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Tuning apicobasal polarity and junctional recycling in the hemogenic endothelium orchestrates the morphodynamic complexity of emerging pre-hematopoietic stem cells —Source data 4 relative to Figure 7 – ArhGEF11 CRISPR interference

Raw image files (TIFF format), corresponding 2D-cartographies (_2Dmap.tiff files) and metadata files for 2D-cartographies (.xml files, readable with the opensource software Icy), relative to Figure 7B and Figure 7 - Figure Supplement 6 (see Materials and Methods — Morphological and morphometric analysis of aortic and hemogenic cells). The source data comprises for each 48 - 55 hpf Tg(kdrl:eGFP-JAM3b; kdrl:nls-mKate2) zebrafish embryo 3 z-stack and 2D cartographies (segments 1 to 3) encompassing the whole length of the aorta, for control condition (n = 2 individuals) and morpholino splicing interference condition (n = 2 individuals). For z-stacks of both control and morphant conditions, two fluorescence channels were acquired, corresponding to the nuclear mKate2 expressed in endothelial cells and the eGFP-JAMs signal localized at the intercellular junctions of endothelial cells. Z-stack were acquired using a confocal spinning disk microscope. Voxel size: x: 0.1635, y: 0.1635, z:0.3 µm. 2D-cartographies were obtained using the Icy plugin “TubeSkinner”, and the semi-manual segmentation of all aortic cells can be uploaded from the corresponding metadata file on the 2D-cartographies using the load ROI function of Icy.

Tuning apicobasal polarity and junctional recycling in the hemogenic endothelium orchestrates the morphodynamic complexity of emerging pre-hematopoietic stem cells —Source data 3 relative to Figure 7 – ArhGEF11 morpholino splicing interference

Raw image files (TIFF format), corresponding 2D-cartographies (_2Dmap.tiff files) and metadata files for 2D-cartographies (.xml files, readable with the opensource software Icy), relative to Figure 7A and Figure 7 - Figure Supplement 5 (see Materials and Methods — Morphological and morphometric analysis of aortic and hemogenic cells). The source data comprises for each 48 - 55 hpf Tg(kdrl:eGFP-JAM2a; kdrl:nls-mKate2) zebrafish embryo 3 z-stack and 2D cartographies (segments 1 to 3) encompassing the whole length of the aorta, for control condition (n = 2 individuals) and morpholino splicing interference condition (n = 3 individuals). For z-stacks of both control and morphant conditions, two fluorescence channels were acquired, corresponding to the nuclear mKate2 expressed in endothelial cells and the eGFP-JAMs signal localized at the intercellular junctions of endothelial cells. Z-stack were acquired using a confocal spinning disk microscope. Voxel size: x: 0.1635, y: 0.1635, z:0.3 µm. 2D-cartographies were obtained using the Icy plugin “TubeSkinner”, and the semi-manual segmentation of all aortic cells can be uploaded from the corresponding metadata file on the 2D-cartographies using the load ROI function of Icy.

Tuning apicobasal polarity and junctional recycling in the hemogenic endothelium orchestrates the morphodynamic complexity of emerging pre-hematopoietic stem cells —Source data 1 relative to Figure 3

Raw image files (TIFF format) relative to Figure 3 (see Materials and Methods — Dt-runx1 phenotype analysis – cell count). The source data comprises for each 52 - 55 hpf zebrafish embryo 3 z-stack (segments 1 to 3) encompassing the whole length of the aorta, for control condition (Tg(Kdrl:Gal4;UAS:RFP), n = 3 individuals) and mutant condition (Tg(kdrl:Gal4;UAS:RFP;4xNR:dt-runx1-eGFP), n = 7 individuals). For control condition, one fluorescence channel was acquired, corresponding to the cytoplasmic RFP expressed in endothelial cells. For mutant condition, two fluorescence channels were acquired, corresponding first to the cytoplasmic RFP expressed in endothelial cells using the same reporter as for the control condition, and second the cleaved cytoplasmic GFP reporting the expression of our dt-runx1 mutant construct in endothelial cells. Z-stack were acquired using a confocal spinning disk microscope. Voxel size: x: 0.1635, y: 0.1635, z:0.3 µm.

