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UNC5A promotes neuronal apoptosis during spinal cord development independent of netrin-1

Abstract

In addition to their role as chemorepellent netrin-1 receptors, UNC5 proteins may mediate cell death because they induce apoptosis in cultured cells. To test this in vivo, we generated Unc5a (formerly Unc5h1) knockout mice and found that this deletion decreased apoptosis and increased the number of neurons in the spinal cord. In contrast, loss of netrin-1 (Ntn1) did not affect the amount of apoptosis, suggesting that NTN1 is not required for neuronal apoptosis in vivo.

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Figure 1: Endogenous expression and targeted disruption of the Unc5a gene locus.
Figure 2: Loss of Unc5a results in decreased apoptotic cell death, supernumerary neurons and abnormal spinal architecture.
Figure 3: Loss of Ntn1 does not affect apoptosis in vivo.

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Acknowledgements

Antibodies to spinal accessory neurons (802C11) were a gift from S.C. Fujita (Mitsubishi Kagaku Institute of Life Sciences, Tokyo, Japan). Supported by grants from the US National Institutes of Health (NS39572- to L.H., MH12813 to M.W.), the Damon-Runyon Cancer Research Fund (X.L.) and the Howard Hughes Medical Institute (M.T.-L.).

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Correspondence to Lindsay Hinck.

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Williams, M., Lu, X., McKenna, W. et al. UNC5A promotes neuronal apoptosis during spinal cord development independent of netrin-1. Nat Neurosci 9, 996–998 (2006). https://doi.org/10.1038/nn1736

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