[{"publication_status":"published","doi":"10.1073/pnas.0808909106","publication":"PNAS","type":"journal_article","abstract":[{"lang":"eng","text":"Inhibiting the alpha(4) subunit of the integrin heterodimers alpha(4)beta(1) and alpha(4)beta(7) with the monoclonal antibody natalizumab is an effective treatment for multiple sclerosis (MS). However, the pharmacological action of natalizumab is not understood conclusively. Previous studies suggested that natalizumab inhibits activation, proliferation, or extravasation of inflammatory cells. To specify which mechanisms, cell types, and alpha(4) heterodimers are affected by the antibody treatment, we studied MS-like experimental autoimmune encephalomyelitis (EAE) in mice lacking the beta(1)-integrin gene either in all hematopoietic cells or selectively in T lymphocytes. Our results show that T cells critically rely on beta(1) integrins to accumulate in the central nervous system (CNS) during EAE, whereas CNS infiltration of beta(1)-deficient myeloid cells remains unaffected, suggesting that T cells are the main target of anti-alpha(4)-antibody blockade. We demonstrate that beta(1)-integrin expression on encephalitogenic T cells is critical for EAE development, and we therefore exclude alpha(4)beta(7) as a target integrin of the antibody treatment. T cells lacking beta(1) integrin are unable to firmly adhere to CNS endothelium in vivo, whereas their priming and expansion remain unaffected. Collectively, these results suggest that the primary action of natalizumab is interference with T cell extravasation via inhibition of alpha(4)beta(1) integrins."}],"extern":1,"citation":{"chicago":"Bauer, Martina, Cord Brakebusch, Caroline Coisne, Michael K Sixt, Hartmut Wekerle, Britta Engelhardt, and Reinhard Fässler. “Β1 Integrins Differentially Control Extravasation of Inflammatory Cell Subsets into the CNS during Autoimmunity.” <i>PNAS</i>. National Academy of Sciences, 2009. <a href=\"https://doi.org/10.1073/pnas.0808909106\">https://doi.org/10.1073/pnas.0808909106</a>.","short":"M. Bauer, C. Brakebusch, C. Coisne, M.K. Sixt, H. Wekerle, B. Engelhardt, R. Fässler, PNAS 106 (2009) 1920–1925.","ista":"Bauer M, Brakebusch C, Coisne C, Sixt MK, Wekerle H, Engelhardt B, Fässler R. 2009. β1 integrins differentially control extravasation of inflammatory cell subsets into the CNS during autoimmunity. PNAS. 106(6), 1920–1925.","ieee":"M. Bauer <i>et al.</i>, “β1 integrins differentially control extravasation of inflammatory cell subsets into the CNS during autoimmunity,” <i>PNAS</i>, vol. 106, no. 6. National Academy of Sciences, pp. 1920–1925, 2009.","ama":"Bauer M, Brakebusch C, Coisne C, et al. β1 integrins differentially control extravasation of inflammatory cell subsets into the CNS during autoimmunity. <i>PNAS</i>. 2009;106(6):1920-1925. doi:<a href=\"https://doi.org/10.1073/pnas.0808909106\">10.1073/pnas.0808909106</a>","mla":"Bauer, Martina, et al. “Β1 Integrins Differentially Control Extravasation of Inflammatory Cell Subsets into the CNS during Autoimmunity.” <i>PNAS</i>, vol. 106, no. 6, National Academy of Sciences, 2009, pp. 1920–25, doi:<a href=\"https://doi.org/10.1073/pnas.0808909106\">10.1073/pnas.0808909106</a>.","apa":"Bauer, M., Brakebusch, C., Coisne, C., Sixt, M. K., Wekerle, H., Engelhardt, B., &#38; Fässler, R. (2009). β1 integrins differentially control extravasation of inflammatory cell subsets into the CNS during autoimmunity. <i>PNAS</i>. National Academy of Sciences. <a href=\"https://doi.org/10.1073/pnas.0808909106\">https://doi.org/10.1073/pnas.0808909106</a>"},"volume":106,"status":"public","day":"10","quality_controlled":0,"date_created":"2018-12-11T12:06:03Z","_id":"3948","publist_id":"2180","page":"1920 - 1925","year":"2009","publisher":"National Academy of Sciences","month":"02","intvolume":"       106","date_published":"2009-02-10T00:00:00Z","issue":"6","author":[{"full_name":"Bauer, Martina","first_name":"Martina","last_name":"Bauer"},{"full_name":"Brakebusch, Cord","last_name":"Brakebusch","first_name":"Cord"},{"first_name":"Caroline","last_name":"Coisne","full_name":"Coisne, Caroline"},{"orcid":"0000-0002-6620-9179","last_name":"Sixt","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Michael Sixt"},{"full_name":"Wekerle, Hartmut","first_name":"Hartmut","last_name":"Wekerle"},{"full_name":"Engelhardt, Britta","last_name":"Engelhardt","first_name":"Britta"},{"first_name":"Reinhard","last_name":"Fässler","full_name":"Fässler, Reinhard"}],"title":"β1 integrins differentially control extravasation of inflammatory cell subsets into the CNS during autoimmunity","date_updated":"2021-01-12T07:53:24Z"},{"publication":"Blood","doi":"10.1182/blood-2008-08-176123","publication_status":"published","date_created":"2018-12-11T12:06:03Z","_id":"3949","quality_controlled":0,"day":"04","status":"public","volume":113,"extern":1,"citation":{"apa":"Quast, T., Tappertzhofen, B., Schild, C., Grell, J., Czeloth, N., Förster, R., … Kolanus, W. (2009). Cytohesin-1 controls the activation of RhoA and modulates integrin-dependent adhesion and migration of dendritic cells. <i>Blood</i>. American Society of Hematology. <a href=\"https://doi.org/10.1182/blood-2008-08-176123\">https://doi.org/10.1182/blood-2008-08-176123</a>","mla":"Quast, Thomas, et al. “Cytohesin-1 Controls the Activation of RhoA and Modulates Integrin-Dependent Adhesion and Migration of Dendritic Cells.” <i>Blood</i>, vol. 113, no. 23, American Society of Hematology, 2009, pp. 5801–10, doi:<a href=\"https://doi.org/10.1182/blood-2008-08-176123\">10.1182/blood-2008-08-176123</a>.","ista":"Quast T, Tappertzhofen B, Schild C, Grell J, Czeloth N, Förster R, Alon R, Fraemohs L, Dreck K, Weber C, Lämmermann T, Sixt MK, Kolanus W. 2009. Cytohesin-1 controls the activation of RhoA and modulates integrin-dependent adhesion and migration of dendritic cells. Blood. 113(23), 5801–5810.","short":"T. Quast, B. Tappertzhofen, C. Schild, J. Grell, N. Czeloth, R. Förster, R. Alon, L. Fraemohs, K. Dreck, C. Weber, T. Lämmermann, M.K. Sixt, W. Kolanus, Blood 113 (2009) 5801–5810.","ieee":"T. Quast <i>et al.</i>, “Cytohesin-1 controls the activation of RhoA and modulates integrin-dependent adhesion and migration of dendritic cells,” <i>Blood</i>, vol. 113, no. 23. American Society of Hematology, pp. 5801–5810, 2009.","ama":"Quast T, Tappertzhofen B, Schild C, et al. Cytohesin-1 controls the activation of RhoA and modulates integrin-dependent adhesion and migration of dendritic cells. <i>Blood</i>. 2009;113(23):5801-5810. doi:<a href=\"https://doi.org/10.1182/blood-2008-08-176123\">10.1182/blood-2008-08-176123</a>","chicago":"Quast, Thomas, Barbara Tappertzhofen, Cora Schild, Jessica Grell, Niklas Czeloth, Reinhold Förster, Ronen Alon, et al. “Cytohesin-1 Controls the Activation of RhoA and Modulates Integrin-Dependent Adhesion and Migration of Dendritic Cells.” <i>Blood</i>. American Society of Hematology, 2009. <a href=\"https://doi.org/10.1182/blood-2008-08-176123\">https://doi.org/10.1182/blood-2008-08-176123</a>."},"abstract":[{"lang":"eng","text":"Adhesion and motility of mammalian leukocytes are essential requirements for innate and adaptive immune defense mechanisms. We show here that the guanine nucleotide exchange factor cytohesin-1, which had previously been demonstrated to be an important component of beta-2 integrin activation in lymphocytes, regulates the activation of the small GTPase RhoA in primary dendritic cells (DCs). Cytohesin-1 and RhoA are both required for the induction of chemokine-dependent conformational changes of the integrin beta-2 subunit of DCs during adhesion under physiological flow conditions. Furthermore, use of RNAi in murine bone marrow DCs (BM-DCs) revealed that interference with cytohesin-1 signaling impairs migration of wild-type dendritic cells in complex 3D environments and in vivo. This phenotype was not observed in the complete absence of integrins. We thus demonstrate an essential role of cytohesin-1/RhoA during ameboid migration in the presence of integrins and further suggest that DCs without integrins switch to a different migration mode."}],"type":"journal_article","year":"2009","page":"5801 - 5810","publist_id":"2177","date_updated":"2021-01-12T07:53:24Z","author":[{"full_name":"Quast, Thomas","last_name":"Quast","first_name":"Thomas"},{"full_name":"Tappertzhofen, Barbara","last_name":"Tappertzhofen","first_name":"Barbara"},{"first_name":"Cora","last_name":"Schild","full_name":"Schild, Cora"},{"first_name":"Jessica","last_name":"Grell","full_name":"Grell, Jessica"},{"full_name":"Czeloth, Niklas","first_name":"Niklas","last_name":"Czeloth"},{"full_name":"Förster, Reinhold","last_name":"Förster","first_name":"Reinhold"},{"last_name":"Alon","first_name":"Ronen","full_name":"Alon, Ronen"},{"last_name":"Fraemohs","first_name":"Line","full_name":"Fraemohs, Line"},{"first_name":"Katrin","last_name":"Dreck","full_name":"Dreck, Katrin"},{"full_name":"Weber, Christian","first_name":"Christian","last_name":"Weber"},{"last_name":"Lämmermann","first_name":"Tim","full_name":"Lämmermann, Tim"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt","full_name":"Michael Sixt"},{"last_name":"Kolanus","first_name":"Waldemar","full_name":"Kolanus, Waldemar"}],"title":"Cytohesin-1 controls the activation of RhoA and modulates integrin-dependent adhesion and migration of dendritic cells","issue":"23","date_published":"2009-06-04T00:00:00Z","month":"06","intvolume":"       113","publisher":"American Society of Hematology"},{"quality_controlled":0,"day":"22","status":"public","date_created":"2018-12-11T12:06:04Z","_id":"3950","type":"journal_article","abstract":[{"lang":"eng","text":"Integrin activation is essential for the function of all blood cells, including platelets and leukocytes. The blood cell-specific FERM domain protein Kindlin-3 is required for the activation of the beta1 and beta3 integrins on platelets. Impaired activation of beta1, beta2 and beta3 integrins on platelets and leukocytes is the hallmark of a rare autosomal recessive leukocyte adhesion deficiency syndrome in humans called LAD-III, characterized by severe bleeding and impaired adhesion of leukocytes to inflamed endothelia. Here we show that Kindlin-3 also binds the beta2 integrin cytoplasmic domain and is essential for neutrophil binding and spreading on beta2 integrin-dependent ligands such as intercellular adhesion molecule-1 and the complement C3 activation product iC3b. Moreover, loss of Kindlin-3 expression abolished firm adhesion and arrest of neutrophils on activated endothelial cells in vitro and in vivo, whereas selectin-mediated rolling was unaffected. Thus, Kindlin-3 is essential to activate the beta1, beta2 and beta3 integrin classes, and loss of Kindlin-3 function is sufficient to cause a LAD-III-like phenotype in mice."