@article{TejosRodriguezFurlanAdamowskietal.2018, author = {Tejos, Ricardo and Rodriguez-Furlan, Cecilia and Adamowski, Maciej and Sauer, Michael and Norambuena, Lorena and Friml, Jiri}, title = {PATELLINS are regulators of auxin-mediated PIN1 relocation and plant development in Arabidopsis thaliana}, series = {Journal of cell science}, volume = {131}, journal = {Journal of cell science}, number = {2}, publisher = {Company of Biologists Limited}, address = {Cambridge}, issn = {0021-9533}, doi = {10.1242/jcs.204198}, pages = {10}, year = {2018}, abstract = {Coordinated cell polarization in developing tissues is a recurrent theme in multicellular organisms. In plants, a directional distribution of the plant hormone auxin is at the core of many developmental programs. A feedback regulation of auxin on the polarized localization of PIN auxin transporters in individual cells has been proposed as a self-organizing mechanism for coordinated tissue polarization, but the molecular mechanisms linking auxin signalling to PIN-dependent auxin transport remain unknown. We used a microarray-based approach to find regulators of the auxin-induced PIN relocation in Arabidopsis thaliana root, and identified a subset of a family of phosphatidylinositol transfer proteins (PITPs), the PATELLINs (PATLs). Here, we show that PATLs are expressed in partially overlapping cell types in different tissues going through mitosis or initiating differentiation programs. PATLs are plasma membrane-associated proteins accumulated in Arabidopsis embryos, primary roots, lateral root primordia and developing stomata. Higher order patl mutants display reduced PIN1 repolarization in response to auxin, shorter root apical meristem, and drastic defects in embryo and seedling development. This suggests that PATLs play a redundant and crucial role in polarity and patterning in Arabidopsis.}, language = {en} } @article{DejongheKuenenMylleetal.2016, author = {Dejonghe, Wim and Kuenen, Sabine and Mylle, Evelien and Vasileva, Mina and Keech, Olivier and Viotti, Corrado and Swerts, Jef and Fendrych, Matyas and Ortiz-Morea, Fausto Andres and Mishev, Kiril and Delang, Simon and Scholl, Stefan and Zarza, Xavier and Heilmann, Mareike and Kourelis, Jiorgos and Kasprowicz, Jaroslaw and Nguyen, Le Son Long and Drozdzecki, Andrzej and Van Houtte, Isabelle and Szatmari, Anna-Maria and Majda, Mateusz and Baisa, Gary and Bednarek, Sebastian York and Robert, Stephanie and Audenaert, Dominique and Testerink, Christa and Munnik, Teun and Van Damme, Daniel and Heilmann, Ingo and Schumacher, Karin and Winne, Johan and Friml, Jiri and Verstreken, Patrik and Russinova, Eugenia}, title = {Mitochondrial uncouplers inhibit clathrin-mediated endocytosis largely through cytoplasmic acidification}, series = {Nature Communications}, volume = {7}, journal = {Nature Communications}, publisher = {Nature Publ. Group}, address = {London}, issn = {2041-1723}, doi = {10.1038/ncomms11710}, pages = {1959 -- 1968}, year = {2016}, abstract = {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.}, language = {en} } @article{RobertGrunewaldSaueretal.2015, author = {Robert, Helene S. and Grunewald, Wim and Sauer, Michael and Cannoot, Bernard and Soriano, Mercedes and Swarup, Ranjan and Weijers, Dolf and Bennett, Malcolm and Boutilier, Kim and Friml, Jiri}, title = {Plant embryogenesis requires AUX/LAX-mediated auxin influx}, series = {Development : Company of Biologists}, volume = {142}, journal = {Development : Company of Biologists}, number = {4}, publisher = {Company of Biologists Limited}, address = {Cambridge}, issn = {0950-1991}, doi = {10.1242/dev.115832}, pages = {702 -- 711}, year = {2015}, abstract = {The plant hormone auxin and its directional transport are known to play a crucial role in defining the embryonic axis and subsequent development of the body plan. Although the role of PIN auxin efflux transporters has been clearly assigned during embryonic shoot and root specification, the role of the auxin influx carriers AUX1 and LIKE-AUX1 (LAX) proteins is not well established. Here, we used chemical and genetic tools on Brassica napus microspore-derived embryos and Arabidopsis thaliana zygotic embryos, and demonstrate that AUX1, LAX1 and LAX2 are required for both shoot and root pole formation, in concert with PIN efflux carriers. Furthermore, we uncovered a positive-feedback loop between MONOPTEROS-(ARF5)dependent auxin signalling and auxin transport. This MONOPTEROS dependent transcriptional regulation of auxin influx (AUX1, LAX1 and LAX2) and auxin efflux (PIN1 and PIN4) carriers by MONOPTEROS helps to maintain proper auxin transport to the root tip. These results indicate that auxin-dependent cell specification during embryo development requires balanced auxin transport involving both influx and efflux mechanisms, and that this transport is maintained by a positive transcriptional feedback on auxin signalling.}, language = {en} }