RT Journal Article
SR Electronic
T1 Par3A and Par3B orchestrate podocyte architecture by regulating RhoA levels
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2020.02.10.933671
DO 10.1101/2020.02.10.933671
A1 Sybille Koehler
A1 Johanna Odenthal
A1 David Unnersjö Jess
A1 Martin Höhne
A1 Christian Jüngst
A1 Ferdi Grawe
A1 Martin Helmstädter
A1 H. Henning Hagmann
A1 Gerd Walz
A1 Wilhelm Bloch
A1 Carien Niessen
A1 Bernhard Schermer
A1 Andreas Wodarz
A1 Barry Denholm
A1 Thomas Benzing
A1 Sandra Iden
A1 Paul Thomas Brinkkoetter
YR 2020
UL http://biorxiv.org/content/early/2020/02/10/2020.02.10.933671.abstract
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.