Tuning apicobasal polarity and junctional recycling in the hemogenic endothelium orchestrates the morphodynamic complexity of emerging pre-hematopoietic stem cells —Source data 2 relative to Figure 4

Raw image files (TIFF format) and segmented 3D images (.ims, Imaris proprietary files) relative to Figure 4 and Figure 4 Figure Supplement 3 (see Materials and Methods — RNAscope image analysis – Pard3). The source data comprises for each 52 - 55 hpf zebrafish embryos 2 z-stack (segments 1 to 2) encompassing the whole length of the aorta, for control condition (Tg(Kdrl:eGFP), n = 7 individuals) and mutant condition (Tg(kdrl:Gal4; 4xNR:dt-runx1-eGFP), n = 12 individuals). For both control and mutant conditions, two fluorescence channels are displayed, corresponding to the cytoplasmic GFP expressed in endothelial cells (in green) and the RNAscope signal (OPAL-570, in magenta). Z-stack were acquired using a confocal spinning disk microscope. Voxel size: x: 0.1635, y: 0.1635, z:0.4 µm. The .ims files contain the 3D rendering of the z-stacks as well as the segmentations of Pard3ba mRNA RNAscope spots (in magenta), in the aorta (Spots 1 Selection) or outside (Spots 1), as well as the segmentation of endothelial cells (green) (Cells 1) and hemogenic endothelial cells (Cells 1 Cell export).

opencc-zeroMar 2024View details →

dryad36/100

Data from: ESCRT-III-dependent adhesive and mechanical changes are triggered by a mechanism detecting alteration of Septate Junction integrity in Drosophila epithelial cells

Barrier functions of proliferative epithelia are constantly challenged by mechanical and chemical constraints. How epithelia respond to and cope with disturbances of barrier functions to allow tissue integrity maintenance is poorly characterized. Cellular junctions play an important role in this process and intracellular traffic contribute to their homeostasis. Here, we reveal that, in Drosophila pupal notum, alteration of the bi- or tricellular septate junctions (SJs) triggers a mechanism with two prominent outcomes. On one hand, there is an increase in the levels of E-cadherin, F-Actin and non-muscle Myosin II in the plane of adherens junctions. On the other hand, β-integrin/Vinculin-positive cell contacts are reinforced along the lateral and basal membranes. We found that the weakening of SJ integrity, caused by the depletion of bi- or tricellular SJ components, alters ESCRT-III/Vps32/Shrub distribution, reduces degradation, and instead favours recycling of SJ components, an effect that extends to other recycled transmembrane protein cargoes including Crumbs, its effector β-Heavy Spectrin Karst, and β-integrin. We propose a mechanism by which epithelial cells, upon sensing alterations of the septate junction, reroute the function of Shrub to adjust the balance of degradation/recycling of junctional cargoes and thereby compensate for barrier junction defects to maintain epithelial integrity.

zenodo36/100

April 7, 2024 (v1) Image Open Tuning apicobasal polarity and junctional recycling in the hemogenic endothelium orchestrates the morphodynamic complexity of emerging pre-hematopoietic stem cells —Source data 5 relative to Figure 7 - Figure Supplement 4

Source data file relative to Figure 7 – figure supplement 4 Panel A Raw image of agarose gel showing the 2 alternative mRNAs encoding for ArhGEF11 in control animals (left track, control) and after injection of the MO at the one cell stage (right track, +MO at 2 and 5ng). The source data includes the raw files (native format .scn and open source format .tiff) as well as a pdf file showing both the full scale image and the cropped image selected for the figure.

opencc-by-4.0May 2024View details →

dryad36/100

Data from: ESCRT-III-dependent adhesive and mechanical changes are triggered by a mechanism detecting alteration of Septate Junction integrity in Drosophila epithelial cells

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publicMar 2024View details →

opencc-zeroDec 2019View details →

Ab initio electronic stopping power for protons in Ga0.5In0.5P/GaAs/Ge triple-junction solar cells for space applications

Motivated by the radiation damage of solar panels in space, firstly, the results of Monte Carlo particle transport simulations are presented for proton impact on triple-junction Ga0.5In0.5P/GaAs/Ge solar cells, showing the proton projectile penetration in the cells as a function of energy. It is followed by a systematic ab initio investigation of the electronic stopping power for protons in different layers of the cell at the relevant velocities via real-time time-dependent density functional theory (RT-TDDFT) calculations. The electronic stopping power is found to depend significantly on different channeling conditions, which should affect the low velocity damage predictions, and which are understood in terms of impact parameter and electron density along the path. Additionally, we explore the effect of the interface between the layers of the multilayer structure on the energy loss of a proton, along with the effect of strain in the lattice-matched solar cell. Both effects are found to be small compared with the main bulk effect. The interface energy loss has been found to increase with decreasing proton velocity, and in one case, there is an effective interface energy gain.

openOct 2023View details →

Data set for "Photoelectrochemical Schlenk cell functionalization of multi-junction water-splitting photoelectrodes"

