PT  - JOURNAL ARTICLE
AU  - Sybille Koehler
AU  - Johanna Odenthal
AU  - David Unnersjö Jess
AU  - Martin Höhne
AU  - Christian Jüngst
AU  - Ferdi Grawe
AU  - Martin Helmstädter
AU  - H. Henning Hagmann
AU  - Gerd Walz
AU  - Wilhelm Bloch
AU  - Carien Niessen
AU  - Bernhard Schermer
AU  - Andreas Wodarz
AU  - Barry Denholm
AU  - Thomas Benzing
AU  - Sandra Iden
AU  - Paul Thomas Brinkkoetter
TI  - Par3A and Par3B orchestrate podocyte architecture by regulating RhoA levels
AID  - 10.1101/2020.02.10.933671
DP  - 2020 Jan 01
TA  - bioRxiv
PG  - 2020.02.10.933671
4099  - http://biorxiv.org/content/early/2020/02/10/2020.02.10.933671.short
4100  - http://biorxiv.org/content/early/2020/02/10/2020.02.10.933671.full
AB  - 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.