2017. "Chronic activation of JNK JAK/STAT and oxidative stress signalling causes the loser cell status," Nature Communications, Nature, vol. 8(1), pages 1-13, December.
  • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-00145-y
    DOI: 10.1038/s41467-017-00145-y
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    Cited by:

    1. Michael E. Baumgartner & Paul F. Langton & Remi Logeay & Alex Mastrogiannopoulos & Anna Nilsson-Takeuchi & Iwo Kucinski & Jules Lavalou & Eugenia Piddini, 2023. "The PECAn image and statistical analysis pipeline identifies Minute cell competition genes and features," Nature Communications, Nature, vol. 14(1), pages 1-16, December.

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