Journal
NEURON
Volume 99, Issue 6, Pages 1188-+Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2018.08.017
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Funding
- German Research Foundation (DFG) [LI 858/6-3, LI 858/9-1, INST 410/45-1 FUGG, BE 5136/1-2, BE 5136/2-1, KL 1395/8-1, WU 164/5-1, CRC870]
- Bavarian Research Network ForIPS''
- University Hospital Erlangen (IZKF) [E12, E16, E21, E25]
- German Federal Ministry of Education and Research [BMBF 01GQ113, 01GM1520A, 01EK1609B, Integrament 01ZX1314H]
- NIH [AG048284, AG053268]
- Deutsche Forschungsgemeinschaft [DFG GRK2162/1]
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Autophagy is a conserved catabolic pathway with emerging functions in mammalian neurodevelopment and human neurodevelopmental diseases. The mechanisms controlling autophagy in neuronal development are not fully understood. Here, we found that conditional deletion of the Forkhead Box O transcription factors FoxO1, FoxO3, and FoxO4 strongly impaired autophagic flux in developing neurons of the adult mouse hippocampus. Moreover, FoxO deficiency led to altered dendritic morphology, increased spine density, and aberrant spine positioning in adult-generated neurons. Strikingly, pharmacological induction of autophagy was sufficient to correct abnormal dendrite and spine development of FoxO-deficient neurons. Collectively, these findings reveal a novel link between FoxO transcription factors, autophagic flux, and maturation of developing neurons.
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