EN
Dystroglycan (DG) is a cell adhesion receptor composed of αand β-subunits that form a transmembrane link between the extracellular matrix and the intracellular actin cytoskeleton. Loss of DG function is implicated in muscular dystrophies and the aetiology of epithelial cancers. We have previously reported that β-DG is a target for matrix metalloproteinase-9 (MMP-9), an extracellularly operating enzyme, known to be pivotal for synaptic plasticity, learning and memory. This may suggest an important role of β-DG cleavage by MMP-9 in neuronal activity. Although it has been demonstrated that deletion of DG in neurons blunted hippocampal long-term potentiation (LTP), detailed knowledge concerning mechanisms of action of DG in neuronal cells is still lacking. To study the role of DG in neuronal structure and function we used the lentiviral vector (LV) to deliver shRNA, specifically silencing DG in cultured hippocampal neurons. We found that knockdown of DG simplifies dendritic arbor morphology as well as decreases the total length of dendrites. To determine whether DG deletion influences the dendritic spine shape and motility we performed life imaging of MMP-9-treated cultures. We observed differences in spine remodeling between control and LV-infected neurons. Our results suggest that DG is required for proper neuronal maturation and dendritic spine plasticity.