c-Jun contributes to amyloid beta-induced neuronal apoptosis but is not necessary for amyloid beta-induced c-jun induction

The role of gene expression in neuronal apoptosis may be cell- and apoptoti c stimulus-specific. Previously, we and others showed that amyloid beta (A beta) -induced neuronal apoptosis is accompanied by c-jun induction. Moreov er, c-Jun contributes to neuronal death in several apoptosis paradigms invo lving survival factor withdrawal. To evaluate the role of c-Jun in A beta t oxicity, we compared A beta-induced apoptosis in neurons from murine fetal littermates that were deficient or wild-type with respect to c-Jun. We repo rt that neurons deficient for c-jun are relatively resistant to A beta toxi city, suggesting that c-Jun contributes to apoptosis in this model. When ch anges in gene expression were quantified in neurons treated in parallel, we found that A beta treatment surprisingly led to an apparent activation of the c-jun promoter in both the c-jun-deficient and wild-type neurons, sugge sting that c-Jun is not necessary for activation of the c-jun promoter. Ind eed, several genes induced by A beta in wildtype neurons were also induced in c-jun-deficient neurons, including c-fos, fosB, ngfi-B, and i(K)B. In su mmary, these results indicate that c-Jun contributes to A beta-induced neur onal death but that c-Jun is not necessary for c-jun induction.