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Par3A and Par3B orchestrate podocyte architecture by regulating RhoA levels

Sybille Koehler, Johanna Odenthal, David Unnersjö Jess, Martin Höhne, Christian Jüngst, Ferdi Grawe, Martin Helmstädter, H. Henning Hagmann, Gerd Walz, Wilhelm Bloch, Carien Niessen, Bernhard Schermer, Andreas Wodarz, Barry Denholm, Thomas Benzing, Sandra Iden, Paul Thomas Brinkkoetter
doi: https://doi.org/10.1101/2020.02.10.933671
Sybille Koehler
1Department II of Internal Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
2Center for Molecular Medicine Cologne (CMMC), University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
3Biomedical Sciences, University of Edinburgh, Edinburgh, Scotland, UK
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Johanna Odenthal
1Department II of Internal Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
2Center for Molecular Medicine Cologne (CMMC), University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
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David Unnersjö Jess
1Department II of Internal Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
2Center for Molecular Medicine Cologne (CMMC), University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
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Martin Höhne
1Department II of Internal Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
2Center for Molecular Medicine Cologne (CMMC), University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
4Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany
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Christian Jüngst
4Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany
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Ferdi Grawe
2Center for Molecular Medicine Cologne (CMMC), University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
4Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany
5Molecular Cell Biology, Institute I for Anatomy, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
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Martin Helmstädter
6Renal Division, Department of Medicine, Faculty of Medicine and Medical Center, University of Freiburg, Freiburg, Germany
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H. Henning Hagmann
1Department II of Internal Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
2Center for Molecular Medicine Cologne (CMMC), University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
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Gerd Walz
6Renal Division, Department of Medicine, Faculty of Medicine and Medical Center, University of Freiburg, Freiburg, Germany
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Wilhelm Bloch
7Department of Molecular and Cellular Sport Medicine, Institute of Cardiovascular Research and Sport Medicine, German Sport University Cologne, Cologne, Germany
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Carien Niessen
2Center for Molecular Medicine Cologne (CMMC), University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
4Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany
8Department of Dermatology, University Hospital of Cologne, Cologne, Germany
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Bernhard Schermer
1Department II of Internal Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
2Center for Molecular Medicine Cologne (CMMC), University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
4Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany
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Andreas Wodarz
2Center for Molecular Medicine Cologne (CMMC), University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
4Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany
5Molecular Cell Biology, Institute I for Anatomy, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
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Barry Denholm
3Biomedical Sciences, University of Edinburgh, Edinburgh, Scotland, UK
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Thomas Benzing
1Department II of Internal Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
2Center for Molecular Medicine Cologne (CMMC), University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
4Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany
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Sandra Iden
2Center for Molecular Medicine Cologne (CMMC), University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
4Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany
9Institute for Cell and Developmental Biology, Saarland University, Homburg/Saar, Germany
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Paul Thomas Brinkkoetter
1Department II of Internal Medicine, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
2Center for Molecular Medicine Cologne (CMMC), University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany
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  • For correspondence: paul.brinkkoetter@uk-koeln.de
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Abstract

Glomerular diseases are a major cause for chronic kidney disorders. In the majority of cases podocyte injury is causative for disease development. Cytoskeletal rearrangements and morphological changes are hallmark features of podocyte injury and result in dedifferentiation and subsequent loss of podocytes. Here, we establish a link between components of the Par3 polarity complex and actin regulators, which are necessary to establish and maintain the podocytes architecture utilizing both, mouse and Drosophila models. We demonstrate that the two mammalian Par3 proteins, Par3A and Par3B, share redundant functions despite differing in their ability to interact with other components of the Par complex. Only simultaneous inactivation of both Par3 proteins causes a severe disease phenotype in mouse podocytes by regulating Rho-GTP levels involving the actin regulators Synaptopodin and CD2AP in an aPKC independent manner.

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Par3A and Par3B orchestrate podocyte architecture by regulating RhoA levels
Sybille Koehler, Johanna Odenthal, David Unnersjö Jess, Martin Höhne, Christian Jüngst, Ferdi Grawe, Martin Helmstädter, H. Henning Hagmann, Gerd Walz, Wilhelm Bloch, Carien Niessen, Bernhard Schermer, Andreas Wodarz, Barry Denholm, Thomas Benzing, Sandra Iden, Paul Thomas Brinkkoetter
bioRxiv 2020.02.10.933671; doi: https://doi.org/10.1101/2020.02.10.933671
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Par3A and Par3B orchestrate podocyte architecture by regulating RhoA levels
Sybille Koehler, Johanna Odenthal, David Unnersjö Jess, Martin Höhne, Christian Jüngst, Ferdi Grawe, Martin Helmstädter, H. Henning Hagmann, Gerd Walz, Wilhelm Bloch, Carien Niessen, Bernhard Schermer, Andreas Wodarz, Barry Denholm, Thomas Benzing, Sandra Iden, Paul Thomas Brinkkoetter
bioRxiv 2020.02.10.933671; doi: https://doi.org/10.1101/2020.02.10.933671

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