TY - JOUR A1 - Dejonghe, Wim A1 - Kuenen, Sabine A1 - Mylle, Evelien A1 - Vasileva, Mina A1 - Keech, Olivier A1 - Viotti, Corrado A1 - Swerts, Jef A1 - Fendrych, Matyas A1 - Ortiz-Morea, Fausto Andres A1 - Mishev, Kiril A1 - Delang, Simon A1 - Scholl, Stefan A1 - Zarza, Xavier A1 - Heilmann, Mareike A1 - Kourelis, Jiorgos A1 - Kasprowicz, Jaroslaw A1 - Nguyen, Le Son Long A1 - Drozdzecki, Andrzej A1 - Van Houtte, Isabelle A1 - Szatmari, Anna-Maria A1 - Majda, Mateusz A1 - Baisa, Gary A1 - Bednarek, Sebastian York A1 - Robert, Stephanie A1 - Audenaert, Dominique A1 - Testerink, Christa A1 - Munnik, Teun A1 - Van Damme, Daniel A1 - Heilmann, Ingo A1 - Schumacher, Karin A1 - Winne, Johan A1 - Friml, Jiri A1 - Verstreken, Patrik A1 - Russinova, Eugenia T1 - Mitochondrial uncouplers inhibit clathrin-mediated endocytosis largely through cytoplasmic acidification JF - Nature Communications N2 - ATP production requires the establishment of an electrochemical proton gradient across the inner mitochondrial membrane. Mitochondrial uncouplers dissipate this proton gradient and disrupt numerous cellular processes, including vesicular trafficking, mainly through energy depletion. Here we show that Endosidin9 (ES9), a novel mitochondrial uncoupler, is a potent inhibitor of clathrin-mediated endocytosis (CME) in different systems and that ES9 induces inhibition of CME not because of its effect on cellular ATP, but rather due to its protonophore activity that leads to cytoplasm acidification. We show that the known tyrosine kinase inhibitor tyrphostinA23, which is routinely used to block CME, displays similar properties, thus questioning its use as a specific inhibitor of cargo recognition by the AP-2 adaptor complex via tyrosine motif-based endocytosis signals. Furthermore, we show that cytoplasm acidification dramatically affects the dynamics and recruitment of clathrin and associated adaptors, and leads to reduction of phosphatidylinositol 4,5-biphosphate from the plasma membrane. Y1 - 2016 U6 - https://doi.org/10.1038/ncomms11710 SN - 2041-1723 VL - 7 SP - 1959 EP - 1968 PB - Nature Publ. Group CY - London ER - TY - GEN A1 - Prát, Tomáš A1 - Hajny ́, Jakub A1 - Grunewald, Wim A1 - Vasileva, Mina A1 - Molnár, Gergely A1 - Tejos, Ricardo A1 - Schmid, Markus A1 - Sauer, Michael A1 - Friml, Jiří T1 - WRKY23 is a component of the transcriptional network mediating auxin feedback on PIN polarity T2 - Postprints der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe N2 - Auxin is unique among plant hormones due to its directional transport that is mediated by the polarly distributed PIN auxin transporters at the plasma membrane. The canalization hypothesis proposes that the auxin feedback on its polar flow is a crucial, plant-specific mechanism mediating multiple self-organizing developmental processes. Here, we used the auxin effect on the PIN polar localization in Arabidopsis thaliana roots as a proxy for the auxin feedback on the PIN polarity during canalization. We performed microarray experiments to find regulators of this process that act downstream of auxin. We identified genes that were transcriptionally regulated by auxin in an AXR3/IAA17-and ARF7/ARF19-dependent manner. Besides the known components of the PIN polarity, such as PID and PIP5K kinases, a number of potential new regulators were detected, among which the WRKY23 transcription factor, which was characterized in more detail. Gain-and loss-of-function mutants confirmed a role for WRKY23 in mediating the auxin effect on the PIN polarity. Accordingly, processes requiring auxin-mediated PIN polarity rearrangements, such as vascular tissue development during leaf venation, showed a higher WRKY23 expression and required the WRKY23 activity. Our results provide initial insights into the auxin transcriptional network acting upstream of PIN polarization and, potentially, canalization-mediated plant development. T3 - Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe - 1123 KW - apical-basal axis KW - arabidopsis-thaliana KW - root gravitropism KW - DNA-binding KW - gene-expression KW - transport KW - efflux KW - canalization KW - plants KW - phosphorylation Y1 - 2021 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-446331 SN - 1866-8372 IS - 1123 ER - TY - JOUR A1 - Prat, Tomas A1 - Hajny, Jakub A1 - Grunewald, Wim A1 - Vasileva, Mina A1 - Molnar, Gergely A1 - Tejos, Ricardo A1 - Schmid, Markus A1 - Sauer, Michael A1 - Friml, Jiří T1 - WRKY23 is a component of the transcriptional network mediating auxin feedback on PIN polarity JF - PLoS Genetics : a peer-reviewed, open-access journal N2 - Auxin is unique among plant hormones due to its directional transport that is mediated by the polarly distributed PIN auxin transporters at the plasma membrane. The canalization hypothesis proposes that the auxin feedback on its polar flow is a crucial, plant-specific mechanism mediating multiple self-organizing developmental processes. Here, we used the auxin effect on the PIN polar localization in Arabidopsis thaliana roots as a proxy for the auxin feedback on the PIN polarity during canalization. We performed microarray experiments to find regulators of this process that act downstream of auxin. We identified genes that were transcriptionally regulated by auxin in an AXR3/IAA17-and ARF7/ARF19-dependent manner. Besides the known components of the PIN polarity, such as PID and PIP5K kinases, a number of potential new regulators were detected, among which the WRKY23 transcription factor, which was characterized in more detail. Gain-and loss-of-function mutants confirmed a role for WRKY23 in mediating the auxin effect on the PIN polarity. Accordingly, processes requiring auxin-mediated PIN polarity rearrangements, such as vascular tissue development during leaf venation, showed a higher WRKY23 expression and required the WRKY23 activity. Our results provide initial insights into the auxin transcriptional network acting upstream of PIN polarization and, potentially, canalization-mediated plant development. Y1 - 2018 U6 - https://doi.org/10.1371/journal.pgen.1007177 SN - 1553-7404 VL - 14 IS - 1 PB - PLoS CY - San Fransisco ER -