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Coordinated mRNA translation at the synapse is increasingly recognized as a critical mechanism for neuronal regulation. Pumilio, a translational regulator, is known to be involved in neuronal homeostasis and memory formation in Drosophila. Most recently, the mammalian Pumilio homolog  Pumilio-2  ( Pum2 ) has been found to play a role in the mammalian nervous system, in particular in regulating morphology, arborization and excitability of neuronal dendrites,  in vitro . However, the role of  Pum2 in vivo  remains unclear. Here, we report our investigation of the functional and molecular consequences of  Pum2  disruption in vivo using an array of neurophysiology, behavioral and gene expression profiling techniques. We used  Pum2 -deficient mice to monitor  in vivo  brain activity using EEG and to study behavior traits, including memory, locomotor activity and nesting capacities. Because of the suspected role of  Pum2  in neuronal excitability, we also examined the susceptibility to seizure induction. Finally, we used a quantitative gene expression profiling assay to identify key molecular partners of  Pum2 . We found that  Pum2 -deficient mice have abnormal behavioral strategies in spatial and object memory test. Additionally,  Pum2  deficiency is associated with increased locomotor activity and decreased body weight. We also observed environmentally-induced impairment in nesting behavior. Most importantly,  Pum2 -deficient mice showed spontaneous EEG abnormalities and had lower seizure thresholds using a convulsing dosage of pentylenetetrazole. Finally, some genes, including neuronal ion channels, were differentially expressed in the hippocampus of  Pum2 -deficient mice. These findings demonstrate that  Pum2  serves key functions in the adult mammalian central nervous system encompassing neuronal excitability and behavioral response to environmental challenges.

Pumilio-2 Function in the Mouse Nervous System