The RNA-binding protein NANOS1 controls hippocampal synaptogenesis

Proteins from the NANOS family are conserved translational repressors with a well-known role in gonad development in both vertebrates and invertebrates. In addition, Drosophila Nanos controls neuron maturation and function, and rodent Nanos1 affects cortical neuron differentiation. Here we show that...

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Bibliographic Details
Published in:PloS one 2023-04, Vol.18 (4), p.e0284589-e0284589
Main Authors: Maschi, Darío, Fernández-Alvarez, Ana J, Boccaccio, Graciela Lidia
Format: Article
Language:English
Subjects:
Analysis
Animals
Apoptosis
Biology and Life Sciences
Clusters
Dendritic spines
Dendritic Spines - metabolism
Dendritic structure
Depolarization
Females
Genes
Hippocampus
Hippocampus - metabolism
Insects
Medicine and Health Sciences
Nervous system
Neurons
Postsynaptic density proteins
Protein binding
Proteins
Rats
Repressors
Research and Analysis Methods
RNA
RNA-binding protein
RNA-Binding Proteins - metabolism
siRNA
Spine
Synapsin
Synaptogenesis
Vertebrates
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Summary:Proteins from the NANOS family are conserved translational repressors with a well-known role in gonad development in both vertebrates and invertebrates. In addition, Drosophila Nanos controls neuron maturation and function, and rodent Nanos1 affects cortical neuron differentiation. Here we show that rat Nanos1 is expressed in hippocampal neurons and that the siRNA-mediated knockdown of Nanos1 impairs synaptogenesis. We found that both dendritic spine size and number were affected by Nanos1 KD. Dendritic spines were smaller and more numerous. Moreover, whereas in control neurons most dendritic PSD95 clusters contact pre-synaptic structures, a larger proportion of PSD95 clusters lacked a synapsin counterpart upon Nanos1 loss-of-function. Finally, Nanos1 KD impaired the induction of ARC typically triggered by neuron depolarization. These results expand our knowledge on the role of NANOS1 in CNS development and suggest that RNA regulation by NANOS1 governs hippocampal synaptogenesis.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0284589