}],"citation":{"chicago":"Moser, Markus, Martina Bauer, Stephan Schmid, Raphael Ruppert, Sarah Schmidt, Michael K Sixt, Hao Wang, Markus Sperandio, and Reinhard Fässler. “Kindlin-3 Is Required for Β2 Integrin-Mediated Leukocyte Adhesion to Endothelial Cells.” <i>Nature Medicine</i>. Nature Publishing Group, 2009. <a href=\"https://doi.org/10.1038/nm.1921\">https://doi.org/10.1038/nm.1921</a>.","ieee":"M. Moser <i>et al.</i>, “Kindlin-3 is required for β2 integrin-mediated leukocyte adhesion to endothelial cells,” <i>Nature Medicine</i>, vol. 15, no. 3. Nature Publishing Group, pp. 300–305, 2009.","ista":"Moser M, Bauer M, Schmid S, Ruppert R, Schmidt S, Sixt MK, Wang H, Sperandio M, Fässler R. 2009. Kindlin-3 is required for β2 integrin-mediated leukocyte adhesion to endothelial cells. Nature Medicine. 15(3), 300–305.","short":"M. Moser, M. Bauer, S. Schmid, R. Ruppert, S. Schmidt, M.K. Sixt, H. Wang, M. Sperandio, R. Fässler, Nature Medicine 15 (2009) 300–305.","ama":"Moser M, Bauer M, Schmid S, et al. Kindlin-3 is required for β2 integrin-mediated leukocyte adhesion to endothelial cells. <i>Nature Medicine</i>. 2009;15(3):300-305. doi:<a href=\"https://doi.org/10.1038/nm.1921\">10.1038/nm.1921</a>","mla":"Moser, Markus, et al. “Kindlin-3 Is Required for Β2 Integrin-Mediated Leukocyte Adhesion to Endothelial Cells.” <i>Nature Medicine</i>, vol. 15, no. 3, Nature Publishing Group, 2009, pp. 300–05, doi:<a href=\"https://doi.org/10.1038/nm.1921\">10.1038/nm.1921</a>.","apa":"Moser, M., Bauer, M., Schmid, S., Ruppert, R., Schmidt, S., Sixt, M. K., … Fässler, R. (2009). Kindlin-3 is required for β2 integrin-mediated leukocyte adhesion to endothelial cells. <i>Nature Medicine</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/nm.1921\">https://doi.org/10.1038/nm.1921</a>"},"extern":1,"volume":15,"doi":"10.1038/nm.1921","publication_status":"published","publication":"Nature Medicine","issue":"3","title":"Kindlin-3 is required for β2 integrin-mediated leukocyte adhesion to endothelial cells","author":[{"first_name":"Markus","last_name":"Moser","full_name":"Moser, Markus"},{"first_name":"Martina","last_name":"Bauer","full_name":"Bauer, Martina"},{"full_name":"Schmid, Stephan","first_name":"Stephan","last_name":"Schmid"},{"last_name":"Ruppert","first_name":"Raphael","full_name":"Ruppert, Raphael"},{"full_name":"Schmidt, Sarah","first_name":"Sarah","last_name":"Schmidt"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","last_name":"Sixt","full_name":"Michael Sixt"},{"first_name":"Hao","last_name":"Wang","full_name":"Wang, Hao-Ven"},{"full_name":"Sperandio, Markus","first_name":"Markus","last_name":"Sperandio"},{"full_name":"Fässler, Reinhard","first_name":"Reinhard","last_name":"Fässler"}],"date_updated":"2021-01-12T07:53:25Z","publisher":"Nature Publishing Group","month":"02","intvolume":"        15","date_published":"2009-02-22T00:00:00Z","year":"2009","publist_id":"2178","page":"300 - 305"},{"date_published":"2009-10-01T00:00:00Z","intvolume":"        21","month":"10","publisher":"Elsevier","date_updated":"2021-01-12T07:53:25Z","title":"Mechanical modes of 'amoeboid' cell migration","author":[{"last_name":"Lämmermann","first_name":"Tim","full_name":"Lämmermann, Tim"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","last_name":"Sixt","full_name":"Michael Sixt"}],"issue":"5","page":"636 - 644","publist_id":"2176","year":"2009","volume":21,"extern":1,"citation":{"ama":"Lämmermann T, Sixt MK. Mechanical modes of “amoeboid” cell migration. <i>Current Opinion in Cell Biology</i>. 2009;21(5):636-644. doi:<a href=\"https://doi.org/10.1016/j.ceb.2009.05.003\">10.1016/j.ceb.2009.05.003</a>","short":"T. Lämmermann, M.K. Sixt, Current Opinion in Cell Biology 21 (2009) 636–644.","ista":"Lämmermann T, Sixt MK. 2009. Mechanical modes of ‘amoeboid’ cell migration. Current Opinion in Cell Biology. 21(5), 636–644.","ieee":"T. Lämmermann and M. K. Sixt, “Mechanical modes of ‘amoeboid’ cell migration,” <i>Current Opinion in Cell Biology</i>, vol. 21, no. 5. Elsevier, pp. 636–644, 2009.","chicago":"Lämmermann, Tim, and Michael K Sixt. “Mechanical Modes of ‘amoeboid’ Cell Migration.” <i>Current Opinion in Cell Biology</i>. Elsevier, 2009. <a href=\"https://doi.org/10.1016/j.ceb.2009.05.003\">https://doi.org/10.1016/j.ceb.2009.05.003</a>.","apa":"Lämmermann, T., &#38; Sixt, M. K. (2009). Mechanical modes of “amoeboid” cell migration. <i>Current Opinion in Cell Biology</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.ceb.2009.05.003\">https://doi.org/10.1016/j.ceb.2009.05.003</a>","mla":"Lämmermann, Tim, and Michael K. Sixt. “Mechanical Modes of ‘amoeboid’ Cell Migration.” <i>Current Opinion in Cell Biology</i>, vol. 21, no. 5, Elsevier, 2009, pp. 636–44, doi:<a href=\"https://doi.org/10.1016/j.ceb.2009.05.003\">10.1016/j.ceb.2009.05.003</a>."},"abstract":[{"lang":"eng","text":"The morphological term 'amoeboid' migration subsumes a number of rather distinct biophysical modes of cellular locomotion that range from blebbing motility to entirely actin-polymerization-based gliding. Here, we discuss the diverse principles of force generation and force transduction that lead to the distinct amoeboid phenotypes. We argue that shifting the balance between actin protrusion, actomyosin contraction, and adhesion to the extracellular substrate can explain the different modes of amoeboid movement and that blebbing and gliding are barely extreme variants of one common migration strategy. Depending on the cell type, physiological conditions or experimental manipulation, amoeboid cells can adopt the distinct mechanical modes of amoeboid migration."}],"type":"journal_article","_id":"3951","date_created":"2018-12-11T12:06:04Z","day":"01","status":"public","quality_controlled":0,"publication":"Current Opinion in Cell Biology","publication_status":"published","doi":"10.1016/j.ceb.2009.05.003"},{"date_updated":"2021-01-12T07:53:26Z","issue":"19","author":[{"full_name":"Schymeinsky, Jürgen","first_name":"Jürgen","last_name":"Schymeinsky"},{"full_name":"Gerstl, Ronald","last_name":"Gerstl","first_name":"Ronald"},{"full_name":"Mannigel, Ingrid","last_name":"Mannigel","first_name":"Ingrid"},{"full_name":"Niedung, Katy","first_name":"Katy","last_name":"Niedung"},{"full_name":"Frommhold, David","first_name":"David","last_name":"Frommhold"},{"first_name":"Klaus","last_name":"Panthel","full_name":"Panthel, Klaus"},{"first_name":"Jürgen","last_name":"Heesemann","full_name":"Heesemann, Jürgen"},{"full_name":"Michael Sixt","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","last_name":"Sixt"},{"full_name":"Quast, Thomas","last_name":"Quast","first_name":"Thomas"},{"first_name":"Waldemar","last_name":"Kolanus","full_name":"Kolanus, Waldemar"},{"full_name":"Mocsai, Attila","first_name":"Attila","last_name":"Mocsai"},{"full_name":"Wienands, Jürgen","first_name":"Jürgen","last_name":"Wienands"},{"last_name":"Sperandio","first_name":"Markus","full_name":"Sperandio, Markus"},{"full_name":"Walzog, Barbara","first_name":"Barbara","last_name":"Walzog"}],"title":"A fundamental role of mAbp1 in neutrophils: impact on β(2) integrin-mediated phagocytosis and adhesion in vivo","intvolume":"       114","month":"11","date_published":"2009-11-05T00:00:00Z","publisher":"American Society of Hematology","year":"2009","page":"4209 - 4220","publist_id":"2175","_id":"3952","date_created":"2018-12-11T12:06:04Z","quality_controlled":0,"status":"public","day":"05","citation":{"chicago":"Schymeinsky, Jürgen, Ronald Gerstl, Ingrid Mannigel, Katy Niedung, David Frommhold, Klaus Panthel, Jürgen Heesemann, et al. “A Fundamental Role of MAbp1 in Neutrophils: Impact on β(2) Integrin-Mediated Phagocytosis and Adhesion in Vivo.” <i>Blood</i>. American Society of Hematology, 2009. <a href=\"https://doi.org/10.1182/blood-2009-02-206169\">https://doi.org/10.1182/blood-2009-02-206169</a>.","ama":"Schymeinsky J, Gerstl R, Mannigel I, et al. A fundamental role of mAbp1 in neutrophils: impact on β(2) integrin-mediated phagocytosis and adhesion in vivo. <i>Blood</i>. 2009;114(19):4209-4220. doi:<a href=\"https://doi.org/10.1182/blood-2009-02-206169\">10.1182/blood-2009-02-206169</a>","short":"J. Schymeinsky, R. Gerstl, I. Mannigel, K. Niedung, D. Frommhold, K. Panthel, J. Heesemann, M.K. Sixt, T. Quast, W. Kolanus, A. Mocsai, J. Wienands, M. Sperandio, B. Walzog, Blood 114 (2009) 4209–4220.","ieee":"J. Schymeinsky <i>et al.</i>, “A fundamental role of mAbp1 in neutrophils: impact on β(2) integrin-mediated phagocytosis and adhesion in vivo,” <i>Blood</i>, vol. 114, no. 19. American Society of Hematology, pp. 4209–4220, 2009.","ista":"Schymeinsky J, Gerstl R, Mannigel I, Niedung K, Frommhold D, Panthel K, Heesemann J, Sixt MK, Quast T, Kolanus W, Mocsai A, Wienands J, Sperandio M, Walzog B. 2009. A fundamental role of mAbp1 in neutrophils: impact on β(2) integrin-mediated phagocytosis and adhesion in vivo. Blood. 