Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 108, Issue 52, Pages 21099-21104Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1112063108
Keywords
cell death; synaptogenesis; neuronal differentiation; hippocampus
Categories
Funding
- Medical Research Council, United Kingdom
- Odysseus
- VIB, Belgium
- Alleanza contro il Cancro [ACC12]
- MIUR [20078P7T3K_001)/FIRB, RBIP06LCA9_0023, RBIP06LCA9_0C, 2008MRLSNZ_004]
- AIRC [2008-2010_33-08, 5471, 2011-IG11955, 9979]
- Italian Human ProteomeNet [RBRN07BMCT]
- Telethon [GGPO9133]
- Min. Salute [26/07]
- IDI-IRCCS [RF06 c. 73, RF07 c. 57, RF08 c. 15]
- Ministry of Education and Science of the Russian Federation [11.G34.31.0069]
- MRC [MC_U132670600, MC_U132681855] Funding Source: UKRI
- Medical Research Council [MC_U132681855, MC_U132670600] Funding Source: researchfish
Ask authors/readers for more resources
The p53 family member TAp73 is a transcription factor that plays a key role in many biological processes, including neuronal development. In particular, we have shown that p73 drives the expression of miR-34a, but not miR-34b and c, in mouse cortical neurons. miR-34a in turn modulates the expression of synaptic targets including synaptotagmin-1 and syntaxin-1A. Here we show that this axis is retained in mouse ES cells committed to differentiate toward a neurological phenotype. Moreover, overexpression of miR-34a alters hippocampal spinal morphology, and results in electrophysiological changes consistent with a reduction in spinal function. Therefore, the TAp73/miR-34a axis has functional relevance in primary neurons. These data reinforce a role for miR-34a in neuronal development.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available