Abstract
Asymmetric division (AD) is a fundamental mechanism whereby unequal inheritance of various cellular compounds during mitosis generates unequal fate in the two daughter cells. Unequal repartitions of transcription factors, receptors as well as mRNA have been abundantly described in AD. In contrast, the involvement of intermediate filaments in this process is still largely unknown. AD occurs in stem cells during development but was also recently observed in cancer stem cells. Here, we demonstrate the asymmetric distribution of the main astrocytic intermediate filament, namely the glial fibrillary acid protein (GFAP), in mitotic glioma multipotent cells isolated from glioblastoma (GBM), the most frequent type of brain tumor. Unequal mitotic repartition of GFAP was also observed in mice non-tumoral neural stem cells indicating that this process occurs across species and is not restricted to cancerous cells. Immunofluorescence and videomicroscopy were used to capture these rare and transient events. Considering the role of intermediate filaments in cytoplasm organization and cell signaling, we propose that asymmetric distribution of GFAP could possibly participate in the regulation of normal and cancerous neural stem cell fate.
Highlights
Asymmetric distribution of molecules during division is a fundamental mechanism which has a major impact on the formation of cell diversity and final size of the organs [1,2,3]
We focused on the glial fibrillary acid protein (GFAP) intermediate filament which is expressed in mature astrocytes in the nervous system
We demonstrate that the intermediate filament GFAP can segregate asymmetrically in multipotent GBM and non tumoral neural cell division
Summary
Asymmetric distribution of molecules during division is a fundamental mechanism which has a major impact on the formation of cell diversity and final size of the organs [1,2,3]. Unequal repartition of proteins, such as transcription factors and growth factor receptors, and other cellular constituents such as mRNA or even organelles, will generate unequal cell fates from genetically identical daughter cells [4,5,6,7]. In accordance with their central role in development, several proteins involved in the Notch and Wnt pathways have been described to be asymmetrically distributed during division [8, 9]. Reduction of asymmetric repartition of the proteoglycan NG2 during division of oligodendrocyte progenitor cells correlates with
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