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A Dilp8-dependent time window ensures tissue size adjustment in Drosophila

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  • D. Blanco-Obregon

    (PSL Research University, CNRS UMR3215, INSERM U934, UPMC Paris-Sorbonne)

  • K. El Marzkioui

    (PSL Research University, CNRS UMR3215, INSERM U934, UPMC Paris-Sorbonne)

  • F. Brutscher

    (University of Zurich)

  • V. Kapoor

    (PSL Research University, CNRS UMR3215, INSERM U934, UPMC Paris-Sorbonne)

  • L. Valzania

    (PSL Research University, CNRS UMR3215, INSERM U934, UPMC Paris-Sorbonne)

  • D. S. Andersen

    (University of Copenhagen
    University of Copenhagen)

  • J. Colombani

    (University of Copenhagen
    University of Copenhagen)

  • S. Narasimha

    (PSL Research University, CNRS UMR3215, INSERM U934, UPMC Paris-Sorbonne)

  • D. McCusker

    (University of Michigan)

  • P. Léopold

    (PSL Research University, CNRS UMR3215, INSERM U934, UPMC Paris-Sorbonne)

  • L. Boulan

    (PSL Research University, CNRS UMR3215, INSERM U934, UPMC Paris-Sorbonne)

Abstract

The control of organ size mainly relies on precise autonomous growth programs. However, organ development is subject to random variations, called developmental noise, best revealed by the fluctuating asymmetry observed between bilateral organs. The developmental mechanisms ensuring bilateral symmetry in organ size are mostly unknown. In Drosophila, null mutations for the relaxin-like hormone Dilp8 increase wing fluctuating asymmetry, suggesting that Dilp8 plays a role in buffering developmental noise. Here we show that size adjustment of the wing primordia involves a peak of dilp8 expression that takes place sharply at the end of juvenile growth. Wing size adjustment relies on a cross-organ communication involving the epidermis as the source of Dilp8. We identify ecdysone signaling as both the trigger for epidermal dilp8 expression and its downstream target in the wing primordia, thereby establishing reciprocal hormonal feedback as a systemic mechanism, which controls organ size and bilateral symmetry in a narrow developmental time window.

Suggested Citation

  • D. Blanco-Obregon & K. El Marzkioui & F. Brutscher & V. Kapoor & L. Valzania & D. S. Andersen & J. Colombani & S. Narasimha & D. McCusker & P. Léopold & L. Boulan, 2022. "A Dilp8-dependent time window ensures tissue size adjustment in Drosophila," Nature Communications, Nature, vol. 13(1), pages 1-10, December.
  • Handle: RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-33387-6
    DOI: 10.1038/s41467-022-33387-6
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    References listed on IDEAS

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    1. Suzanne L. Rutherford & Susan Lindquist, 1998. "Hsp90 as a capacitor for morphological evolution," Nature, Nature, vol. 396(6709), pages 336-342, November.
    2. Andres Garelli & Fabiana Heredia & Andreia P. Casimiro & Andre Macedo & Catarina Nunes & Marcia Garcez & Angela R. Mantas Dias & Yanel A. Volonte & Thomas Uhlmann & Esther Caparros & Takashi Koyama & , 2015. "Dilp8 requires the neuronal relaxin receptor Lgr3 to couple growth to developmental timing," Nature Communications, Nature, vol. 6(1), pages 1-14, December.
    3. Fabiana Heredia & Yanel Volonté & Joana Pereirinha & Magdalena Fernandez-Acosta & Andreia P. Casimiro & Cláudia G. Belém & Filipe Viegas & Kohtaro Tanaka & Juliane Menezes & Maite Arana & Gisele A. Ca, 2021. "The steroid-hormone ecdysone coordinates parallel pupariation neuromotor and morphogenetic subprograms via epidermis-to-neuron Dilp8-Lgr3 signal induction," Nature Communications, Nature, vol. 12(1), pages 1-20, December.
    4. Emilie Boone & Julien Colombani & Ditte S. Andersen & Pierre Léopold, 2016. "The Hippo signalling pathway coordinates organ growth and limits developmental variability by controlling dilp8 expression," Nature Communications, Nature, vol. 7(1), pages 1-8, December.
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