UNC5A promotes neuronal apoptosis during spinal cord development independent of netrin-1.
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.
Williams
Megan E
ME
Department of Molecular, Cell and Developmental Biology, University of California Santa Cruz, Santa Cruz, California 95064, USA.
Lu
Xiaowei
X
McKenna
William L
WL
Washington
Raesha
R
Boyette
Adam
A
Strickland
Phyllis
P
Dillon
Allison
A
Kaprielian
Zaven
Z
Tessier-Lavigne
Marc
M
Hinck
Lindsay
L
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D051379:Mice; D018345:Mice, Knockout; D009414:Nerve Growth Factors / Q000235:genetics / Q000378:metabolism*; D000075386:Netrin Receptors; D000075388:Netrin-1; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism*; D013116:Spinal Cord / Q000002:abnormalities / Q000166:cytology* / Q000196:embryology* / Q000378:metabolism; D025521:Tumor Suppressor Proteins / Q000235:genetics / Q000378:metabolism*
D009414:Nerve Growth Factors; D000075386:Netrin Receptors; C000617353:Ntn1 protein, mouse; D011956:Receptors, Cell Surface; D025521:Tumor Suppressor Proteins; C000617308:Unc5A protein, mouse; D000075388:Netrin-1