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VandenHeuvel, K.

Publications and source records attributed to VandenHeuvel, K..

2 recordsLinked to original sources

The midbody and midbody remnant are assembly sites for RNA and active translation

The midbody (MB) is a transient structure at the spindle midzone that is required for cytokinesis, the terminal stage of cell division. Long ignored as a vestigial remnant of cytokinesis, we now know MBs are released post-abscission as extracellular vesicles called MB remnants (MBRs) and can modulate cell proliferation, fate decisions, tissue polarity, neuronal architecture, and tumorigenic behavior. Here, we demonstrate that the MB matrix--the structurally amorphous MB core of unknown composition--is the site of ribonucleoprotein assembly and is enriched in mRNAs that encode proteins involved in cell fate, oncogenesis, and pluripotency, that we are calling the MB granule. Using a quantitative transcriptomic approach, we identified a population of mRNAs enriched in mitotic MBs and confirmed their presence in signaling MBR vesicles released by abscission. The MB granule is unique in that it is translationally active, contains both small and large ribosomal subunits, and has both membrane-less and membrane-bound states. Both MBs and post-abscission MBRs are sites of spatiotemporally regulated translation, which is initiated when nascent daughter cells re-enter G1 and continues after extracellular release. We demonstrate that the MB is the assembly site of an RNP granule. MKLP1 and ARC are necessary for the localization and translation of RNA in the MB dark zone, whereas ESCRT-III was necessary to maintain translation levels in the MB. Our data suggest a model in which the MB functions as a novel RNA-based organelle with a uniquely complex life cycle. We present a model in which the assembly and transfer of RNP complexes are central to post-mitotic MBR function and suggest the MBR serves as a novel mode of RNA-based intercellular communication with a defined biogenesis that is coupled to abscission, and inherently links cell division status with signaling capacity. To our knowledge, this is the first example of an autonomous extracellular vesicle with active translation activity. HighlightsO_LIThe MB, the center region of the intercellular bridge, is the assembly site of a ribonucleoprotein granule, we call the MB granule C_LIO_LIDistinct oncogenic and pluripotent transcription factor RNAs, including Jun/Fos and KLF4, are packaged in MBs and MBRs C_LIO_LIThe MB granule is coincident with the MB matrix, or dark zone, of the MB C_LIO_LIThe Kif23/MKLP1 kinesin is a core hexanediol-sensitive MB granule component C_LIO_LIThe MB and MBR are site of active translation that begins in early G1 and continues post-mitotically C_LIO_LIMKLP1 and ARC are necessary for RNA targeting/maintenance and translation at the MB C_LIO_LIDepletion of ESCRT-III increases the levels of translation during abscission C_LIO_LIAbscission releases MBRs as MB granule-harboring, translating extracellular vesicles C_LIO_LIMultiple cell types including cancer, stem, neural stem, all have actively translating MBRs C_LIO_LIMBRs are proposed as a novel mode of intercellular communication by extracellular vesicle-mediated direct transfer of RNA C_LI

cell biology↗

MAP1LC3C regulates lysosomal exocytosis and induces zinc reprogramming in renal cancer cells

MAP1LC3C (LC3C) is a member of the microtubule associated family of proteins that are essential in the formation of autophagosomes and lysosomal degradation of cargo. LC3C has tumor suppressing activity and its expression is dependent on kidney cancer tumor suppressors, such as VHL and FLCN. Recently we demonstrated that LC3C autophagy is regulated by noncannonical upstream regulatory complexes and targets for degradation postdivision midbody rings associated with cancer cells stemness. Here we show that loss of LC3C leads to peripheral positioning of the lysosomes and lysosomal exocytosis (LE) in a subset of cells. This process is independent of the autophagic activity of LC3C. Analysis of isogenic cells with low and high LE shows substantial transcriptomic reprogramming with altered expression of Zn-related genes and activity of Polycomb Repressor Complex 2 (PRC2), accompanied by a robust decrease in intracellular Zn. Metabolomic analysis revealed alterations in amino acid steady-state levels. Cells with augmented LE show tumor initiation properties and form aggressive tumors in xenograft models. Immunocytochemistry identified high levels of LAMP1 on the plasma membrane of cancer cells in human ccRCC and reduced levels of Zn, an indication that LE is a frequent event in ccRCC, potentially contributing to the loss of Zn. Overall, these data indicate that an important tumor suppressing activity of LC3C is contributing to the reprogramming of lysosomal activity and Zn metabolism with implication for epigenetic remodeling in a subpopulation of tumor propagating properties of cancer cells.

cell biology↗