The data set is organised along the figures of the publication. <ul> <li>The '.ers' and '.ert' files are reflection anisotropy spectra and and transients, respectively, in the native format of Laytec's EpiRAS.</li> <li>The '.xy' files are XPS data in the export format of SpecsLab Prodigy.</li> <li>The electrochemistry data is in the '.txt' file format "Zahner Online Display data file version: 2" exported from the Zahner ZenniumPro potentiostat. Currents are absolute currents, For sample areas see the additional file description.</li> </ul>

opencc-by-4.0Oct 2022View details →

Golgi cell gap junction coupling in cerebellum cortex model WT and KO conditions

Golgi cell gap junction coupling in cerebellum cortex model WT and KO conditions

opencc-by-4.0Oct 2022View details →

Gap junction coupling of Golgi cells in cerebellar cortex model

Gap junction coupling of Golgi cells in cerebellar cortex model

Data supporting the analysis of lymphatic endothelial cell junctions and shape

Data in support of:  Dynamic cytoskeletal regulation of cell shape supports resilience of lymphatic endothelium Hans Schoofs1#, Nina Daubel1#, Sarah Schnabellehner1, Max Grönloh2, Sebastián Palacios Martínez3, Aleksi Halme4, Amanda M. Marks1, Marie Jeansson1, Sara Barcos5, Cord Brakebusch6, Rui Benedito7, Britta Engelhardt5, Dietmar Vestweber8, Konstantin Gängel1, Fabian Linsenmeier9, Sebastian Schürmann9, Pipsa Saharinen4,10, Jaap D. van Buul2,3,11, Oliver Friedrich9, Richard S. Smith12, Mateusz Majda13, and Taija Mäkinen1,4,10*   1Uppsala University, Department of Immunology, Genetics and Pathology, Dag Hammarskjölds väg 20, 751 85 Uppsala, Sweden. 2Department of Medical Biochemistry at the Amsterdam UMC, location AMC, The Netherlands. 3Department of Molecular Cytology, Leeuwenhoek Centre for Advanced Microscopy at Swammerdam Institute for Life Sciences at the University of Amsterdam, The Netherlands. 4Translational Cancer Medicine Program and Department of Biochemistry and Developmental Biology, University of Helsinki, Haartmaninkatu 8, 00014 Helsinki, Finland. 5Theodor Kocher Institute, University of Bern, Bern, Switzerland. 6Biotech Research and Innovation Center, University of Copenhagen, Ole Maaløes Vej 5, 2200 Denmark. 7Centro Nacional de Investigaciones Cardiovasculares, Melchor Fernández Almagro 3, E-28029 Madrid, Spain. 8Max Planck Institute for Molecular Biomedicine, Münster, Germany. 9Institute of Medical Biotechnology, Department of Chemical and Biological Engineering, Friedrich-Alexander-University, Erlangen-Nürnberg, Paul-Gordan-Str.3, 91052 Erlangen, Germany. 10Wihuri Research Institute, Haartmaninkatu 8, 00290 Helsinki, Finland. 11Amsterdam UMC, Sanquin Research and Landsteiner Laboratory, The Netherlands. 12John Innes Centre, Norwich Research Park, Norwich NR4 7UH, UK. 13Department of Plant Molecular Biology, University of Lausanne, CH-1015 Lausanne, Switzerland. #These authors contributed equally. *Corresponding author: Taija Mäkinen, E-mail: <a href="mailto:taija.makinen@igp.uu.se">taija.makinen@igp.uu.se</a>, <a href="mailto:taija.makinen@helsinki.fi">taija.makinen@helsinki.fi</a>   DATASET A: Annotated cell-cell junction types in lymphatic capillaries of wild type mouse ear skin at different ages  __________________________________________________________________________________________________________ Contents <ul> <li>SOURCE DATA Fig1 FINAL. xlsx</li> <li>3w <ul> <li>animal 1</li> <li>animal 2</li> <li>animal 3</li> <li>animal 4</li> <li>animal 5</li> <li>sprouts</li> </ul> </li> <li>5w <ul> <li>animal 1</li> <li>animal 2</li> <li>animal 3</li> <li>animal 4</li> <li>animal 5</li> <li>diaphragm <ul> <li>Overview of diaphragm and high mag. of different capillary ends</li> </ul> </li> <li>trachea</li> </ul> </li> <li>25w <ul> <li>animal 1</li> <li>animal 2</li> <li>animal 3</li> <li>animal 4</li> <li>animal 5</li> <li>diaphragm</li> <li>trachea</li> </ul> </li> </ul> File legends C1 images: inverted LYVE1 signal (.tif) C2 images: inverted VE-cadherin signal (.tif) MAX images: RGB merge of LYVE1 (cyan) and VE-cadherin (red) (.tif) "NAME".roi: Regions of interest (ROI) of annotated junctions can be imported in ImageJ Methods Junctional classification:  Analysis of junction morphology was done on blunt-ended initial lymphatic capillaries in the segment between the intial tip and the first valve. Junction types were quantified in Z-stack projection by numbering of individual lobes of LYVE1 and VE-cadherin-stained LECs and subsequent categorizing of lobe-associated junctions based on VE-cadherin signal. Four categories were defined: 1) Button junction – a punctate VE-cadherin+ deposit at the neck of LYVE1+ lobe/overlap, with no detectable VE-cadherin at the borders of the overlap, 2) Curvilinear junction – unsegmented(continous) or segmented (discontinuous) distribution of VE-cadherin within one border of LYVE1+ lobe/cellular overlap, 3) Double junction – unsegmented(continous) or segmented (discontinuous) distribution of VE-cadherin within both borders of LYVE1+ lobe/cellular overlap, and 4) LYVE1- curvilineair junction – unsegmented(continous) linear VE-cadherin distribution at cell-cell contacts in the absence of LYVE1. Wild-type C57BL/6J mice were used for analysis of junction types, and 4-5 blunt ended vessels per mouse from five mice per age group and condition were analysed; in total 1785 junctions were annoted Imaging: Confocal images were obtained using a Leica Stellaris 5 confocal microscope equipped with 405 nm and white light lasers, 63x/1.3 HC PL APO CORR CS2 Glycerol immersion objective, and Leica LAS X software. Images were aquired at 1.51 digital zoom using a 2048x2048 resolution Tissue processing and staining:   Tissues were fixed in 4% paraformaldehyde for 2 h at RT and permeabilized in 0.3% Triton X-100 in PBS (PBST) for 10 min. After blocking in PBST with 2% bovine serum albumin, 1% FBS for 2 h, tissues were incubated with primary antibodies in blocking buffer overnight, followed by PBST washing and incubation with fluorescent dye-conjugated secondary antibodies for 2 h. All incubation steps were carried out at RT. Prior to mounting in Mowiol, samples were repeatedly washed in PBST and water. Antibodies used: Goat anti-mouse VE-cadherin (R&D Systems, AF1002; 1:200), Rat anti-mouse LYVE1 (R&D Systems, MAB2125; 1:200)   DATASET B: Finite element method (FEM) simulations of cellular stresses _______________________________________________________________ The FEM simulations were performed with MorphoMechanX using available models adapted from Sapala et al, eLife 7, e32794 (2018). A regular cylindrical grid 45 µm wide and 200 µm long was created and outlines from the cells of a lymphatic vessel were projected onto it and smoothed. These cells were then extruded inward to make 3D volumetric cells with a depth of 2 µm and triangulated using a threshold area of 4 µm.  The template was then used as the reference configuration for triangular 3 node membrane elements which were given a thickness of 0.1um. An isotropic St. Venant material model (linear, large deformation) was used with the Young's modulus set to 100 kPa to match a 10 kPa cell level Young's modulus estimated from the literature (ignoring the cell ends, the 2 x 0.1 µm membrane thickness occupied roughly 1/10th the cross-sectional area of the cell that were 2 µm deep). A uniform internal pressure was applied normal to the inside faces of the elements, which cancels out on the shared walls between cells. For simulations with a lower pressure inside the vessel, the inside faces were assigned a higher pressure. Stresses were visualized as the trace of the stress tensor.

