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251 results on '"Berninger, Benedikt"'

6. Quiescence Modulates Stem Cell Maintenance and Regenerative Capacity in the Aging Brain

Author

Kalamakis, Georgios, Brüne, Daniel, Ravichandran, Srikanth, Bolz, Jan, Fan, Wenqiang, Ziebell, Frederik, Stiehl, Thomas, Catalá-Martinez, Francisco, Kupke, Janina, Zhao, Sheng, Llorens-Bobadilla, Enric, Bauer, Katharina, Limpert, Stefanie, Berger, Birgit, Christen, Urs, Schmezer, Peter, Mallm, Jan Philipp, Berninger, Benedikt, Anders, Simon, del Sol, Antonio, Marciniak-Czochra, Anna, and Martin-Villalba, Ana

Published
2019
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13. TOX3 regulates neural progenitor identity

Author

Sahu, Sanjeeb Kumar, Fritz, Alina, Tiwari, Neha, Kovacs, Zsuzsa, Pouya, Alireza, Wüllner, Verena, Bora, Pablo, Schacht, Teresa, Baumgart, Jan, Peron, Sophie, Berninger, Benedikt, Tiwari, Vijay K., and Methner, Axel

Published
2016
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15. Lmo4 synergizes with Fezf2 to promote direct in vivo reprogramming of upper layer cortical neurons and cortical glia towards deep layer neuron identities

Author

Felske, Torsten, Tocco, Chiara, Peron, Sophie, Harb, Kawssar, Alfano, Christian, Galante, Chiara, Berninger, Benedikt, and Studer, Michele

Abstract

In vivo direct neuronal reprogramming relies on the implementation of an exogenous transcriptional program allowing to achieve conversion of a particular neuronal or glial cell type towards a new neuronal identity. The transcription factor Fezf2 is known for its role in neuronal subtype specification of deep-layer subcortical projection neurons. In fact, high ectopic Fezf2 expression can convert both upper layer and striatal projection neurons into a corticofugal fate, even if at low efficiency. In this study, we show that Fezf2 synergizes with the nuclear co-adaptor Lmo4 to further enhance reprogramming of upper-layer cortical pyramidal neurons into deep-layer corticofugal neurons, at bothembryonic and early postnatal stages. Reprogrammed neurons express deep-layer molecular markers and project toward subcerebral targets, including the thalamus, cerebral peduncle, and spinal cord. We also show that Fezf2 co-expression with the reprogramming factors Neurog2 and Bcl2 in early postnatal glia promotes glia-to-neuron conversion with hallmarks of deep-layer neurons, and with Lmo4 promoting further morphological complexity. These data support a novel role for Lmo4 in synergizing with Fezf2 during direct lineage conversion in vivo.

Published
2023

32. Enhanced proliferation of oligodendrocyte progenitor cells following retrovirus mediated Achaete-scute complex-like 1 overexpression in the postnatal cerebral cortex in vivo.

Author

Galante, Chiara, Marichal, Nicolás, Scarante, Franciele Franco, Ghayad, Litsa Maria, Youran Shi, Schuurmans, Carol, Berninger, Benedikt, and Péron, Sophie

Subjects
CEREBRAL cortex, PROGENITOR cells, GLIAL fibrillary acidic protein, FATE mapping (Genetics), NEUROGLIA
Abstract

The proneural transcription factor Achaete-scute complex-like 1 (Ascl1) is a major regulator of neural fate decisions, implicated both in neurogenesis and oligodendrogliogenesis. Focusing on its neurogenic activity, Ascl1 has been widely used to reprogram non-neuronal cells into induced neurons. In vitro, Ascl1 induces efficient reprogramming of proliferative astroglia from the early postnatal cerebral cortex into interneuron-like cells. Here, we examined whether Ascl1 can similarly induce neuronal reprogramming of glia undergoing proliferation in the postnatal mouse cerebral cortex in vivo. Toward this goal, we targeted cortical glia during the peak of proliferative expansion (i.e., postnatal day 5) by injecting a retrovirus encoding for Ascl1 into the mouse cerebral cortex. In contrast to the efficient reprogramming observed in vitro, in vivo Ascl1-transduced glial cells were converted into doublecortin-immunoreactive neurons only with very low efficiency. However, we noted a drastic shift in the relative number of retrovirus-transduced Sox10-positive oligodendrocyte progenitor cells (OPCs) as compared to glial fibrillary acidic protein (GFAP)-positive astrocytes. Genetic fate mapping demonstrated that this increase in OPCs was not due to Ascl1-mediated astrocyte-to-OPC fate conversion. Rather, EdU incorporation experiments revealed that Ascl1 caused a selective increase in proliferative activity of OPCs, but not astrocytes. Our data indicate that rather than inducing neuronal reprogramming of glia in the early postnatal cortex, Ascl1 is a selective enhancer of OPC proliferation. [ABSTRACT FROM AUTHOR]

Published
2022
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43. Reprogramming cellular identity in vivo.

Author

Leaman, Sydney, Marichal, Nicolás, and Berninger, Benedikt

Subjects
GENE regulatory networks, GENETIC regulation, CELL physiology
Abstract

Cellular identity is established through complex layers of genetic regulation, forged over a developmental lifetime. An expanding molecular toolbox is allowing us to manipulate these gene regulatory networks in specific cell types in vivo. In principle, if we found the right molecular tricks, we could rewrite cell identity and harness the rich repertoire of possible cellular functions and attributes. Recent work suggests that this rewriting of cell identity is not only possible, but that newly induced cells can mitigate disease phenotypes in animal models of major human diseases. So, is the sky the limit, or do we need to keep our feet on the ground? This Spotlight synthesises key concepts emerging from recent efforts to reprogramme cellular identity in vivo. We provide our perspectives on recent controversies in the field of glia-to-neuron reprogramming and identify important gaps in our understanding that present barriers to progress. [ABSTRACT FROM AUTHOR]

Published
2022
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