[{"publisher":"National Academy of Sciences","corr_author":"1","article_processing_charge":"No","pmid":1,"acknowledgement":"We thank Urban Bezeljak, Natalia Baranova, Mar Lopez-Pelegrin, Catarina Alcarva, and Victoria Faas for sharing reagents and helpful discussions. We thank Veronika Szentirmai for help with protein purifications. We thank Carrie Bernecky, Sascha Martens, and the M.L. lab for comments on the manuscript. We thank the bioimaging facility, the life science facility, and Armel Nicolas from the mass spec facility at the Institute of Science and Technology (IST) Austria for technical support. C.D. acknowledges funding from the IST fellowship program; this work was supported by Human Frontier Science Program Young Investigator Grant\r\nRGY0083/2016. ","doi":"10.1073/pnas.2010054118","oa":1,"project":[{"grant_number":"RGY0083/2016","_id":"2599F062-B435-11E9-9278-68D0E5697425","name":"Reconstitution of cell polarity and axis determination in a cell-free system"}],"article_type":"original","month":"01","department":[{"_id":"MaLo"},{"_id":"MiSi"}],"author":[{"last_name":"Düllberg","full_name":"Düllberg, Christian F","id":"459064DC-F248-11E8-B48F-1D18A9856A87","first_name":"Christian F","orcid":"0000-0001-6335-9748"},{"full_name":"Auer, Albert","last_name":"Auer","id":"3018E8C2-F248-11E8-B48F-1D18A9856A87","first_name":"Albert","orcid":"0000-0002-3580-2906"},{"last_name":"Canigova","full_name":"Canigova, Nikola","id":"3795523E-F248-11E8-B48F-1D18A9856A87","first_name":"Nikola","orcid":"0000-0002-8518-5926"},{"id":"3760F32C-F248-11E8-B48F-1D18A9856A87","first_name":"Katrin","orcid":"0000-0002-2429-7668","full_name":"Loibl, Katrin","last_name":"Loibl"},{"first_name":"Martin","id":"462D4284-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-7309-9724","full_name":"Loose, Martin","last_name":"Loose"}],"volume":118,"publication_identifier":{"issn":["0027-8424"],"eissn":["1091-6490"]},"oa_version":"Published Version","title":"In vitro reconstitution reveals phosphoinositides as cargo-release factors and activators of the ARF6 GAP ADAP1","date_created":"2021-01-03T23:01:23Z","publication_status":"published","status":"public","scopus_import":"1","issue":"1","acknowledged_ssus":[{"_id":"Bio"},{"_id":"LifeSc"},{"_id":"EM-Fac"}],"isi":1,"date_updated":"2025-05-14T10:59:29Z","publication":"Proceedings of the National Academy of Sciences of the United States of America","year":"2021","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","intvolume":"       118","article_number":"e2010054118","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1073/pnas.2010054118"}],"date_published":"2021-01-05T00:00:00Z","type":"journal_article","quality_controlled":"1","language":[{"iso":"eng"}],"_id":"8988","abstract":[{"lang":"eng","text":"The differentiation of cells depends on a precise control of their internal organization, which is the result of a complex dynamic interplay between the cytoskeleton, molecular motors, signaling molecules, and membranes. For example, in the developing neuron, the protein ADAP1 (ADP-ribosylation factor GTPase-activating protein [ArfGAP] with dual pleckstrin homology [PH] domains 1) has been suggested to control dendrite branching by regulating the small GTPase ARF6. Together with the motor protein KIF13B, ADAP1 is also thought to mediate delivery of the second messenger phosphatidylinositol (3,4,5)-trisphosphate (PIP3) to the axon tip, thus contributing to PIP3 polarity. However, what defines the function of ADAP1 and how its different roles are coordinated are still not clear. Here, we studied ADAP1’s functions using in vitro reconstitutions. We found that KIF13B transports ADAP1 along microtubules, but that PIP3 as well as PI(3,4)P2 act as stop signals for this transport instead of being transported. We also demonstrate that these phosphoinositides activate ADAP1’s enzymatic activity to catalyze GTP hydrolysis by ARF6. Together, our results support a model for the cellular function of ADAP1, where KIF13B transports ADAP1 until it encounters high PIP3/PI(3,4)P2 concentrations in the plasma membrane. Here, ADAP1 disassociates from the motor to inactivate ARF6, promoting dendrite branching."