4.8 Article

Maintaining symmetry during body axis elongation

Journal

CURRENT BIOLOGY
Volume 33, Issue 16, Pages 3536-+

Publisher

CELL PRESS
DOI: 10.1016/j.cub.2023.07.050

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Bilateral symmetry is crucial for the function of bilaterian organisms, but how it is maintained during morphogenetic events is largely unknown. This study reveals that the terminal patterning system in Drosophila is critical for preserving bilateral symmetry during body axis elongation. Attenuation of this system leads to a corkscrew phenotype that disrupts tissue flow and affects viability.
Bilateral symmetry defines much of the animal kingdom and is crucial for numerous functions of bilaterian organisms. Genetic approaches have discovered highly conserved patterning networks that establish bilateral symmetry in early embryos,1 but how this symmetry is maintained throughout subsequent morphogenetic events remains largely unknown.2 Here we show that the terminal patterning system-which relies on Ras/ERK signaling through activation of the Torso receptor by its ligand Trunk3-is critical for preserving bilateral symmetry during Drosophila body axis elongation, a process driven by cell rearrangements in the two identical lateral regions of the embryo and specified by the dorsal-ventral and anterior-posterior patterning systems.4 We demonstrate that fluctuating asymmetries in this rapid convergent-extension process are attenuated in normal embryos over time, possibly through noise-dissipating forces from the posterior midgut invagination and movement. However, when Torso signaling is attenuated via mutation of Trunk or RNAi directed against downstream Ras/ERK pathway components, body axis elongation results in a characteristic corkscrew phenotype,5 which reflects dramatic reorganization of global tissue flow and is incompatible with viability. Our results reveal a new function downstream of the Drosophila terminal patterning system in potentially active control of bilateral symmetry and should motivate systematic search for similar symmetry-preserving regulatory mechanisms in other bilaterians.

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