UNC5A promotes neuronal apoptosis during spinal cord development independent of netrin-1
ME Williams, X Lu, WL McKenna, R Washington… - Nature …, 2006 - nature.com
ME Williams, X Lu, WL McKenna, R Washington, A Boyette, P Strickland, A Dillon…
Nature neuroscience, 2006•nature.comIn 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.
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.
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.
nature.com