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  • 1. Majda, Mateusz
    et al.
    Grones, Peter
    Sintorn, Ida-Maria
    Vain, Thomas
    Milani, Pascale
    Krupinski, Pawel
    Zagorska-Marek, Beata
    Viotti, Corrado
    Umeå University, Faculty of Science and Technology, Umeå Plant Science Centre (UPSC). Institute of Biochemistry and Biology, Plant Physiology, University of Potsdam, 14476 Potsdam, Germany.
    Jonsson, Henrik
    Mellerowicz, Ewa J.
    Hamant, Olivier
    Robert, Stephanie
    Mechanochemical Polarization of Contiguous Cell Walls Shapes Plant Pavement Cells2017In: Developmental Cell, ISSN 1534-5807, E-ISSN 1878-1551, Vol. 43, no 3, p. 290-304Article in journal (Refereed)
    Abstract [en]

    The epidermis of aerial plant organs is thought to be limiting for growth, because it acts as a continuous load-bearing layer, resisting tension. Leaf epidermis contains jigsaw puzzle piece-shaped pavement cells whose shape has been proposed to be a result of subcellular variations in expansion rate that induce local buckling events. Paradoxically, such local compressive buckling should not occur given the tensile stresses across the epidermis. Using computational modeling, we show that the simplest scenario to explain pavement cell shapes within an epidermis under tension must involve mechanical wall heterogeneities across and along the anticlinal pavement cell walls between adjacent cells. Combining genetics, atomic force microscopy, and immunolabeling, we demonstrate that contiguous cell walls indeed exhibit hybrid mechanochemical properties. Such biochemical wall heterogeneities precede wall bending. Altogether, this provides a possible mechanism for the generation of complex plant cell shapes.

  • 2. Schwab, R.
    et al.
    Palatnik, J. F.
    Riester, M.
    Schommer, C.
    Schmid, M.
    Department of Molecular Biology, Max Planck Institute for Developmental Biology, 72076 Tübingen, Germany.
    Weigel, D.
    Specific effects of MicroRNAs on the plant transcriptome2005In: Developmental Cell, ISSN 1534-5807, E-ISSN 1878-1551, Vol. 8, no 4, p. 517-527Article in journal (Refereed)
  • 3.
    Sjödal, My
    et al.
    Umeå University, Faculty of Medicine, Umeå Centre for Molecular Medicine (UCMM).
    Edlund, Thomas
    Umeå University, Faculty of Medicine, Umeå Centre for Molecular Medicine (UCMM).
    Gunhaga, Lena
    Umeå University, Faculty of Medicine, Umeå Centre for Molecular Medicine (UCMM).
    Time of exposure to BMP signals plays a key role in the specification of the olfactory and lens placodes ex vivo.2007In: Developmental Cell, ISSN 1534-5807, E-ISSN 1878-1551, Vol. 13, no 1, p. 141-149Article in journal (Refereed)
  • 4. van Erp, Susan
    et al.
    van den Heuvel, Dianne M. A.
    Fujita, Yuki
    Robinson, Ross A.
    Hellemons, Anita J. C. G. M.
    Adolfs, Youri
    Van Battum, Eljo Y.
    Blokhuis, Anna M.
    Kuijpers, Marijn
    Demmers, Jeroen A. A.
    Hedman, Håkan
    Umeå University, Faculty of Medicine, Department of Radiation Sciences.
    Hoogenraad, Casper C.
    Siebold, Christian
    Yamashita, Toshihide
    Pasterkamp, R. Jeroen
    Lrig2 Negatively Regulates Ectodomain Shedding of Axon Guidance Receptors by ADAM Proteases2015In: Developmental Cell, ISSN 1534-5807, E-ISSN 1878-1551, Vol. 35, no 5, p. 537-552Article in journal (Refereed)
    Abstract [en]

    Many guidance receptors are proteolytically cleaved by membrane-associated metalloproteases of the ADAM family, leading to the shedding of their ectodomains. Ectodomain shedding is crucial for receptor signaling and function, but how this process is controlled in neurons remains poorly understood. Here, we show that the transmembrane protein Lrig2 negatively regulates ADAM-mediated guidance receptor proteolysis in neurons. Lrig2 binds Neogenin, a receptor for repulsive guidance molecules (RGMs), and prevents premature Neogenin shedding by ADAM17 (TACE). RGMa reduces Lrig2-Neogenin interactions, providing ADAM17 access to Neogenin and allowing this protease to induce ectodomain shedding. Regulation of ADAM17-mediated Neogenin cleavage by Lrig2 is required for neurite growth inhibition by RGMa in vitro and for cortical neuron migration in vivo. Furthermore, knockdown of Lrig2 significantly improves CNS axon regeneration. Together, our data identify a unique ligand-gated mechanism to control receptor shedding by ADAMs and reveal functions for Lrigs in neuron migration and regenerative failure.

  • 5. Vera-Sirera, Francisco
    et al.
    De Rybel, Bert
    Urbez, Cristina
    Kouklas, Evangelos
    Pesquera, Marta
    Camilo Alvarez-Mahecha, Juan
    Minguet, Eugenio G.
    Tuominen, Hannele
    Umeå University, Faculty of Science and Technology, Department of Plant Physiology. Umeå University, Faculty of Science and Technology, Umeå Plant Science Centre (UPSC).
    Carbonell, Juan
    Borst, Jan Willem
    Weijers, Dolf
    Blazquez, Miguel A.
    A bHLH-Based Feedback Loop Restricts Vascular Cell Proliferation in Plants2015In: Developmental Cell, ISSN 1534-5807, E-ISSN 1878-1551, Vol. 35, no 4, p. 432-443Article in journal (Refereed)
    Abstract [en]

    Control of tissue dimensions in multicellular organisms requires the precise quantitative regulation of mitotic activity. In plants, where cells are immobile, tissue size is achieved through control of both cell division orientation and mitotic rate. The bHLH transcription factor heterodimer formed by TARGET OF MONOPTEROS5 (TMO5) and LONESOME HIGHWAY (LHVV) is a central regulator of vascular width-increasing divisions. An important unanswered question is how its activity is limited to specify vascular tissue dimensions. Here we identify a regulatory network that restricts TMO5/LHW activity. We show that thermospermine synthase ACAULIS5 antagonizes TMO5/LHW activity by promoting the accumulation of SAC51-LIKE (SACL) bHLH transcription factors. SACL proteins heterodimerize with LHW therefore likely competing with TMO5/LHW interactions prevent activation of TMO5/LHW target genes, and suppress the over-proliferation caused by excess TMO5/LHW activity. These findings connect two thus-far disparate pathways and provide a mechanistic understanding of the quantitative control of vascular tissue growth.

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