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

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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.

Original languageEnglish
Article number5629
JournalNature Communications
Number of pages10
Publication statusPublished - 2022

Bibliographical note

Funding Information:
We thank David Lubensky, Ojan Khatib-Damavandi, Lorette Noiret, and Marie-Anne Félix for insightful discussions; Paula Santa Bárbara-Ruiz for help with the experiments and members of the laboratory for discussions and comments on the manuscript; Cyril Kana Tepakbong for help with wing image segmentation codes; Julio Lopes Sampaio for help with ecdysteroids extractions; the Bloomington Stock Center and the Vienna Drosophila RNAi Center for fly stocks; the PICT-IBiSA@BDD light-microscopy facility of Institut Curie. This work was supported by Institut Curie, CNRS, INSERM, FRM, European Research Council (Advanced Grant no. 694677 to P.L.), HFSP grant no. RGP0031/2020 to D. Lubensky and P.L., Labex DEEP program (ANR-11-LABX-0044, ANR-10-IDEX-0001-02), PSL (Ph.D. fellowship to K.E.M.) and the Marie Sklodowska-Curie Actions (fellowship no. 897309 to D.B-O).

Publisher Copyright:
© 2022, The Author(s).

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