The Petritsch Lab uses pharmacological, molecular, and in vivo and ex vivo techniques, to uncover the mechanism for cell fate decisions in oligodendrocyte precursor cells, in the healthy and diseased brain.
Oligodendrocytes arise from oligodendrocyte precursor cells (OPCs) and accomplish myelination in the central nervous system to regulate axonal function. Although OPCs are the most abundant proliferative population in the adult and ageing brain, we are only beginning to understand their heterogeneity and the underlying molecular regulation of OPC functions.
Do OPCs in the adult central nervous system decide about their fate that is to proliferate or differentiate, by undergoing asymmetric divisions? Does the underlying mechanism of asymmetric cell divisions in mammalian cells diverge from the conserved process found in Drosophila neuroblasts? Does it involve epigenetic regulators? Is there a cell intrinsic or extrinsic mechanism that determines whether OPC divisions are symmetrical or asymmetrical?
Deviations from the normal OPC fate leads to a number of diseases, such as gliomas, and demyelinating disorders, including multiple sclerosis (MS).
What are the consequences of deregulation of asymmetric OPC division for the central nervous system? Are defective asymmetric divisions the cause for deviation from the normal OPC fate? If so, can we pinpoint the molecules that are crucial for the deregulation of cell fate and characterize them as novel targets for anti-glioma therapy?
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