opencc-by-4.0May 2021View details →

Passivating polysilicon recombination junctions for crystalline silicon solar cells

Data underlying the publication

opencc-zeroOct 2019View details →

Data from: GATA2 controls lymphatic endothelial cell junctional integrity and lymphovenous valve morphogenesis through miR-126

Mutations in the transcription factor GATA2 cause lymphedema. GATA2 is necessary for the development of lymphatic valves (LVs) and lymphovenous valves (LVVs), and for the patterning of lymphatic vessels. Here, we report that GATA2 is not necessary for valvular endothelial cell (VEC) differentiation. Instead, GATA2 is required for VEC maintenance and morphogenesis. GATA2 is also necessary for the expression of cell junction molecules VE-Cadherin and Claudin5 in lymphatic vessels. We identified miR-126 as a target of GATA2, and miR-126-/- embryos recapitulate the phenotypes of mice lacking GATA2. Primary human lymphatic endothelial cells (HLECs) lacking GATA2 (GATA2ΔHLEC) have altered expression of Claudin5 and VE-Cadherin, and blocking miR-126 activity in HLECs phenocopies these changes in expression. Importantly, overexpression of miR-126 in GATA2ΔHLEC significantly rescues the cell junction defects. Thus, our work defines a new mechanism of GATA2 and uncovers miR-126 as a novel regulator of mammalian lymphatic vascular development.

publicOct 2019View details →

Data from: GATA2 controls lymphatic endothelial cell junctional integrity and lymphovenous valve morphogenesis through miR-126

Open the record for dataset details and reuse information.