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Published on: May 12, 2015
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Brain development is impaired in c-fos -/- mice
Fabiola N Velazquez1, César G Prucca1, Olivier Etienne2,3,4,5
1CIQUIBIC (CONICET), Departamento de Química Biológica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Córdoba, Argentina.
Oncotarget
|July 6, 2015
Summary
The proto-oncogene c-Fos is crucial for normal neocortex development. Loss of c-Fos in mice leads to reduced neocortex thickness and altered Neural Stem Progenitor Cells differentiation, impacting brain growth.
Area of Science:
- Neuroscience
- Developmental Biology
- Molecular Biology
Background:
- c-Fos is a proto-oncogene regulating cellular functions.
- Deregulation of c-Fos is linked to abnormal development and cancer.
- c-Fos knockout mice exhibit reduced body weight and brain size.
Purpose of the Study:
- To investigate the role of c-Fos in mouse neocortex development.
- To analyze the impact of c-Fos deficiency on Neural Stem Progenitor Cells (NSPCs) differentiation.
- To understand c-Fos's contribution to embryonic brain growth.
Main Methods:
- Comparative analysis of c-fos-/- and wild-type mouse embryos at gestational days 13.5, 14.5, and 16.5.
- Assessment of neocortex thickness, apoptosis, and mitosis rates.
- Evaluation of NSPC differentiation markers and AP-1/DNA complex formation.
Main Results:
- c-fos-/- embryos showed a ~15% reduction in neocortex thickness.
- Increased apoptosis and altered NSPC differentiation trends (vertical mitotic angle) were observed in c-fos-/- embryos.
- Changes in differentiation markers were evident by E13.5 and E16.5, with increased AP-1/DNA complexes in knockout embryos.
Conclusions:
- c-Fos plays a significant role in normal neocortex development.
- c-Fos influences NSPC differentiation and survival through its AP-1 activity.
- Disruption of c-Fos impacts embryonic brain development, suggesting its proto-oncogenic relevance.
