Nature Neuroscience 9, 996 - 998 (2006)
Published online: 9 July 2006; | doi:10.1038/nn1736
UNC5A promotes neuronal apoptosis during spinal cord development independent of netrin-1Megan E Williams1, 6, Xiaowei Lu2, 5, 6, William L McKenna1, 6, Raesha Washington1, Adam Boyette1, Phyllis Strickland1, Allison Dillon3, Zaven Kaprielian3, Marc Tessier-Lavigne4 &
Lindsay Hinck11
Department of Molecular, Cell and Developmental Biology, University of California Santa Cruz, Santa Cruz, California 95064, USA. 2
Department of Biological Sciences, Howard Hughes Medical Institute, Stanford University, Stanford, California 94305, USA. 3
Departments of Neuroscience and Pathology, Albert Einstein College of Medicine, Bronx, New York 10461, USA. 4
Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA. 5
Present address: Department of Cell Biology, University of Virginia, Charlottesville, Virginia 22908, USA. 6
These authors contributed equally to this work.
Correspondence should be addressed to Lindsay Hinck hinck@biology.ucsc.edu netrin-1UNC5Unc5aUnc5h1Ntn1NTN1In 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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