}],"external_id":{"isi":["000607270100018"],"pmid":["33443153"]},"day":"05","citation":{"apa":"Düllberg, C. F., Auer, A., Canigova, N., Loibl, K., &#38; Loose, M. (2021). In vitro reconstitution reveals phosphoinositides as cargo-release factors and activators of the ARF6 GAP ADAP1. <i>Proceedings of the National Academy of Sciences of the United States of America</i>. National Academy of Sciences. <a href=\"https://doi.org/10.1073/pnas.2010054118\">https://doi.org/10.1073/pnas.2010054118</a>","ieee":"C. F. Düllberg, A. Auer, N. Canigova, K. Loibl, and M. Loose, “In vitro reconstitution reveals phosphoinositides as cargo-release factors and activators of the ARF6 GAP ADAP1,” <i>Proceedings of the National Academy of Sciences of the United States of America</i>, vol. 118, no. 1. National Academy of Sciences, 2021.","short":"C.F. Düllberg, A. Auer, N. Canigova, K. Loibl, M. Loose, Proceedings of the National Academy of Sciences of the United States of America 118 (2021).","mla":"Düllberg, Christian F., et al. “In Vitro Reconstitution Reveals Phosphoinositides as Cargo-Release Factors and Activators of the ARF6 GAP ADAP1.” <i>Proceedings of the National Academy of Sciences of the United States of America</i>, vol. 118, no. 1, e2010054118, National Academy of Sciences, 2021, doi:<a href=\"https://doi.org/10.1073/pnas.2010054118\">10.1073/pnas.2010054118</a>.","chicago":"Düllberg, Christian F, Albert Auer, Nikola Canigova, Katrin Loibl, and Martin Loose. “In Vitro Reconstitution Reveals Phosphoinositides as Cargo-Release Factors and Activators of the ARF6 GAP ADAP1.” <i>Proceedings of the National Academy of Sciences of the United States of America</i>. National Academy of Sciences, 2021. <a href=\"https://doi.org/10.1073/pnas.2010054118\">https://doi.org/10.1073/pnas.2010054118</a>.","ista":"Düllberg CF, Auer A, Canigova N, Loibl K, Loose M. 2021. In vitro reconstitution reveals phosphoinositides as cargo-release factors and activators of the ARF6 GAP ADAP1. Proceedings of the National Academy of Sciences of the United States of America. 118(1), e2010054118.","ama":"Düllberg CF, Auer A, Canigova N, Loibl K, Loose M. In vitro reconstitution reveals phosphoinositides as cargo-release factors and activators of the ARF6 GAP ADAP1. <i>Proceedings of the National Academy of Sciences of the United States of America</i>. 2021;118(1). doi:<a href=\"https://doi.org/10.1073/pnas.2010054118\">10.1073/pnas.2010054118</a>"}},{"pmid":1,"article_processing_charge":"No","publisher":"National Academy of Sciences","author":[{"first_name":"Jamie","full_name":"Rickman, Jamie","last_name":"Rickman"},{"full_name":"Düllberg, Christian F","last_name":"Düllberg","first_name":"Christian F","id":"459064DC-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6335-9748"},{"last_name":"Cade","full_name":"Cade, Nicholas","first_name":"Nicholas"},{"first_name":"Lewis","full_name":"Griffin, Lewis","last_name":"Griffin"},{"first_name":"Thomas","full_name":"Surrey, Thomas","last_name":"Surrey"}],"volume":114,"department":[{"_id":"MaLo"}],"month":"03","doi":"10.1073/pnas.1620274114","oa":1,"acknowledgement":"We thank Philippe Cluzel for helpful discussions and Gunnar Pruessner for data analysis advice. This work was supported by the Francis Crick Institute, which receives its core funding from Cancer Research UK Grant FC001163, Medical Research Council Grant FC001163, and Wellcome Trust Grant FC001163. This work was also supported by European Research Council Advanced Grant Project 323042 (to C.D. and T.S.).","title":"Steady state EB cap size fluctuations are determined by stochastic microtubule growth and maturation","date_created":"2018-12-11T11:47:46Z","oa_version":"Submitted Version","publication_identifier":{"issn":["0027-8424"]},"publication_status":"published","publist_id":"7073","issue":"13","scopus_import":"1","status":"public","page":"3427 - 3432","publication":"PNAS","date_updated":"2025-09-11T07:08:20Z","isi":1,"date_published":"2017-03-28T00:00:00Z","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5380103/"}],"intvolume":"       114","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","year":"2017","day":"28","citation":{"apa":"Rickman, J., Düllberg, C. F., Cade, N., Griffin, L., &#38; Surrey, T. (2017). Steady state EB cap size fluctuations are determined by stochastic microtubule growth and maturation. <i>PNAS</i>. National Academy of Sciences. <a