114(19), 4209–4220.","mla":"Schymeinsky, Jürgen, et al. “A Fundamental Role of MAbp1 in Neutrophils: Impact on β(2) Integrin-Mediated Phagocytosis and Adhesion in Vivo.” <i>Blood</i>, vol. 114, no. 19, American Society of Hematology, 2009, pp. 4209–20, doi:<a href=\"https://doi.org/10.1182/blood-2009-02-206169\">10.1182/blood-2009-02-206169</a>.","apa":"Schymeinsky, J., Gerstl, R., Mannigel, I., Niedung, K., Frommhold, D., Panthel, K., … Walzog, B. (2009). A fundamental role of mAbp1 in neutrophils: impact on β(2) integrin-mediated phagocytosis and adhesion in vivo. <i>Blood</i>. American Society of Hematology. <a href=\"https://doi.org/10.1182/blood-2009-02-206169\">https://doi.org/10.1182/blood-2009-02-206169</a>"},"extern":1,"volume":114,"type":"journal_article","abstract":[{"text":"The mammalian actin-binding protein 1 (mAbp1, Hip-55, SH3P7) is phosphorylated by the nonreceptor tyrosine kinase Syk that has a fundamental effect for several beta(2) integrin (CD11/CD18)-mediated neutrophil functions. Live cell imaging showed a dynamic enrichment of enhanced green fluorescence protein-tagged mAbp1 at the phagocytic cup of neutrophil-like differentiated HL-60 cells during beta(2) integrin-mediated phagocytosis of serum-opsonized Escherichia coli. The genetic absence of Syk or its pharmacologic inhibition using piceatannol abrogated the proper localization of mAbp1 at the phagocytic cup. The genetic absence or down-regulation of mAbp1 using the RNA interference technique significantly compromised beta(2) integrin-mediated phagocytosis of serum-opsonized E coli or Salmonella typhimurium in vitro as well as clearance of S typhimurium infection in vivo. Moreover, the genetic absence of mAbp1 almost completely abrogated firm neutrophil adhesion under physiologic shear stress conditions in vitro as well as leukocyte adhesion and extravasation in inflamed cremaster muscle venules of mice treated with tumor-necrosis factor alpha. Functional analysis showed that the down-regulation of mAbp1 diminished the number of beta(2) integrin clusters in the high-affinity conformation under flow conditions. These unanticipated results define mAbp1 as a novel molecular player in integrin biology that is critical for phagocytosis and firm neutrophil adhesion under flow conditions.","lang":"eng"}],"publication_status":"published","doi":"10.1182/blood-2009-02-206169","publication":"Blood"},{"intvolume":"       183","month":"09","date_published":"2009-09-15T00:00:00Z","publisher":"American Association of Immunologists","date_updated":"2021-01-12T07:53:26Z","issue":"6","title":"The sphingosine 1-phosphate receptor agonist FTY720 potently inhibits regulatory T cell proliferation in vitro and in vivo","author":[{"full_name":"Wolf, Anna Maria","last_name":"Wolf","first_name":"Anna"},{"full_name":"Eller, Kathrin","last_name":"Eller","first_name":"Kathrin"},{"last_name":"Zeiser","first_name":"Robert","full_name":"Zeiser, Robert"},{"full_name":"Dürr, Christoph","first_name":"Christoph","last_name":"Dürr"},{"full_name":"Gerlach, Ulrike V","first_name":"Ulrike","last_name":"Gerlach"},{"full_name":"Michael Sixt","last_name":"Sixt","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"},{"first_name":"Lydia","last_name":"Markut","full_name":"Markut, Lydia"},{"last_name":"Gastl","first_name":"Guenther","full_name":"Gastl, Guenther"},{"full_name":"Rosenkranz, Alexander R","first_name":"Alexander","last_name":"Rosenkranz"},{"full_name":"Wolf, Dominik","first_name":"Dominik","last_name":"Wolf"}],"page":"3751 - 3760","publist_id":"2174","year":"2009","extern":1,"citation":{"mla":"Wolf, Anna, et al. “The Sphingosine 1-Phosphate Receptor Agonist FTY720 Potently Inhibits Regulatory T Cell Proliferation in Vitro and in Vivo.” <i>Journal of Immunology</i>, vol. 183, no. 6, American Association of Immunologists, 2009, pp. 3751–60, doi:<a href=\"https://doi.org/10.4049/jimmunol.0901011\">10.4049/jimmunol.0901011</a>.","apa":"Wolf, A., Eller, K., Zeiser, R., Dürr, C., Gerlach, U., Sixt, M. K., … Wolf, D. (2009). The sphingosine 1-phosphate receptor agonist FTY720 potently inhibits regulatory T cell proliferation in vitro and in vivo. <i>Journal of Immunology</i>. American Association of Immunologists. <a href=\"https://doi.org/10.4049/jimmunol.0901011\">https://doi.org/10.4049/jimmunol.0901011</a>","chicago":"Wolf, Anna, Kathrin Eller, Robert Zeiser, Christoph Dürr, Ulrike Gerlach, Michael K Sixt, Lydia Markut, Guenther Gastl, Alexander Rosenkranz, and Dominik Wolf. “The Sphingosine 1-Phosphate Receptor Agonist FTY720 Potently Inhibits Regulatory T Cell Proliferation in Vitro and in Vivo.” <i>Journal of Immunology</i>. American Association of Immunologists, 2009. <a href=\"https://doi.org/10.4049/jimmunol.0901011\">https://doi.org/10.4049/jimmunol.0901011</a>.","ieee":"A. Wolf <i>et al.</i>, “The sphingosine 1-phosphate receptor agonist FTY720 potently inhibits regulatory T cell proliferation in vitro and in vivo,” <i>Journal of Immunology</i>, vol. 183, no. 6. American Association of Immunologists, pp. 3751–3760, 2009.","ista":"Wolf A, Eller K, Zeiser R, Dürr C, Gerlach U, Sixt MK, Markut L, Gastl G, Rosenkranz A, Wolf D. 2009. The sphingosine 1-phosphate receptor agonist FTY720 potently inhibits regulatory T cell proliferation in vitro and in vivo. Journal of Immunology. 183(6), 3751–3760.","short":"A. Wolf, K. Eller, R. Zeiser, C. Dürr, U. Gerlach, M.K. Sixt, L. Markut, G. Gastl, A. Rosenkranz, D. Wolf, Journal of Immunology 183 (2009) 3751–3760.","ama":"Wolf A, Eller K, Zeiser R, et al. The sphingosine 1-phosphate receptor agonist FTY720 potently inhibits regulatory T cell proliferation in vitro and in vivo. <i>Journal of Immunology</i>. 2009;183(6):3751-3760. doi:<a href=\"https://doi.org/10.4049/jimmunol.0901011\">10.4049/jimmunol.0901011</a>"},"volume":183,"type":"journal_article","abstract":[{"lang":"eng","text":"CD4(+)CD25(+) regulatory T cell (Treg) entry into secondary lymphoid organs and local expansion is critical for their immunosuppressive function. Long-term application of the sphingosine-1 phosphate receptor agonist FTY720 exerts pleiotropic anti-inflammatory effects, whereas short-term FTY720 boosts antiviral immunity. In this study, we provide evidence that FTY720 potently inhibits Treg proliferation in vitro and in vivo without affecting their viability, phenotype, or in vitro immunosuppression. In contrast, adoptively transferred Treg exposed ex vivo to FTY720 lost their protective effects in murine models of acute glomerulonephritis and acute graft-vs-host disease. On a cellular level, FTY720 inhibits IL-2-induced STAT-5 phosphorylation, paralleled by a loss of FoxP3 expression during Treg expansion in vitro. Notably, loss of in vivo immunosuppression is not due to impaired migration to or localization within secondary lymphoid organs. We could even show a selective trapping of adoptively transferred Treg in inflammatory lymph nodes by FTY720. Finally, Treg isolated from animals systemically exposed to FTY720 also exhibit a significantly impaired proliferative response upon restimulation when compared with Treg isolated from solvent-treated animals. In summary, our data suggest that sphingosine-1 phosphate receptor-mediated signals induced by FTY720 abrogate their in vivo immunosuppressive potential by blocking IL-2 induced expansion, which is indispensable for their in vivo immunosuppressive activity."}],"_id":"3953","date_created":"2018-12-11T12:06:05Z","status":"public","day":"15","quality_controlled":0,"publication_status":"published","doi":"10.4049/jimmunol.0901011","publication":"Journal of Immunology"},{"language":[{"iso":"eng"}],"year":"2009","page":"1438 - 1443","publist_id":"2173","date_updated":"2021-01-12T07:53:27Z","author":[{"full_name":"Renkawitz, Jörg","id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","first_name":"Jörg","orcid":"0000-0003-2856-3369","last_name":"Renkawitz"},{"last_name":"Schumann","first_name":"Kathrin","id":"F44D762E-4F9D-11E9-B64C-9EB26CEFFB5F","full_name":"Schumann, Kathrin"},{"full_name":"Weber, Michele","last_name":"Weber","first_name":"Michele","id":"3A3FC708-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Lämmermann","first_name":"Tim","full_name":"Lämmermann, Tim"},{"last_name":"Pflicke","first_name":"Holger","full_name":"Pflicke, Holger"},{"full_name":"Piel, Matthieu","last_name":"Piel","first_name":"Matthieu"},{"first_name":"Julien","last_name":"Polleux","full_name":"Polleux, Julien"},{"first_name":"Joachim","last_name":"Spatz","full_name":"Spatz, Joachim"},{"orcid":"0000-0002-6620-9179","last_name":"Sixt","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K"}],"title":"Adaptive force transmission in amoeboid cell migration","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","issue":"12","date_published":"2009-11-15T00:00:00Z","intvolume":"        11","month":"11","publisher":"Nature Publishing Group","acknowledgement":"We thank S. Cremer for statistical analysis, K. Hirsch for technical assistance, D. Critchley for talin1-deficient mice and R. Fässler for integrindeficient mice, discussions and critical reading of the manuscript. This work was supported by the German Research Foundation, the Peter Hans Hofschneider Foundation for Experimental Biomedicine, the Max Planck Society, the Alexander von Humboldt Foundation and the allergology programme of the Landesstiftung Baden-Württemberg.","oa_version":"None","publication":"Nature Cell Biology","doi":"10.1038/ncb1992","publication_status":"published","date_created":"2018-12-11T12:06:05Z","_id":"3954","day":"15","status":"public","volume":11,"extern":"1","citation":{"mla":"Renkawitz, Jörg, et al. “Adaptive Force Transmission in Amoeboid Cell Migration.” <i>Nature Cell Biology</i>, vol. 11, no. 12, Nature Publishing Group, 2009, pp. 1438–43, doi:<a href=\"https://doi.org/10.1038/ncb1992\">10.1038/ncb1992</a>.","apa":"Renkawitz, J., Schumann, K., Weber, M., Lämmermann, T., Pflicke, H., Piel, M., … Sixt, M. K. (2009). Adaptive force transmission in amoeboid cell migration. <i>Nature Cell Biology</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/ncb1992\">https://doi.org/10.1038/ncb1992</a>","chicago":"Renkawitz, Jörg, Kathrin Schumann, Michele Weber, Tim Lämmermann, Holger Pflicke, Matthieu Piel, Julien Polleux, Joachim Spatz, and Michael K Sixt. “Adaptive Force Transmission in Amoeboid Cell Migration.” <i>Nature Cell Biology</i>. Nature Publishing Group, 2009. <a href=\"https://doi.org/10.1038/ncb1992\">https://doi.org/10.1038/ncb1992</a>.","ama":"Renkawitz J, Schumann K, Weber M, et al. Adaptive force transmission in amoeboid cell migration. <i>Nature Cell Biology</i>. 