Deficiency of the miR-29a/b-1 cluster leads to ataxic features and cerebellar alterations in mice.

作者: Aikaterini S Papadopoulou , Lutgarde Serneels , Tilmann Achsel , Wim Mandemakers , Zsuzsanna Callaerts-Vegh

DOI: 10.1016/J.NBD.2014.10.006

关键词: Olfactory bulbCerebellumSpinocerebellar ataxiaBiologyNeuroscienceAtaxiaMotor coordinationCell biologyHippocampusPhenotypeKnockout mouse

摘要: miR-29 is expressed strongly in the brain and alterations expression have been linked to several neurological disorders. To further explore function of this miRNA brain, we generated miR-29a/b-1 knockout animals. Knockout mice develop a progressive disorder characterized by locomotor impairment ataxia. The different members family are neurons olfactory bulb, hippocampus Purkinje cells cerebellum. Morphological analysis showed that smaller display less dendritic arborisation compared their wildtype littermates. In addition, decreased number parallel fibers form synapses on cells. We identified mRNAs significantly up-regulated absence cluster. At protein level, however, voltage-gated potassium channel Kcnc3 (Kv3.3) was cerebella miR-29a/b mice. Dysregulation KCNC3 may contribute ataxic phenotype.

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