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

• DOI: 10.1038/nn1736
• Publication Date: 2006-07-09T17:28:34Z
• Authors: Megan E Williams; Xiaowei Lu; William L McKenna; Raesha Washington; Adam Boyette; Phyllis Strickland; Allison Dillon; Zaven Kaprielian; Marc Tessier-Lavigne; Lindsay Hinck
• Keywords: Mice, Knockout; Neurons; 0303 health sciences; Tumor Suppressor Proteins; Apoptosis; Receptors, Cell Surface; Netrin-1; Mice; 03 medical and health sciences; Spinal Cord; Animals; Nerve Growth Factors; Netrin Receptors

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.