2009;11(12):1438-1443. doi:<a href=\"https://doi.org/10.1038/ncb1992\">10.1038/ncb1992</a>","short":"J. Renkawitz, K. Schumann, M. Weber, T. Lämmermann, H. Pflicke, M. Piel, J. Polleux, J. Spatz, M.K. Sixt, Nature Cell Biology 11 (2009) 1438–1443.","ieee":"J. Renkawitz <i>et al.</i>, “Adaptive force transmission in amoeboid cell migration,” <i>Nature Cell Biology</i>, vol. 11, no. 12. Nature Publishing Group, pp. 1438–1443, 2009.","ista":"Renkawitz J, Schumann K, Weber M, Lämmermann T, Pflicke H, Piel M, Polleux J, Spatz J, Sixt MK. 2009. Adaptive force transmission in amoeboid cell migration. Nature Cell Biology. 11(12), 1438–1443."},"abstract":[{"text":"The leading front of a cell can either protrude as an actin-free membrane bleb that is inflated by actomyosin-driven contractile forces, or as an actin-rich pseudopodium, a site where polymerizing actin filaments push out the membrane. Pushing filaments can only cause the membrane to protrude if the expanding actin network experiences a retrograde counter-force, which is usually provided by transmembrane receptors of the integrin family. Here we show that chemotactic dendritic cells mechanically adapt to the adhesive properties of their substrate by switching between integrin-mediated and integrin-independent locomotion. We found that on engaging the integrin-actin clutch, actin polymerization was entirely turned into protrusion, whereas on disengagement actin underwent slippage and retrograde flow. Remarkably, accelerated retrograde flow was balanced by an increased actin polymerization rate; therefore, cell shape and protrusion velocity remained constant on alternating substrates. Due to this adaptive response in polymerization dynamics, tracks of adhesive substrate did not dictate the path of the cells. Instead, directional guidance was exclusively provided by a soluble gradient of chemoattractant, which endowed these 'amoeboid' cells with extraordinary flexibility, enabling them to traverse almost every type of tissue.","lang":"eng"}],"type":"journal_article"},{"doi":"10.1084/jem.20091739","publication_status":"published","publication":"The Journal of Experimental Medicine","extern":1,"citation":{"chicago":"Pflicke, Holger, and Michael K Sixt. “Preformed Portals Facilitate Dendritic Cell Entry into Afferent Lymphatic Vessels.” <i>The Journal of Experimental Medicine</i>. Rockefeller University Press, 2009. <a href=\"https://doi.org/10.1084/jem.20091739\">https://doi.org/10.1084/jem.20091739</a>.","short":"H. Pflicke, M.K. Sixt, The Journal of Experimental Medicine 206 (2009) 2925–2935.","ieee":"H. Pflicke and M. K. Sixt, “Preformed portals facilitate dendritic cell entry into afferent lymphatic vessels,” <i>The Journal of Experimental Medicine</i>, vol. 206, no. 13. Rockefeller University Press, pp. 2925–2935, 2009.","ista":"Pflicke H, Sixt MK. 2009. Preformed portals facilitate dendritic cell entry into afferent lymphatic vessels. The Journal of Experimental Medicine. 206(13), 2925–2935.","ama":"Pflicke H, Sixt MK. Preformed portals facilitate dendritic cell entry into afferent lymphatic vessels. <i>The Journal of Experimental Medicine</i>. 2009;206(13):2925-2935. doi:<a href=\"https://doi.org/10.1084/jem.20091739\">10.1084/jem.20091739</a>","mla":"Pflicke, Holger, and Michael K. Sixt. “Preformed Portals Facilitate Dendritic Cell Entry into Afferent Lymphatic Vessels.” <i>The Journal of Experimental Medicine</i>, vol. 206, no. 13, Rockefeller University Press, 2009, pp. 2925–35, doi:<a href=\"https://doi.org/10.1084/jem.20091739\">10.1084/jem.20091739</a>.","apa":"Pflicke, H., &#38; Sixt, M. K. (2009). Preformed portals facilitate dendritic cell entry into afferent lymphatic vessels. <i>The Journal of Experimental Medicine</i>. Rockefeller University Press. <a href=\"https://doi.org/10.1084/jem.20091739\">https://doi.org/10.1084/jem.20091739</a>"},"volume":206,"type":"journal_article","abstract":[{"text":"Although both processes occur at similar rates, leukocyte extravasation from the blood circulation is well investigated, whereas intravasation into lymphatic vessels has hardly been studied. In contrast to a common assumption-that intra- and extravasation follow similar molecular principles-we previously showed that lymphatic entry of dendritic cells (DCs) does not require integrin-mediated adhesive interactions. In this study, we demonstrate that DC-entry is also independent of pericellular proteolysis, raising the question of whether lymphatic vessels offer preexisting entry routes. We find that the perilymphatic basement membrane of initial lymphatic vessels is discontinuous and therefore leaves gaps for entering cells. Using a newly developed in situ live cell imaging approach that allows us to dynamically visualize the cells and their extracellular environment, we demonstrate that DCs enter through these discontinuities, which are transiently mechanically dilated by the passaging cells. We further show that penetration of the underlying lymphatic endothelial layer occurs through flap valves lacking continuous intercellular junctions. Together, we demonstrate free cellular communication between interstitium and lymphatic lumen.","lang":"eng"}],"date_created":"2018-12-11T12:06:05Z","_id":"3955","quality_controlled":0,"day":"07","status":"public","page":"2925 - 2935","publist_id":"2172","year":"2009","month":"12","intvolume":"       206","date_published":"2009-12-07T00:00:00Z","publisher":"Rockefeller University Press","date_updated":"2021-01-12T07:53:27Z","issue":"13","author":[{"last_name":"Pflicke","first_name":"Holger","full_name":"Pflicke, Holger"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt","full_name":"Michael Sixt"}],"title":"Preformed portals facilitate dendritic cell entry into afferent lymphatic vessels"},{"publist_id":"2162","page":"79 - 103","year":"2009","publisher":"Springer","acknowledgement":"Research by all three authors is partially supported by DARPA under grant HR0011-05-1-0007. Research by the second author is also partially supported by NSF under grant CCR-00-86013.","intvolume":"         9","month":"01","date_published":"2009-01-01T00:00:00Z","issue":"1","author":[{"full_name":"Cohen-Steiner, David","first_name":"David","last_name":"Cohen Steiner"},{"orcid":"0000-0002-9823-6833","last_name":"Edelsbrunner","id":"3FB178DA-F248-11E8-B48F-1D18A9856A87","first_name":"Herbert","full_name":"Herbert Edelsbrunner"},{"last_name":"Harer","first_name":"John","full_name":"Harer, John"}],"title":"Extending persistence using Poincare and Lefschetz duality","date_updated":"2021-01-12T07:53:32Z","publication_status":"published","doi":"10.1007/s10208-008-9027-z","publication":"Foundations of Computational Mathematics","type":"journal_article","abstract":[{"lang":"eng","text":"Persistent homology has proven to be a useful tool in a variety of contexts, including the recognition and measurement of shape characteristics of surfaces in ℝ3. Persistence pairs homology classes that are born and die in a filtration of a topological space, but does not pair its actual homology classes. For the sublevelset filtration of a surface in ℝ3, persistence has been extended to a pairing of essential classes using Reeb graphs. In this paper, we give an algebraic formulation that extends persistence to essential homology for any filtered space, present an algorithm to calculate it, and describe how it aids our ability to recognize shape features for codimension 1 submanifolds of Euclidean space. The extension derives from Poincaré duality but generalizes to nonmanifold spaces. We prove stability for general triangulated spaces and duality as well as symmetry for triangulated manifolds. "}],"citation":{"mla":"Cohen Steiner, David, et al. “Extending Persistence Using Poincare and Lefschetz Duality.” <i>Foundations of Computational Mathematics</i>, vol. 9, no. 1, Springer, 2009, pp. 79–103, doi:<a href=\"https://doi.org/10.1007/s10208-008-9027-z\">10.1007/s10208-008-9027-z</a>.","apa":"Cohen Steiner, D., Edelsbrunner, H., &#38; Harer, J. (2009). Extending persistence using Poincare and Lefschetz duality. <i>Foundations of Computational Mathematics</i>. Springer. <a href=\"https://doi.org/10.1007/s10208-008-9027-z\">https://doi.org/10.1007/s10208-008-9027-z</a>","chicago":"Cohen Steiner, David, Herbert Edelsbrunner, and John Harer. “Extending Persistence Using Poincare and Lefschetz Duality.” <i>Foundations of Computational Mathematics</i>. Springer, 2009. <a href=\"https://doi.org/10.1007/s10208-008-9027-z\">https://doi.org/10.1007/s10208-008-9027-z</a>.","ista":"Cohen Steiner D, Edelsbrunner H, Harer J. 2009. Extending persistence using Poincare and Lefschetz duality. Foundations of Computational Mathematics. 9(1), 79–103.","ieee":"D. Cohen Steiner, H. Edelsbrunner, and J. Harer, “Extending persistence using Poincare and Lefschetz duality,” <i>Foundations of Computational Mathematics</i>, vol. 9, no. 1. Springer, pp. 79–103, 2009.","short":"D. Cohen Steiner, H. Edelsbrunner, J. Harer, Foundations of Computational Mathematics 9 (2009) 79–103.","ama":"Cohen Steiner D, Edelsbrunner H, Harer J. Extending persistence using Poincare and Lefschetz duality. <i>Foundations of Computational Mathematics</i>. 