| First Author | Wenzel A | Year | 2002 |
| Journal | J Neurochem | Volume | 80 |
| Issue | 6 | Pages | 1089-94 |
| PubMed ID | 11953459 | Mgi Jnum | J:126010 |
| Mgi Id | MGI:3760353 | Doi | 10.1046/j.0022-3042.2002.00807.x |
| Citation | Wenzel A, et al. (2002) Fra-1 substitutes for c-Fos in AP-1-mediated signal transduction in retinal apoptosis. J Neurochem 80(6):1089-94 |
| abstractText | Lack of the AP-1 member c-Fos protects photoreceptors against light-induced apoptosis, a model for retinal degeneration. In mice, light damage increases the activity of the transcription factor AP-1, while pharmacological suppression of AP-1 prevents apoptosis, suggesting the involvement of pro-apoptotic AP-1 target genes. Recently, however, it was shown that photoreceptors expressing Fra-1 in place of c-Fos (Fos (Fosl1/Fosl1) ) are apoptosis competent despite the lack of transactivation domains in Fra-1. Here, we show that morphological features of light-induced apoptosis were indistinguishable in Fos (Fosl1/Fosl1) and wild-type mice. Furthermore, light exposure comparably increased AP-1 activity in both genotypes. Opposite to wild-type mice, Fra-1, but not c-Fos, was detectable in AP-1 complexes of Fos (Fosl1/Fosl1) mice. Importantly, AP-1 responsiveness for glucocorticoid receptor-mediated inhibition was preserved in Fos (Fosl1/Fosl1) mice. Thus, Fra-1 takes over for c-Fos in pro- and anti-apoptotic signal transduction. As Fra-1 lacks transactivation domains, AP-1 may not induce, but rather suppress genes in retinal light damage. |
