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PMID:15147761

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Citation

Orgogozo, V, Schweisguth, F and Bellaïche, Y (2004) Slit-Robo signalling prevents sensory cells from crossing the midline in Drosophila. Mech. Dev. 121:427-36

Abstract

Maintenance of bilateral symmetry throughout animal development requires that both left and right halves of the body follow nearly identical patterns of cell proliferation, differentiation, death and migration. During formation of the perfectly bilateral Drosophila larval peripheral nervous system (PNS), the sensory precursor cells of the ventral multidendritic neuron vmd1a originating from each hemisegment migrate away from the ventral midline. Our observations indicate that in slit mutant embryos, as well as in robo, robo2 double mutants, sensory precursor cells of the left and right vmd1a neurons aberrantly cluster at the midline and then the pair of vmd1a neurons migrate to their final position on the same side of the embryo. This results in disruption of PNS bilateral symmetry. Expression of slit at the midline rescues the slit mutant vmd1a phenotype, suggesting that midline-secreted Slit activates Robo/Robo2 signalling to control the migration of the vmd1a sensory precursor cells. Our study indicates that midline-secreted Slit prevents vmd1a sensory cells from crossing the midline and thereby maintains PNS bilateral symmetry during development.

Links

PubMed Online version:10.1016/j.mod.2004.04.001

Keywords

Animals; Cell Lineage; Cell Movement; Drosophila Proteins/metabolism; Drosophila melanogaster/cytology; Drosophila melanogaster/embryology; Drosophila melanogaster/genetics; Drosophila melanogaster/metabolism; Female; Male; Mutation/genetics; Nerve Tissue Proteins/metabolism; Neurons/cytology; Neurons/metabolism; Peripheral Nervous System/cytology; Peripheral Nervous System/embryology; Peripheral Nervous System/metabolism; Phenotype; Receptors, Immunologic/genetics; Receptors, Immunologic/metabolism; Signal Transduction; Stem Cells/cytology; Stem Cells/metabolism

Significance

Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status


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References

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