2009;9(1):79-103. doi:<a href=\"https://doi.org/10.1007/s10208-008-9027-z\">10.1007/s10208-008-9027-z</a>"},"extern":1,"volume":9,"status":"public","day":"01","quality_controlled":0,"date_created":"2018-12-11T12:06:10Z","_id":"3966"},{"author":[{"full_name":"Cohen-Steiner, David","last_name":"Cohen Steiner","first_name":"David"},{"orcid":"0000-0002-9823-6833","last_name":"Edelsbrunner","id":"3FB178DA-F248-11E8-B48F-1D18A9856A87","first_name":"Herbert","full_name":"Herbert Edelsbrunner"},{"first_name":"John","last_name":"Harer","full_name":"Harer, John"},{"full_name":"Morozov, Dmitriy","last_name":"Morozov","first_name":"Dmitriy"}],"title":"Persistent homology for kernels, images, and cokernels","date_updated":"2021-01-12T07:53:32Z","publisher":"SIAM","date_published":"2009-01-01T00:00:00Z","month":"01","year":"2009","conference":{"name":"SODA: Symposium on Discrete Algorithms"},"publist_id":"2159","page":"1011 - 1020","day":"01","quality_controlled":0,"status":"public","date_created":"2018-12-11T12:06:10Z","_id":"3967","abstract":[{"text":"Motivated by the measurement of local homology and of functions on noisy domains, we extend the notion of persistent homology to sequences of kernels, images, and cokernels of maps induced by inclusions in a filtration of pairs of spaces. Specifically, we note that persistence in this context is well defined, we prove that the persistence diagrams are stable, and we explain how to compute them.","lang":"eng"}],"type":"conference","extern":1,"citation":{"apa":"Cohen Steiner, D., Edelsbrunner, H., Harer, J., &#38; Morozov, D. (2009). Persistent homology for kernels, images, and cokernels (pp. 1011–1020). Presented at the SODA: Symposium on Discrete Algorithms, SIAM.","mla":"Cohen Steiner, David, et al. <i>Persistent Homology for Kernels, Images, and Cokernels</i>. SIAM, 2009, pp. 1011–20.","ista":"Cohen Steiner D, Edelsbrunner H, Harer J, Morozov D. 2009. Persistent homology for kernels, images, and cokernels. SODA: Symposium on Discrete Algorithms, 1011–1020.","short":"D. Cohen Steiner, H. Edelsbrunner, J. Harer, D. Morozov, in:, SIAM, 2009, pp. 1011–1020.","ieee":"D. Cohen Steiner, H. Edelsbrunner, J. Harer, and D. Morozov, “Persistent homology for kernels, images, and cokernels,” presented at the SODA: Symposium on Discrete Algorithms, 2009, pp. 1011–1020.","ama":"Cohen Steiner D, Edelsbrunner H, Harer J, Morozov D. Persistent homology for kernels, images, and cokernels. In: SIAM; 2009:1011-1020.","chicago":"Cohen Steiner, David, Herbert Edelsbrunner, John Harer, and Dmitriy Morozov. “Persistent Homology for Kernels, Images, and Cokernels,” 1011–20. SIAM, 2009."},"publication_status":"published"},{"has_accepted_license":"1","publisher":"Springer","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"full_name":"Edelsbrunner, Herbert","last_name":"Edelsbrunner","orcid":"0000-0002-9823-6833","first_name":"Herbert","id":"3FB178DA-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Harer, John","first_name":"John","last_name":"Harer"}],"title":"The persistent Morse complex segmentation of a 3-manifold","file":[{"file_id":"4694","content_type":"application/pdf","creator":"system","file_size":165090,"access_level":"open_access","relation":"main_file","checksum":"11fc85bcc19bab1f020e706a4b8a4660","file_name":"IST-2016-535-v1+1_2009-P-04-3ManifoldSegmentation.pdf","date_created":"2018-12-12T10:08:33Z","date_updated":"2020-07-14T12:46:21Z"}],"publist_id":"2160","department":[{"_id":"HeEd"}],"language":[{"iso":"eng"}],"pubrep_id":"535","citation":{"apa":"Edelsbrunner, H., &#38; Harer, J. (2009). The persistent Morse complex segmentation of a 3-manifold (Vol. 5903, pp. 36–50). Presented at the 3DPH: Modelling the Physiological Human, Zermatt, Switzerland: Springer. <a href=\"https://doi.org/10.1007/978-3-642-10470-1_4\">https://doi.org/10.1007/978-3-642-10470-1_4</a>","mla":"Edelsbrunner, Herbert, and John Harer. <i>The Persistent Morse Complex Segmentation of a 3-Manifold</i>. Vol. 5903, Springer, 2009, pp. 36–50, doi:<a href=\"https://doi.org/10.1007/978-3-642-10470-1_4\">10.1007/978-3-642-10470-1_4</a>.","ama":"Edelsbrunner H, Harer J. The persistent Morse complex segmentation of a 3-manifold. In: Vol 5903. Springer; 2009:36-50. doi:<a href=\"https://doi.org/10.1007/978-3-642-10470-1_4\">10.1007/978-3-642-10470-1_4</a>","ieee":"H. Edelsbrunner and J. Harer, “The persistent Morse complex segmentation of a 3-manifold,” presented at the 3DPH: Modelling the Physiological Human, Zermatt, Switzerland, 2009, vol. 5903, pp. 36–50.","ista":"Edelsbrunner H, Harer J. 2009. The persistent Morse complex segmentation of a 3-manifold. 3DPH: Modelling the Physiological Human, LNCS, vol. 5903, 36–50.","short":"H. Edelsbrunner, J. Harer, in:, Springer, 2009, pp. 36–50.","chicago":"Edelsbrunner, Herbert, and John Harer. “The Persistent Morse Complex Segmentation of a 3-Manifold,” 5903:36–50. Springer, 2009. <a href=\"https://doi.org/10.1007/978-3-642-10470-1_4\">https://doi.org/10.1007/978-3-642-10470-1_4</a>."},"abstract":[{"lang":"eng","text":"We describe an algorithm for segmenting three-dimensional medical imaging data modeled as a continuous function on a 3-manifold. It is related to watershed algorithms developed in image processing but is closer to its mathematical roots, which are Morse theory and homological algebra. It allows for the implicit treatment of an underlying mesh, thus combining the structural integrity of its mathematical foundations with the computational efficiency of image processing."}],"scopus_import":1,"file_date_updated":"2020-07-14T12:46:21Z","type":"conference","_id":"3968","quality_controlled":"1","publication_status":"published","alternative_title":["LNCS"],"date_published":"2009-11-17T00:00:00Z","intvolume":"      5903","month":"11","acknowledgement":"This research was partially supported by Geomagic, Inc., and by the Defense Advanced Research Projects Agency (DARPA) under grants HR0011-05-1-0007 and HR0011-05-1-0057.","date_updated":"2021-01-12T07:53:32Z","oa":1,"page":"36 - 50","conference":{"name":"3DPH: Modelling the Physiological Human","start_date":"2009-11-29","end_date":"2009-12-02","location":"Zermatt, Switzerland"},"year":"2009","volume":5903,"ddc":["000"],"date_created":"2018-12-11T12:06:10Z","status":"public","day":"17","doi":"10.1007/978-3-642-10470-1_4","oa_version":"Submitted Version"},{"date_published":"2009-11-05T00:00:00Z","intvolume":"       174","month":"11","oa":1,"issue":"5","date_updated":"2021-01-12T07:54:46Z","external_id":{"pmid":[" 19788353"]},"page":"E186 - E204","year":"2009","volume":174,"pmid":1,"status":"public","day":"05","date_created":"2018-12-11T12:07:09Z","ddc":["570"],"publication":"American Naturalist","doi":"10.1086/605958","main_file_link":[{"open_access":"1","url":"https://www.doi.org/10.1086/605958"}],"oa_version":"Published Version","related_material":{"link":[{"url":"https://doi.org/10.1086/659642","relation":"erratum"}]},"publisher":"University of Chicago Press","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"full_name":"Polechova, Jitka","orcid":"0000-0003-0951-3112","last_name":"Polechova","id":"3BBFB084-F248-11E8-B48F-1D18A9856A87","first_name":"Jitka"},{"orcid":"0000-0002-8548-5240","last_name":"Barton","first_name":"Nicholas H","id":"4880FE40-F248-11E8-B48F-1D18A9856A87","full_name":"Barton, Nicholas H"},{"first_name":"Glenn","last_name":"Marion","full_name":"Marion, Glenn"}],"title":"Species' range: Adaptation in space and time","department":[{"_id":"NiBa"}],"publist_id":"1986","article_processing_charge":"No","article_type":"original","pubrep_id":"552","language":[{"iso":"eng"}],"scopus_import":1,"abstract":[{"text":"Populations living in a spatially and temporally changing environment can adapt to the changing optimum and/or migrate toward favorable habitats. Here we extend previous analyses with a static optimum to allow the environment to vary in time as well as in space. The model follows both population dynamics and the trait mean under stabilizing selection, and the outcomes can be understood by comparing the loads due to genetic variance, dispersal, and temporal change. With fixed genetic variance, we obtain two regimes: (1) adaptation that is uniform along the environmental gradient and that responds to the moving optimum as expected for panmictic populations and when the spatial gradient is sufficiently steep, and (2) a population with limited range that adapts more slowly than the environmental optimum changes in both time and space; the population therefore becomes locally extinct and migrates toward suitable habitat. We also use a population‐genetic model with many loci to allow genetic variance to evolve, and we show that the only solution now has uniform adaptation.","lang":"eng"}],"type":"journal_article","citation":{"mla":"Polechova, Jitka, et al. “Species’ Range: Adaptation in Space and Time.” <i>American Naturalist</i>, vol. 174, no. 5, University of Chicago Press, 2009, pp. E186–204, doi:<a href=\"https://doi.org/10.1086/605958\">10.1086/605958</a>.","apa":"Polechova, J., Barton, N. H., &#38; Marion, G. (2009). Species’ range: Adaptation in space and time. <i>American Naturalist</i>. University of Chicago Press. <a href=\"https://doi.org/10.1086/605958\">https://doi.org/10.1086/605958</a>","chicago":"Polechova, Jitka, Nicholas H Barton, and Glenn Marion. “Species’ Range: Adaptation in Space and Time.” <i>American Naturalist</i>. University of Chicago Press, 2009. <a href=\"https://doi.org/10.1086/605958\">https://doi.org/10.1086/605958</a>.","short":"J. Polechova, N.H. Barton, G. Marion, American Naturalist 174 (2009) E186–E204.","ieee":"J. Polechova, N. H. Barton, and G. Marion, “Species’ range: Adaptation in space and time,” <i>American Naturalist</i>, vol. 174, no. 5. University of Chicago Press, pp. E186–E204, 2009.","ista":"Polechova J, Barton NH, Marion G. 2009. Species’ range: Adaptation in space and time. American Naturalist. 174(5), E186–E204.","ama":"Polechova J, Barton NH, Marion G. Species’ range: Adaptation in space and time. <i>American Naturalist</i>. 