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Expression of c‐fos, c‐jun, and N‐terminal kinase (JNK) in a Development Model of Induced Apoptotic Death in Neurons of the Substantia Nigra
Author(s) -
Oo Tinmarla,
Henchcliffe Claire,
James Daylon,
Burke Robert E.
Publication year - 1999
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1999.0720557.x
Subject(s) - c jun , substantia nigra , terminal (telecommunication) , apoptosis , kinase , microbiology and biotechnology , chemistry , programmed cell death , c fos , neuroscience , biology , gene expression , biochemistry , gene , computer science , transcription factor , dopamine , computer network , dopaminergic
: The transcription factors c‐fos and c‐jun have been proposed to play a role in the initiation of programmed cell death in neurons. We have shown that programmed cell death, with the morphology of apoptosis, occurs in dopamine neurons of the substantia nigra (SN) during normal postnatal development and that this death event can be induced by early striatal target injury. We have investigated the relationship between c‐fos and c‐jun protein expression and induced death in neurons of the SN. Although c‐fos is induced, it is unlikely to play a role in cell death, because its expression is not well correlated with apoptotic death either temporally or at a cellular level. Expression of c‐jun, however, is both temporally and regionally correlated with induction of death, and, at a cellular level, it colocalizes with apoptotic morphology. The increased expression of c‐jun is likely to be functionally significant, because it is associated with increased c‐jun expression. JNK expression also colocalizes with apoptotic morphology. We conclude that c‐jun is likely to play a role in the initiation of apoptotic cell death in these neurons.