The left-right (LR) asymmetry of internal organs is established during embryogenesis. Failure of LR patterning causes serious birth defects, so it is important to understand how it is initiated. Vandenberg et al. performed experiments in Xenopus embryos to distinguish between two theoretical models explaining the initiation of LR patterning – the EARLY model, which proposes that serotonin acts in right-side blastomeres to initiate the cascade of asymmetric gene expression, and the LATE model, which proposes that, during neurulation, serotonin induces cilia that later break embryonic symmetry. The researchers show that preventing serotonin signalling in blastomeres that do not contribute to cilia randomises asymmetry, and that asymmetric genes become expressed even in explants without cilia. Their results uniformly support the EARLY model, a finding that could affect our understanding of the aetiology of several birth defects. Page 261

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