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First published online 20 March 2008
doi: 10.1242/dev.015412

Development 135, 1605-1613 (2008)
Published by The Company of Biologists 2008
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Neuropilin 1 and 2 control cranial gangliogenesis and axon guidance through neural crest cells

Quenten Schwarz1, Joaquim M. Vieira1, Beatrice Howard2, Britta J. Eickholt3 and Christiana Ruhrberg1,*

1 Institute of Ophthalmology, University College London, Bath Street, London EC1V 9EL, UK.
2 Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research, 237 Fulham Road, London SW3 6JB, UK.
3 MRC Centre for Developmental Neurobiology, King's College London, London SE1 1UL, UK.

* Author for correspondence (email: c.ruhrberg{at}ucl.ac.uk)

Accepted 26 February 2008

Neuropilin (NRP) receptors and their class 3 semaphorin (SEMA3) ligands play well-established roles in axon guidance, with loss of NRP1, NRP2, SEMA3A or SEMA3F causing defasciculation and errors in growth cone guidance of peripherally projecting nerves. Here we report that loss of NRP1 or NRP2 also impairs sensory neuron positioning in the mouse head, and that this defect is a consequence of inappropriate cranial neural crest cell migration. Specifically, neural crest cells move into the normally crest-free territory between the trigeminal and hyoid neural crest streams and recruit sensory neurons from the otic placode; these ectopic neurons then extend axons between the trigeminal and facioacoustic ganglia. Moreover, we found that NRP1 and NRP2 cooperate to guide cranial neural crest cells and position sensory neurons; thus, in the absence of SEMA3/NRP signalling, the segmentation of the cranial nervous system is lost. We conclude that neuropilins play multiple roles in the sensory nervous system by directing cranial neural crest cells, positioning sensory neurons and organising their axonal projections.

Key words: Neural crest cell, Placode, Peripheral nervous system, Sensory neuron, Axon guidance, Neuropilin, Semaphorin, Mouse


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