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[P2.26]: Roles of the onecut transcription factors in catecholaminergic neuron differentiation
Author(s) -
Espana A.,
Clotman F.
Publication year - 2008
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2008.09.151
Subject(s) - citation , library science , catecholaminergic cell groups , transcription (linguistics) , psychology , catecholaminergic , computer science , neuroscience , linguistics , philosophy , catecholamine
been demonstrated in vivo. In sensory neurons Sema3A-induced repellent activity is mediated by PlexinA4, but can be substituted to a large degree by PlexinA3. Here we show that, in contrast, Sema3A-induced death is completely dependent on the PlexinA3 receptor. This PlexinA3-dependent cell death is mediated via BAX activation. In addition to being protected from Sema3A-induced death, PlexinA3 / neurons are also partly protected from death by neurotrophin withdrawal. Consistent with a role for PlexinA3 in cell death, there is decreased apoptosis and an increase in the number of DRG neurons in PlexinA3 / embryos. We found no reduction in cell death in Sema3A / mice, but did find a significant reduction in cell death in Sema3A / mice that are also missing one allele of BAX, when compared to wild-type or BAX+/ only embryos, revealing an important role for the PlexinA3/ Sema3A-signaling pathway in determining neuronal cell numbers in vivo. We thus propose that the widely held view of neuronal cell death being at least partially due to limiting amounts of neurotrophins should be modified to include the idea that a balance between death-inducing signals, such as semaphorins, and survival signals, such as neurotrophins, determines whether a cell dies or survives.