href=\"https://doi.org/10.1073/pnas.1620274114\">https://doi.org/10.1073/pnas.1620274114</a>","short":"J. Rickman, C.F. Düllberg, N. Cade, L. Griffin, T. Surrey, PNAS 114 (2017) 3427–3432.","ieee":"J. Rickman, C. F. Düllberg, N. Cade, L. Griffin, and T. Surrey, “Steady state EB cap size fluctuations are determined by stochastic microtubule growth and maturation,” <i>PNAS</i>, vol. 114, no. 13. National Academy of Sciences, pp. 3427–3432, 2017.","mla":"Rickman, Jamie, et al. “Steady State EB Cap Size Fluctuations Are Determined by Stochastic Microtubule Growth and Maturation.” <i>PNAS</i>, vol. 114, no. 13, National Academy of Sciences, 2017, pp. 3427–32, doi:<a href=\"https://doi.org/10.1073/pnas.1620274114\">10.1073/pnas.1620274114</a>.","chicago":"Rickman, Jamie, Christian F Düllberg, Nicholas Cade, Lewis Griffin, and Thomas Surrey. “Steady State EB Cap Size Fluctuations Are Determined by Stochastic Microtubule Growth and Maturation.” <i>PNAS</i>. National Academy of Sciences, 2017. <a href=\"https://doi.org/10.1073/pnas.1620274114\">https://doi.org/10.1073/pnas.1620274114</a>.","ista":"Rickman J, Düllberg CF, Cade N, Griffin L, Surrey T. 2017. Steady state EB cap size fluctuations are determined by stochastic microtubule growth and maturation. PNAS. 114(13), 3427–3432.","ama":"Rickman J, Düllberg CF, Cade N, Griffin L, Surrey T. Steady state EB cap size fluctuations are determined by stochastic microtubule growth and maturation. <i>PNAS</i>. 2017;114(13):3427-3432. doi:<a href=\"https://doi.org/10.1073/pnas.1620274114\">10.1073/pnas.1620274114</a>"},"external_id":{"isi":["000397607300065"],"pmid":["28280102"]},"_id":"660","abstract":[{"text":"Growing microtubules are protected from depolymerization by the presence of a GTP or GDP/Pi cap. End-binding proteins of the EB1 family bind to the stabilizing cap, allowing monitoring of its size in real time. The cap size has been shown to correlate with instantaneous microtubule stability. Here we have quantitatively characterized the properties of cap size fluctuations during steadystate growth and have developed a theory predicting their timescale and amplitude from the kinetics of microtubule growth and cap maturation. In contrast to growth speed fluctuations, cap size fluctuations show a characteristic timescale, which is defined by the lifetime of the cap sites. Growth fluctuations affect the amplitude of cap size fluctuations; however, cap size does not affect growth speed, indicating that microtubules are far from instability during most of their time of growth. Our theory provides the basis for a quantitative understanding of microtubule stability fluctuations during steady-state growth.","lang":"eng"}],"language":[{"iso":"eng"}],"quality_controlled":"1","type":"journal_article"},{"page":"2055 - 2067","status":"public","scopus_import":"1","issue":"9","file_date_updated":"2020-07-14T12:46:31Z","publication":"Biophysical Journal","date_updated":"2025-08-05T14:08:52Z","year":"2017","ddc":["570"],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","intvolume":"       113","date_published":"2017-11-07T00:00:00Z","OA_place":"publisher","type":"journal_article","quality_controlled":"1","_id":"453","abstract":[{"lang":"eng","text":"Most kinesin motors move in only one direction along microtubules. Members of the kinesin-5 subfamily were initially described as unidirectional plus-end-directed motors and shown to produce piconewton forces. However, some fungal kinesin-5 motors are bidirectional. The force production of a bidirectional kinesin-5 has not yet been measured. Therefore, it remains unknown whether the mechanism of the unconventional minus-end-directed motility differs fundamentally from that of plus-end-directed stepping. Using force spectroscopy, we have measured here the forces that ensembles of purified budding yeast kinesin-5 Cin8 produce in microtubule gliding assays in both plus- and minus-end direction. Correlation analysis of pause forces demonstrated that individual Cin8 molecules produce additive forces in both directions of movement. In ensembles, Cin8 motors were able to produce single-motor forces up to a magnitude of ∼1.5 pN. Hence, these properties appear to be conserved within the kinesin-5 subfamily. Force production was largely independent of the directionality of movement, indicating similarities between the motility mechanisms for both directions. These results provide constraints for the development of models for the bidirectional motility mechanism of fission yeast kinesin-5 and provide insight into the function of this mitotic motor."