2009;174(5):E186-E204. doi:<a href=\"https://doi.org/10.1086/605958\">10.1086/605958</a>"},"quality_controlled":"1","_id":"4136","publication_status":"published"},{"citation":{"chicago":"Ulrich, Florian, and Carl-Philipp J Heisenberg. “Trafficking and Cell Migration.” <i>Traffic</i>. Wiley-Blackwell, 2009. <a href=\"https://doi.org/10.1111/j.1600-0854.2009.00929.x\">https://doi.org/10.1111/j.1600-0854.2009.00929.x</a>.","short":"F. Ulrich, C.-P.J. Heisenberg, Traffic 10 (2009) 811–818.","ieee":"F. Ulrich and C.-P. J. Heisenberg, “Trafficking and cell migration,” <i>Traffic</i>, vol. 10, no. 7. Wiley-Blackwell, pp. 811–818, 2009.","ista":"Ulrich F, Heisenberg C-PJ. 2009. Trafficking and cell migration. Traffic. 10(7), 811–818.","ama":"Ulrich F, Heisenberg C-PJ. Trafficking and cell migration. <i>Traffic</i>. 2009;10(7):811-818. doi:<a href=\"https://doi.org/10.1111/j.1600-0854.2009.00929.x\">10.1111/j.1600-0854.2009.00929.x</a>","mla":"Ulrich, Florian, and Carl-Philipp J. Heisenberg. “Trafficking and Cell Migration.” <i>Traffic</i>, vol. 10, no. 7, Wiley-Blackwell, 2009, pp. 811–18, doi:<a href=\"https://doi.org/10.1111/j.1600-0854.2009.00929.x\">10.1111/j.1600-0854.2009.00929.x</a>.","apa":"Ulrich, F., &#38; Heisenberg, C.-P. J. (2009). Trafficking and cell migration. <i>Traffic</i>. Wiley-Blackwell. <a href=\"https://doi.org/10.1111/j.1600-0854.2009.00929.x\">https://doi.org/10.1111/j.1600-0854.2009.00929.x</a>"},"extern":"1","volume":10,"type":"journal_article","abstract":[{"text":"The migration of single cells and epithelial sheets is of great importance for gastrulation and organ formation in developing embryos and, if misregulated, can have dire consequences e.g. during cancer metastasis. A keystone of cell migration is the regulation of adhesive contacts, which are dynamically assembled and disassembled via endocytosis. Here, we discuss some of the basic concepts about the function of endocytic trafficking during cell migration: transport of integrins from the cell rear to the leading edge in fibroblasts; confinement of signalling to the front of single cells by endocytic transport of growth factors; regulation of movement coherence in multicellular sheets by cadherin turnover; and shaping of extracellular chemokine gradients. Taken together, endocytosis enables migrating cells and tissues to dynamically modulate their adhesion and signalling, allowing them to efficiently migrate through their extracellular environment.","lang":"eng"}],"_id":"4143","date_created":"2018-12-11T12:07:12Z","day":"20","status":"public","publication_status":"published","doi":"10.1111/j.1600-0854.2009.00929.x","publication":"Traffic","oa_version":"None","intvolume":"        10","month":"05","date_published":"2009-05-20T00:00:00Z","publisher":"Wiley-Blackwell","date_updated":"2021-01-12T07:54:49Z","issue":"7","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"full_name":"Ulrich, Florian","last_name":"Ulrich","first_name":"Florian"},{"full_name":"Heisenberg, Carl-Philipp J","orcid":"0000-0002-0912-4566","last_name":"Heisenberg","first_name":"Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87"}],"title":"Trafficking and cell migration","article_processing_charge":"No","page":"811 - 818","publist_id":"1976","language":[{"iso":"eng"}],"year":"2009"},{"publication":"Mechanisms of Development","doi":"10.1016/j.mod.2009.06.391","publication_status":"published","oa_version":"None","abstract":[{"text":"An important step in the formation of all epithelial organs is the coordinated polarisation of their constituent cells. One of the factors thought to be crucial for this process is the extracellular matrix (ECM), which provides positional information for cells and directs polarity specification and epithelial cyst formation in 3D culture. However, in vivo evidence for the role of the ECM in epithelial tissue polarisation is scarce.\r\n\r\nTo gain insight in the factors involved in establishing cell polarity during organogenesis, we are studying a group of epithelial cells called the Dorsal Forerunner Cells (DFCs) in zebrafish embryos. These cells migrate as a cluster towards the vegetal pole of the developing embryo, where they involute. During this process they polarise, and make foci that open up to form a ciliated lumen called Kupffer’s vesicle.\r\n\r\nWe find that interfering with the deposition of components of the extracellular matrix, or with the intracellular anchors of the cells to the matrix, impairs the polarisation of the DFC’s and leads to subsequent defects in lumen formation. In addition, we have developed a method to culture the DFCs ex vivo, allowing us to precisely manipulate the extracellular environment. The possibility of combining the genetic study of Kupffer’s vesicle formation in the live embryo with cell biological techniques in organ culture make this system uniquely relevant for studying the role of the ECM in polarisation during organogenesis.\r\n","lang":"eng"}],"type":"journal_article","volume":126,"extern":"1","citation":{"apa":"Soete, G., &#38; Heisenberg, C.-P. J. (2009). The role of the extracellular matrix in Kupffer’s vesicle formation in zebrafish. <i>Mechanisms of Development</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.mod.2009.06.391\">https://doi.org/10.1016/j.mod.2009.06.391</a>","mla":"Soete, Gwen, and Carl-Philipp J. Heisenberg. “The Role of the Extracellular Matrix in Kupffer’s Vesicle Formation in Zebrafish.” <i>Mechanisms of Development</i>, vol. 126, Elsevier, 2009, pp. S168–S168, doi:<a href=\"https://doi.org/10.1016/j.mod.2009.06.391\">10.1016/j.mod.2009.06.391</a>.","ieee":"G. Soete and C.-P. J. Heisenberg, “The role of the extracellular matrix in Kupffer’s vesicle formation in zebrafish,” <i>Mechanisms of Development</i>, vol. 126. Elsevier, pp. S168–S168, 2009.","short":"G. Soete, C.-P.J. Heisenberg, Mechanisms of Development 126 (2009) S168–S168.","ista":"Soete G, Heisenberg C-PJ. 2009. The role of the extracellular matrix in Kupffer’s vesicle formation in zebrafish. Mechanisms of Development. 126, S168–S168.","ama":"Soete G, Heisenberg C-PJ. The role of the extracellular matrix in Kupffer’s vesicle formation in zebrafish. <i>Mechanisms of Development</i>. 2009;126:S168-S168. doi:<a href=\"https://doi.org/10.1016/j.mod.2009.06.391\">10.1016/j.mod.2009.06.391</a>","chicago":"Soete, Gwen, and Carl-Philipp J Heisenberg. “The Role of the Extracellular Matrix in Kupffer’s Vesicle Formation in Zebrafish.” <i>Mechanisms of Development</i>. Elsevier, 2009. <a href=\"https://doi.org/10.1016/j.mod.2009.06.391\">https://doi.org/10.1016/j.mod.2009.06.391</a>."},"status":"public","day":"01","date_created":"2018-12-11T12:07:14Z","_id":"4149","publist_id":"1970","page":"S168 - S168","article_processing_charge":"No","year":"2009","language":[{"iso":"eng"}],"publisher":"Elsevier","date_published":"2009-08-01T00:00:00Z","intvolume":"       126","month":"08","author":[{"first_name":"Gwen","last_name":"Soete","full_name":"Soete, Gwen"},{"full_name":"Heisenberg, Carl-Philipp J","first_name":"Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87","last_name":"Heisenberg","orcid":"0000-0002-0912-4566"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","title":"The role of the extracellular matrix in Kupffer's vesicle formation in zebrafish","date_updated":"2021-01-12T07:54:52Z"},{"_id":"4158","date_created":"2018-12-11T12:07:17Z","day":"15","status":"public","extern":"1","citation":{"mla":"Paluch, Ewa, and Carl-Philipp J. Heisenberg. “Biology and Physics of Cell Shape Changes in Development.” <i>Current Biology</i>, vol. 19, no. 17, Cell Press, 2009, pp. R790–99, doi:<a href=\"https://doi.org/10.1016/j.cub.2009.07.029\">10.1016/j.cub.2009.07.029</a>.","apa":"Paluch, E., &#38; Heisenberg, C.-P. J. (2009). Biology and physics of cell shape changes in development. <i>Current Biology</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.cub.2009.07.029\">https://doi.org/10.1016/j.cub.2009.07.029</a>","chicago":"Paluch, Ewa, and Carl-Philipp J Heisenberg. “Biology and Physics of Cell Shape Changes in Development.” <i>Current Biology</i>. Cell Press, 2009. <a href=\"https://doi.org/10.1016/j.cub.2009.07.029\">https://doi.org/10.1016/j.cub.2009.07.029</a>.","ama":"Paluch E, Heisenberg C-PJ. Biology and physics of cell shape changes in development. <i>Current Biology</i>. 2009;19(17):R790-R799. doi:<a href=\"https://doi.org/10.1016/j.cub.2009.07.029\">10.1016/j.cub.2009.07.029</a>","short":"E. Paluch, C.-P.J. Heisenberg, Current Biology 19 (2009) R790–R799.","ista":"Paluch E, Heisenberg C-PJ. 2009. Biology and physics of cell shape changes in development. Current Biology. 19(17), R790–R799.","ieee":"E. Paluch and C.-P. J. Heisenberg, “Biology and physics of cell shape changes in development,” <i>Current Biology</i>, vol. 19, no. 17. Cell Press, pp. R790–R799, 2009."},"volume":19,"type":"journal_article","abstract":[{"lang":"eng","text":"Together with cell growth, division and death, changes in cell shape are of central importance for tissue morphogenesis during development. Cell shape is the product of a cell's material and active properties balanced by external forces. Control of cell shape, therefore, relies on both tight regulation of intracellular mechanics and the cell's physical interaction with its environment. In this review, we first discuss the biological and physical mechanisms of cell shape control. We next examine a number of develop mental processes in which cell shape change - either individually or in a coordinated manner - drives embryonic morphogenesis and discuss how cell shape is controlled in these processes. Finally, we emphasize that cell shape control during tissue morphogenesis can only be fully understood by using a combination of cellular, molecular, developmental and biophysical approaches."