Control of neuronal branching by the death receptor CD95 (Fas/Apo-1)
Abstract
The CD95 (Apo-1/Fas)/CD95 ligand (CD95L) system is best characterized as a trigger of apoptosis. Nevertheless, despite broad expression of CD95L and CD95 in the developing brain, absence of functional CD95 (lpr mice) or CD95L (gld mice) does not alter neuronal numbers. Here, we report that in embryonic hippocampal and cortical neurons in vivo and in vitro CD95L does not induce apoptosis. Triggering of CD95 in cultured immature neurons substantially increases neurite branches by promoting their formation. The branching increase occurs in a caspase-independent and death domain-dependent manner and is paralleled by an increase in the nonphosphorylated form of Tau. Most importantly, lpr and gld mutants exhibit a reduced number of dendritic branches in vivo at the time when synapse formation takes place. These data reveal a novel function for the CD95 system and add to the picture of guidance molecules in the developing brain.
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In embryonic hippocampal and cortical neurons, CD95 activation stimulated neurite branching in a caspase-independent and death-domain-dependent manner, paralleled by an increase in non-phosphorylated Tau.
“In embryonic hippocampal and cortical neurons, activation of CD95 stimulated neurite branching, which occurred in a caspase-independent and death-domain-dependent manner and was paralleled by an increase in non-phosphorylated Tau.98”
From Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation (2012) · cites this paper as [98]
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- Authors
- Zuliani, C., Kleber, S., Klussmann, S., Wenger, T., Kenzelmann, M., Schreglmann, N., Martinez, A., del Rio, J. A., Soriano, E., Vodrazka, P., Kuner, R., Groene, H.-J., Herr, I., Krammer, P. H., & Martin-Villalba, A.
- Affiliations
- German Cancer Research Center (DE)
- Parc Científic de Barcelona (ES)
- Heidelberg University (DE)
- Venue
- Cell Death & Differentiation
- Published
- 2005-07-08
- Volume
- 13
- Issue
- 1
- Pages
- 31-40
- ISSN
- 1350-9047 (ISSN-L)
- 1476-5403
- OpenAlex
- W1994416984
- Cited by
- 117
- References
- 45
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 2 · 2023: 1 · 2022: 3 · 2021: 2 · 2020: 3 · 2019: 4 · 2018: 3 · 2017: 6 · 2016: 5 · 2015: 9 · 2014: 5 · 2013: 9 · 2012: 7
- FWCI
- 4.14
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cell Death and Differentiation (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft (SFB405)
- Ministerio de Ciencia y Tecnología
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Axon Guidance and Neuronal Signaling
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- Fas, Fas ligand, neuronal branching, neurite branching, dendritic branching, lpr mice, gld mice, death domain, tau phosphorylation, synaptogenesis, hippocampal neurons, cortical neurons, neuronal development, guidance molecules
- MeSH terms
- Animals, Cell Differentiation, Cells, Cultured, Hippocampus, Membrane Glycoproteins, Mice, Inbred CBA, Mice, Mutant Strains, Neuronal Plasticity, Neurons, Transcription Factors, Signal Transduction, Neurites, Apoptosis, fas Receptor, Caspases, Tumor Necrosis Factors, Mice, Fas Ligand Protein
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