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El Marzkioui, K.

Publications and source records attributed to El Marzkioui, K..

2 recordsLinked to original sources

A switch in the mode of tissue growth extends the growth phase of Drosophila wing primordia during early pupal development

Understanding how final organ size is established during development raises two key questions: how organs increase their mass and how they stop growing upon reaching an appropriate size. While organ growth is driven by conserved signaling pathways, the mechanisms underlying growth arrest remain elusive. Studies on Drosophila imaginal wing discs have provided a model whereby final organ size coincides with an arrest of cell proliferation at the end of the larval phase. Here, through 3D reconstruction and volume measurements, we show that wing discs grow continuously throughout the larva-to-pupa (L/P) transition and proceed to growth arrest later during the pupal period. This supplemental growth phase involves a switch at the L/P transition that uncouples proliferation from tissue growth, with an important contribution from Insulin/IGF signaling. These findings challenge the existing model of imaginal wing development and open new avenues for our understanding of growth arrest and organ size determination.

developmental biology↗

Dilp8 controls a time window for tissue size adjustment in Drosophila

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 crossorgan 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 feedback between the two hormones as a systemic mechanism controlling organ size precision. Our results reveal a hormone-based time window ensuring fine-tuning of organ size and bilateral symmetry.

developmental biology↗