}],"oa_version":"None","publication_status":"published","doi":"10.1016/j.cub.2009.07.029","publication":"Current Biology","date_updated":"2021-01-12T07:54:56Z","issue":"17","title":"Biology and physics of cell shape changes in development","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"full_name":"Paluch, Ewa","last_name":"Paluch","first_name":"Ewa"},{"full_name":"Heisenberg, Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87","first_name":"Carl-Philipp J","orcid":"0000-0002-0912-4566","last_name":"Heisenberg"}],"intvolume":"        19","month":"09","date_published":"2009-09-15T00:00:00Z","publisher":"Cell Press","language":[{"iso":"eng"}],"year":"2009","page":"R790 - R799","article_processing_charge":"No","publist_id":"1960"},{"language":[{"iso":"eng"}],"year":"2009","article_processing_charge":"No","page":"4 - 6","publist_id":"1961","date_updated":"2021-01-12T07:54:56Z","issue":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","title":"Chaos begets order: Asynchronous cell contractions drive epithelial morphogenesis","author":[{"full_name":"Paluch, Ewa","last_name":"Paluch","first_name":"Ewa"},{"full_name":"Heisenberg, Carl-Philipp J","orcid":"0000-0002-0912-4566","last_name":"Heisenberg","id":"39427864-F248-11E8-B48F-1D18A9856A87","first_name":"Carl-Philipp J"}],"month":"01","intvolume":"        16","date_published":"2009-01-20T00:00:00Z","publisher":"Cell Press","oa_version":"None","doi":"10.1016/j.devcel.2008.12.011","publication_status":"published","publication":"Developmental Cell","date_created":"2018-12-11T12:07:18Z","_id":"4159","status":"public","day":"20","citation":{"mla":"Paluch, Ewa, and Carl-Philipp J. Heisenberg. “Chaos Begets Order: Asynchronous Cell Contractions Drive Epithelial Morphogenesis.” <i>Developmental Cell</i>, vol. 16, no. 1, Cell Press, 2009, pp. 4–6, doi:<a href=\"https://doi.org/10.1016/j.devcel.2008.12.011\">10.1016/j.devcel.2008.12.011</a>.","apa":"Paluch, E., &#38; Heisenberg, C.-P. J. (2009). Chaos begets order: Asynchronous cell contractions drive epithelial morphogenesis. <i>Developmental Cell</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.devcel.2008.12.011\">https://doi.org/10.1016/j.devcel.2008.12.011</a>","chicago":"Paluch, Ewa, and Carl-Philipp J Heisenberg. “Chaos Begets Order: Asynchronous Cell Contractions Drive Epithelial Morphogenesis.” <i>Developmental Cell</i>. Cell Press, 2009. <a href=\"https://doi.org/10.1016/j.devcel.2008.12.011\">https://doi.org/10.1016/j.devcel.2008.12.011</a>.","ama":"Paluch E, Heisenberg C-PJ. Chaos begets order: Asynchronous cell contractions drive epithelial morphogenesis. <i>Developmental Cell</i>. 2009;16(1):4-6. doi:<a href=\"https://doi.org/10.1016/j.devcel.2008.12.011\">10.1016/j.devcel.2008.12.011</a>","ista":"Paluch E, Heisenberg C-PJ. 2009. Chaos begets order: Asynchronous cell contractions drive epithelial morphogenesis. Developmental Cell. 16(1), 4–6.","short":"E. Paluch, C.-P.J. Heisenberg, Developmental Cell 16 (2009) 4–6.","ieee":"E. Paluch and C.-P. J. Heisenberg, “Chaos begets order: Asynchronous cell contractions drive epithelial morphogenesis,” <i>Developmental Cell</i>, vol. 16, no. 1. Cell Press, pp. 4–6, 2009."},"extern":"1","volume":16,"type":"journal_article","abstract":[{"text":"Apical cell contraction triggers tissue folding and invagination in epithelia. During Drosophila gastrulation, ventral furrow formation was thought to be driven by smooth, purse-string-like constriction of an actomyosin belt underlying adherens junctions. Now Martin et al. report in Nature that ventral furrow formation is triggered by asynchronous pulsed contractions of the apical acto-myosin cortex in individual cells.","lang":"eng"}]},{"doi":"10.1016/j.mod.2009.06.970","publication_status":"published","publication":"Mechanisms of Development","oa_version":"None","type":"journal_article","abstract":[{"lang":"eng","text":"While the function of patterning in organogenesis is being extensively studied, considerably less is known of reverse effects that organ formation imposes on patterning. In zebrafish, the Kupffer’s vesicle (KV) and parapineal (PP) are embryonic struc- tures that share mechanisms of organogenesis and whose func- tion is essential for normal patterning along the left–right axis. Early morphogenesis of KV and PP organs involve the compaction of progenitor cells into a tight cluster within which three-dimen- sional cellular rosettes are formed. Organisation into rosettes pre- cedes the detachment of progenitor cells from neighbouring tissue and thus represents a key step towards organ formation. Such morphogenetic event is essential for organ function and its disruption has profound effects on left–right patterning."}],"extern":"1","citation":{"apa":"Oteíza, P., Lemus, C., Köppen, M., Palma, K., Krieg, M., Melo, C., … Concha, M. (2009). Linking organ formation to left-right patterning in the embryonic zebrafish. <i>Mechanisms of Development</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.mod.2009.06.970\">https://doi.org/10.1016/j.mod.2009.06.970</a>","mla":"Oteíza, Pablo, et al. “Linking Organ Formation to Left-Right Patterning in the Embryonic Zebrafish.” <i>Mechanisms of Development</i>, vol. 126, no. Supplement 1, Elsevier, 2009, pp. S11–S11, doi:<a href=\"https://doi.org/10.1016/j.mod.2009.06.970\">10.1016/j.mod.2009.06.970</a>.","ista":"Oteíza P, Lemus C, Köppen M, Palma K, Krieg M, Melo C, Farias C, Pulgar E, Preibisch S, Hartel S, Heisenberg C-PJ, Concha M. 2009. Linking organ formation to left-right patterning in the embryonic zebrafish. Mechanisms of Development. 126(Supplement 1), S11–S11.","short":"P. Oteíza, C. Lemus, M. Köppen, K. Palma, M. Krieg, C. Melo, C. Farias, E. Pulgar, S. Preibisch, S. Hartel, C.-P.J. Heisenberg, M. Concha, Mechanisms of Development 126 (2009) S11–S11.","ieee":"P. Oteíza <i>et al.</i>, “Linking organ formation to left-right patterning in the embryonic zebrafish,” <i>Mechanisms of Development</i>, vol. 126, no. Supplement 1. Elsevier, pp. S11–S11, 2009.","ama":"Oteíza P, Lemus C, Köppen M, et al. Linking organ formation to left-right patterning in the embryonic zebrafish. <i>Mechanisms of Development</i>. 2009;126(Supplement 1):S11-S11. doi:<a href=\"https://doi.org/10.1016/j.mod.2009.06.970\">10.1016/j.mod.2009.06.970</a>","chicago":"Oteíza, Pablo, Carmen Lemus, Mathias Köppen, Karina Palma, Michael Krieg, Cristina Melo, Cecilia Farias, et al. “Linking Organ Formation to Left-Right Patterning in the Embryonic Zebrafish.” <i>Mechanisms of Development</i>. Elsevier, 2009. <a href=\"https://doi.org/10.1016/j.mod.2009.06.970\">https://doi.org/10.1016/j.mod.2009.06.970</a>."},"volume":126,"status":"public","day":"05","date_created":"2018-12-11T12:07:18Z","_id":"4160","publist_id":"1959","page":"S11 - S11","article_processing_charge":"No","year":"2009","language":[{"iso":"eng"}],"publisher":"Elsevier","acknowledgement":"Grant sponsors: HHMI, CONICYT (PBCT ACT47, PBCT Red6), ICM P04-048-F, EU FP6-2004-NEST-PATH EDCBNL, DAAD.","month":"08","intvolume":"       126","date_published":"2009-08-05T00:00:00Z","issue":"Supplement 1","title":"Linking organ formation to left-right patterning in the embryonic zebrafish","author":[{"full_name":"Oteíza, Pablo","last_name":"Oteíza","first_name":"Pablo"},{"last_name":"Lemus","first_name":"Carmen","full_name":"Lemus, Carmen"},{"full_name":"Köppen, Mathias","first_name":"Mathias","last_name":"Köppen"},{"full_name":"Palma, Karina","first_name":"Karina","last_name":"Palma"},{"last_name":"Krieg","first_name":"Michael","full_name":"Krieg, Michael"},{"full_name":"Melo, Cristina","first_name":"Cristina","last_name":"Melo"},{"full_name":"Farias, Cecilia","last_name":"Farias","first_name":"Cecilia"},{"last_name":"Pulgar","first_name":"Eduardo","full_name":"Pulgar, Eduardo"},{"full_name":"Preibisch, Steffen","last_name":"Preibisch","first_name":"Steffen"},{"last_name":"Hartel","first_name":"Steffen","full_name":"Hartel, Steffen"},{"full_name":"Heisenberg, Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87","first_name":"Carl-Philipp J","last_name":"Heisenberg","orcid":"0000-0002-0912-4566"},{"full_name":"Concha, Miguel","first_name":"Miguel","last_name":"Concha"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2021-01-12T07:54:57Z"},{"title":"Wnt11/Pk1a-mediated planar cell polarity signalling orchestrates epithelial organ morphogenesis by regulating N-cadherin dependent cell adhesion forces","author":[{"full_name":"Oteíza, Pablo","first_name":"Pablo","last_name":"Oteíza"},{"full_name":"Köppen, Mathias","last_name":"Köppen","first_name":"Mathias"},{"full_name":"Krieg, Michael","last_name":"Krieg","first_name":"Michael"},{"last_name":"Preibisch","first_name":"Steffen","full_name":"Preibisch, Steffen"},{"full_name":"Haertel, Steffen","first_name":"Steffen","last_name":"Haertel"},{"first_name":"Daniel","last_name":"Müller","full_name":"Müller, Daniel"},{"full_name":"Heisenberg, Carl-Philipp J","first_name":"Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87","last_name":"Heisenberg","orcid":"0000-0002-0912-4566"},{"full_name":"Concha, Miguel","last_name":"Concha","first_name":"Miguel"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","issue":"Supplement 1","date_updated":"2021-01-12T07:54:58Z","publisher":"Elsevier","date_published":"2009-08-05T00:00:00Z","month":"08","intvolume":"       126","year":"2009","language":[{"iso":"eng"}],"publist_id":"1957","article_processing_charge":"No","page":"S80 - S80","status":"public","day":"05","_id":"4162","date_created":"2018-12-11T12:07:19Z","abstract":[{"lang":"eng","text":"Organ formation requires the precise assembly of progenitor cells into a functional unit. Mechanical forces are likely to play a critical role in this process, but it is unclear how these are molecularly controlled during development. Here, we show that Wnt11/ Pk1a-mediated planar cell polarity (PCP) signalling coordinates formation of the zebrafish laterality organ (Kupffer’s vesicle, KV) by regulating adhesion forces between organ progenitor cells (the dorsal forerunner cells, DFCs)."}],"type":"journal_article","volume":126,"extern":"1","citation":{"ama":"Oteíza P, Köppen M, Krieg M, et al. Wnt11/Pk1a-mediated planar cell polarity signalling orchestrates epithelial organ morphogenesis by regulating N-cadherin dependent cell adhesion forces. <i>Mechanisms of Development</i>. 