Abstract
Mutation in huntingtin (HTT) gene causes Huntington’s disease (HD). Expression of many micro RNAs is known to alter in cell, animal models and brains of HD patients, but their cellular effects are not known. Here, we show that expression of microRNA-124 (miR-124) is down regulated in HD striatal mutant STHdhQ111/HdhQ111 cells, a cell model of HD compared to STHdhQ7/HdhQ7 cells. STHdhQ7/HdhQ7 and STHdhQ111/HdhQ111 cells express endogenously full length wild type and mutant HTT respectively. We confirmed this result in R6/2 mouse, an animal model of HD, expressing mutant HTT. Gene Ontology terms related to cell cycle were enriched significantly with experimentally validated targets of miR-124. We observed that expression of Cyclin A2 (CCNA2), a putative target of miR-124 was increased in mutant STHdhQ111/HdhQ111 cells and brains of R6/2 mice. Fraction of cells in S phase was higher in asynchronously growing mutant STHdhQ111/HdhQ111 cells compared to wild type STHdhQ7/HdhQ7 cells and could be altered by exogenous expression or inhibition of miR-124. Exogenous expression or knock down of CCNA2, a target of miR-124, also alters proportion of cells in S phase of HD cell model. In summary, decreased miR-124 expression could increase CCNA2 in cell and animal model of HD and is involved in deregulation of cell cycle in STHdhQ111/HdhQ111 cells.
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