Title: Deficiency of the miR-29a/b-1 cluster leads to ataxic features and cerebellar alterations in mice
Authors: Papadopoulou, Smaragda ×
Serneels, Lutgarde
Achsel, Tilmann
Mandemakers, Wim
Callaerts-Vegh, Zsuzsanna
Dooley, James
Lau Poui Cheung, Pierre
Ayoubi, Torik
Radaelli, Enrico
Spinazzi, Marco
Neumann, Melanie
Hébert, Sébastien S
Silahtaroglu, Asli
Liston, Adrian
D'Hooge, Rudi
Glatzel, Markus
De Strooper, Bart #
Issue Date: Jan-2015
Publisher: Blackwell Science
Series Title: Neurobiology of Disease vol:73 pages:275-88
Article number: S0969-9961(14)00299-X
Abstract: miR-29 is expressed strongly in the brain and alterations in expression have been linked to several neurological disorders. To further explore the function of this miRNA in the brain, we generated miR-29a/b-1 knockout animals. Knockout mice develop a progressive disorder characterized by locomotor impairment and ataxia. The different members of the miR-29 family are strongly expressed in neurons of the olfactory bulb, the hippocampus and in the Purkinje cells of the cerebellum. Morphological analysis showed that Purkinje cells are smaller and display less dendritic arborisation compared to their wildtype littermates. In addition, a decreased number of parallel fibers form synapses on the Purkinje cells. We identified several mRNAs significantly upregulated in the absence of the miR-29a/b-1 cluster. At the protein level, however, the voltage-gated potassium channel Kcnc3 (Kv3.3) was significantly upregulated in the cerebella of the miR-29a/b knockout mice. Dysregulation of KCNC3 expression may contribute to the ataxic phenotype.
ISSN: 0969-9961
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Department of Human Genetics - miscellaneous
Laboratory for the Research of Neurodegenerative Diseases (VIB-KU Leuven Center for Brain & Disease Research)
Laboratory for Biological Psychology
Laboratory of Genetics of Autoimmunity (VIB-KU Leuven Center for Brain & Disease Research)
× corresponding author
# (joint) last author

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