2009;126(Supplement 1):S80-S80. doi:<a href=\"https://doi.org/10.1016/j.mod.2009.06.098\">10.1016/j.mod.2009.06.098</a>","short":"P. Oteíza, M. Köppen, M. Krieg, S. Preibisch, S. Haertel, D. Müller, C.-P.J. Heisenberg, M. Concha, Mechanisms of Development 126 (2009) S80–S80.","ista":"Oteíza P, Köppen M, Krieg M, Preibisch S, Haertel S, Müller D, Heisenberg C-PJ, Concha M. 2009. Wnt11/Pk1a-mediated planar cell polarity signalling orchestrates epithelial organ morphogenesis by regulating N-cadherin dependent cell adhesion forces. Mechanisms of Development. 126(Supplement 1), S80–S80.","ieee":"P. Oteíza <i>et al.</i>, “Wnt11/Pk1a-mediated planar cell polarity signalling orchestrates epithelial organ morphogenesis by regulating N-cadherin dependent cell adhesion forces,” <i>Mechanisms of Development</i>, vol. 126, no. Supplement 1. Elsevier, pp. S80–S80, 2009.","chicago":"Oteíza, Pablo, Mathias Köppen, Michael Krieg, Steffen Preibisch, Steffen Haertel, Daniel Müller, Carl-Philipp J Heisenberg, and Miguel Concha. “Wnt11/Pk1a-Mediated Planar Cell Polarity Signalling Orchestrates Epithelial Organ Morphogenesis by Regulating N-Cadherin Dependent Cell Adhesion Forces.” <i>Mechanisms of Development</i>. Elsevier, 2009. <a href=\"https://doi.org/10.1016/j.mod.2009.06.098\">https://doi.org/10.1016/j.mod.2009.06.098</a>.","apa":"Oteíza, P., Köppen, M., Krieg, M., Preibisch, S., Haertel, S., Müller, D., … Concha, M. (2009). Wnt11/Pk1a-mediated planar cell polarity signalling orchestrates epithelial organ morphogenesis by regulating N-cadherin dependent cell adhesion forces. <i>Mechanisms of Development</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.mod.2009.06.098\">https://doi.org/10.1016/j.mod.2009.06.098</a>","mla":"Oteíza, Pablo, et al. “Wnt11/Pk1a-Mediated Planar Cell Polarity Signalling Orchestrates Epithelial Organ Morphogenesis by Regulating N-Cadherin Dependent Cell Adhesion Forces.” <i>Mechanisms of Development</i>, vol. 126, no. Supplement 1, Elsevier, 2009, pp. S80–S80, doi:<a href=\"https://doi.org/10.1016/j.mod.2009.06.098\">10.1016/j.mod.2009.06.098</a>."},"oa_version":"None","publication":"Mechanisms of Development","publication_status":"published","doi":"10.1016/j.mod.2009.06.098"},{"publisher":"Nature Publishing Group","date_published":"2009-08-01T00:00:00Z","month":"08","intvolume":"        10","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"full_name":"Oates, Andrew","last_name":"Oates","first_name":"Andrew"},{"full_name":"Gorfinkiel, Nicole","first_name":"Nicole","last_name":"Gorfinkiel"},{"last_name":"Gonzalez Gaitan","first_name":"Marcos","full_name":"Gonzalez Gaitan, Marcos"},{"orcid":"0000-0002-0912-4566","last_name":"Heisenberg","id":"39427864-F248-11E8-B48F-1D18A9856A87","first_name":"Carl-Philipp J","full_name":"Heisenberg, Carl-Philipp J"}],"title":"Quantitative approaches in developmental biology","issue":"8","date_updated":"2021-01-12T07:54:59Z","publist_id":"1953","article_processing_charge":"No","page":"517 - 530","year":"2009","language":[{"iso":"eng"}],"abstract":[{"lang":"eng","text":"The tissues of a developing embryo are simultaneously patterned, moved and differentiated according to an exchange of information between their constituent cells. We argue that these complex self-organizing phenomena can only be fully understood with quantitative mathematical frameworks that allow specific hypotheses to be formulated and tested. The quantitative and dynamic imaging of growing embryos at the molecular, cellular and tissue level is the key experimental advance required to achieve this interaction between theory and experiment. Here we describe how mathematical modelling has become an invaluable method to integrate quantitative biological information across temporal and spatial scales, serving to connect the activity of regulatory molecules with the morphological development of organisms."}],"type":"journal_article","volume":10,"citation":{"ista":"Oates A, Gorfinkiel N, Gonzalez Gaitan M, Heisenberg C-PJ. 2009. Quantitative approaches in developmental biology. Nature Reviews Genetics. 10(8), 517–530.","ieee":"A. Oates, N. Gorfinkiel, M. Gonzalez Gaitan, and C.-P. J. Heisenberg, “Quantitative approaches in developmental biology,” <i>Nature Reviews Genetics</i>, vol. 10, no. 8. Nature Publishing Group, pp. 517–530, 2009.","short":"A. Oates, N. Gorfinkiel, M. Gonzalez Gaitan, C.-P.J. Heisenberg, Nature Reviews Genetics 10 (2009) 517–530.","ama":"Oates A, Gorfinkiel N, Gonzalez Gaitan M, Heisenberg C-PJ. Quantitative approaches in developmental biology. <i>Nature Reviews Genetics</i>. 2009;10(8):517-530. doi:<a href=\"https://doi.org/10.1038/nrg2548\">10.1038/nrg2548</a>","chicago":"Oates, Andrew, Nicole Gorfinkiel, Marcos Gonzalez Gaitan, and Carl-Philipp J Heisenberg. “Quantitative Approaches in Developmental Biology.” <i>Nature Reviews Genetics</i>. Nature Publishing Group, 2009. <a href=\"https://doi.org/10.1038/nrg2548\">https://doi.org/10.1038/nrg2548</a>.","apa":"Oates, A., Gorfinkiel, N., Gonzalez Gaitan, M., &#38; Heisenberg, C.-P. J. (2009). Quantitative approaches in developmental biology. <i>Nature Reviews Genetics</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/nrg2548\">https://doi.org/10.1038/nrg2548</a>","mla":"Oates, Andrew, et al. “Quantitative Approaches in Developmental Biology.” <i>Nature Reviews Genetics</i>, vol. 10, no. 8, Nature Publishing Group, 2009, pp. 517–30, doi:<a href=\"https://doi.org/10.1038/nrg2548\">10.1038/nrg2548</a>."},"extern":"1","status":"public","day":"01","date_created":"2018-12-11T12:07:20Z","_id":"4165","publication":"Nature Reviews Genetics","publication_status":"published","doi":"10.1038/nrg2548","oa_version":"None"},{"date_updated":"2021-01-12T07:55:11Z","issue":"Supplement 1","author":[{"full_name":"Kai, Masatake","first_name":"Masatake","last_name":"Kai"},{"last_name":"Buchan","first_name":"Nina","full_name":"Buchan, Nina"},{"last_name":"Heisenberg","orcid":"0000-0002-0912-4566","id":"39427864-F248-11E8-B48F-1D18A9856A87","first_name":"Carl-Philipp J","full_name":"Heisenberg, Carl-Philipp J"},{"full_name":"Tada, Masazumi","last_name":"Tada","first_name":"Masazumi"}],"title":"Regulation of planar cell polarity signalling by the prenylation pathway","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","intvolume":"       126","month":"08","date_published":"2009-08-05T00:00:00Z","publisher":"Elsevier","language":[{"iso":"eng"}],"year":"2009","article_processing_charge":"No","page":"S132 - S132","publist_id":"1927","_id":"4192","date_created":"2018-12-11T12:07:30Z","day":"05","status":"public","citation":{"apa":"Kai, M., Buchan, N., Heisenberg, C.-P. J., &#38; Tada, M. (2009). Regulation of planar cell polarity signalling by the prenylation pathway. <i>Mechanisms of Development</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.mod.2009.06.269\">https://doi.org/10.1016/j.mod.2009.06.269</a>","mla":"Kai, Masatake, et al. “Regulation of Planar Cell Polarity Signalling by the Prenylation Pathway.” <i>Mechanisms of Development</i>, vol. 126, no. Supplement 1, Elsevier, 2009, pp. S132–S132, doi:<a href=\"https://doi.org/10.1016/j.mod.2009.06.269\">10.1016/j.mod.2009.06.269</a>.","ista":"Kai M, Buchan N, Heisenberg C-PJ, Tada M. 2009. Regulation of planar cell polarity signalling by the prenylation pathway. Mechanisms of Development. 126(Supplement 1), S132–S132.","short":"M. Kai, N. Buchan, C.-P.J. Heisenberg, M. Tada, Mechanisms of Development 126 (2009) S132–S132.","ieee":"M. Kai, N. Buchan, C.-P. J. Heisenberg, and M. Tada, “Regulation of planar cell polarity signalling by the prenylation pathway,” <i>Mechanisms of Development</i>, vol. 126, no. Supplement 1. Elsevier, pp. S132–S132, 2009.","ama":"Kai M, Buchan N, Heisenberg C-PJ, Tada M. Regulation of planar cell polarity signalling by the prenylation pathway. <i>Mechanisms of Development</i>. 2009;126(Supplement 1):S132-S132. doi:<a href=\"https://doi.org/10.1016/j.mod.2009.06.269\">10.1016/j.mod.2009.06.269</a>","chicago":"Kai, Masatake, Nina Buchan, Carl-Philipp J Heisenberg, and Masazumi Tada. “Regulation of Planar Cell Polarity Signalling by the Prenylation Pathway.” <i>Mechanisms of Development</i>. Elsevier, 2009. <a href=\"https://doi.org/10.1016/j.mod.2009.06.269\">https://doi.org/10.1016/j.mod.2009.06.269</a>."},"extern":"1","volume":126,"type":"journal_article","abstract":[{"text":"During vertebrate gastrulation, the body axis is established by a variety of co-ordinated and directed movements of cells. One of these movements is convergence and extension (CE), which is regulated by a non-canonical Wnt/planar cell polarity (PCP) pathway. From our forward genetic screen, we have identified 3-hydroxy-3-methyglutaryl-coenzyme A reductase 1b (hmgcr1b) gene as a dominant enhancer of the silberblick (slb)/wnt11 CE phenotype. hmgcr1b mutant embryos exhibit only very mild CE phenotype during gastrulation while showing a thicker yolk extension at pharyngula stages. Notably, abrogation of hmgcr1b also enhances the CE defects of other core PCP mutants/morphants. The prenylation pathway is one of branches downstream of HMGCR, and has been implicated for lipid modification at the C-terminus of proteins. To test the possibility that the prenylation pathway regulates activities of the PCP pathway, we abrogated farnesyl transferase (FT) or geranylgeranyl transferase (GGT) function using morpholinos on PCP mutant/morphant backgrounds. Consistent with the notion that FT preferentially performs lipid modification on to proteins with the CAAX motif including the core PCP protein Prickle (Pk), abrogation of FT, but not GGT, enhances the pk1a or pk1b morphant CE phenotype, suggesting the specif icity for targets of the prenylation enzymes.\r\n","lang":"eng"}],"oa_version":"None","doi":"10.1016/j.mod.2009.06.269","publication_status":"published","publication":"Mechanisms of Development"}]