}],"language":[{"iso":"eng"}],"external_id":{"pmid":["29117528"]},"has_accepted_license":"1","day":"07","citation":{"chicago":"Fallesen, Todd, Johanna Roostalu, Christian F Düllberg, Gunnar Pruessner, and Thomas Surrey. “Ensembles of Bidirectional Kinesin Cin8 Produce Additive Forces in Both Directions of Movement.” <i>Biophysical Journal</i>. Biophysical Society, 2017. <a href=\"https://doi.org/10.1016/j.bpj.2017.09.006\">https://doi.org/10.1016/j.bpj.2017.09.006</a>.","ama":"Fallesen T, Roostalu J, Düllberg CF, Pruessner G, Surrey T. Ensembles of bidirectional kinesin Cin8 produce additive forces in both directions of movement. <i>Biophysical Journal</i>. 2017;113(9):2055-2067. doi:<a href=\"https://doi.org/10.1016/j.bpj.2017.09.006\">10.1016/j.bpj.2017.09.006</a>","ista":"Fallesen T, Roostalu J, Düllberg CF, Pruessner G, Surrey T. 2017. Ensembles of bidirectional kinesin Cin8 produce additive forces in both directions of movement. Biophysical Journal. 113(9), 2055–2067.","apa":"Fallesen, T., Roostalu, J., Düllberg, C. F., Pruessner, G., &#38; Surrey, T. (2017). Ensembles of bidirectional kinesin Cin8 produce additive forces in both directions of movement. <i>Biophysical Journal</i>. Biophysical Society. <a href=\"https://doi.org/10.1016/j.bpj.2017.09.006\">https://doi.org/10.1016/j.bpj.2017.09.006</a>","mla":"Fallesen, Todd, et al. “Ensembles of Bidirectional Kinesin Cin8 Produce Additive Forces in Both Directions of Movement.” <i>Biophysical Journal</i>, vol. 113, no. 9, Biophysical Society, 2017, pp. 2055–67, doi:<a href=\"https://doi.org/10.1016/j.bpj.2017.09.006\">10.1016/j.bpj.2017.09.006</a>.","short":"T. Fallesen, J. Roostalu, C.F. Düllberg, G. Pruessner, T. Surrey, Biophysical Journal 113 (2017) 2055–2067.","ieee":"T. Fallesen, J. Roostalu, C. F. Düllberg, G. Pruessner, and T. Surrey, “Ensembles of bidirectional kinesin Cin8 produce additive forces in both directions of movement,” <i>Biophysical Journal</i>, vol. 113, no. 9. Biophysical Society, pp. 2055–2067, 2017."},"publisher":"Biophysical Society","tmp":{"short":"CC BY (4.0)","image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"article_processing_charge":"No","pmid":1,"pubrep_id":"965","acknowledgement":"The plasmid for full-length kinesin-1 was a gift from G. Holzwarth and J. Macosko with permission from J. Howard. We thank I. Lueke and N. I. Cade for technical assistance. G.P. thanks the Francis Crick Institute, and in particular the Surrey and Salbreux groups, for their hospitality during his sabbatical stay, as well as Imperial College London for making it possible. This work was supported by the Francis Crick Institute, which receives its core funding from Cancer Research UK (FC001163), the United Kingdom Medical Research Council (FC001163), and the Wellcome Trust (FC001163), and by Imperial College London. J.R. was also supported by a Sir Henry Wellcome Postdoctoral Fellowship (100145/Z/12/Z) and T.S. by the European Research Council (Advanced Grant, project 323042). ","oa":1,"doi":"10.1016/j.bpj.2017.09.006","article_type":"original","month":"11","department":[{"_id":"MaLo"}],"author":[{"first_name":"Todd","last_name":"Fallesen","full_name":"Fallesen, Todd"},{"first_name":"Johanna","full_name":"Roostalu, Johanna","last_name":"Roostalu"},{"full_name":"Düllberg, Christian F","last_name":"Düllberg","orcid":"0000-0001-6335-9748","first_name":"Christian F","id":"459064DC-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Gunnar","last_name":"Pruessner","full_name":"Pruessner, Gunnar"},{"full_name":"Surrey, Thomas","last_name":"Surrey","first_name":"Thomas"}],"volume":113,"publication_identifier":{"issn":["0006-3495"],"eissn":["1542-0086"]},"oa_version":"Published Version","OA_type":"hybrid","date_created":"2018-12-11T11:46:33Z","title":"Ensembles of bidirectional kinesin Cin8 produce additive forces in both directions of movement","publist_id":"7369","publication_status":"published","file":[{"checksum":"99a2474088e20ac74b1882c4fbbb45b1","file_name":"IST-2018-965-v1+1_2017_Duellberg_Ensembles_of.pdf","relation":"main_file","creator":"system","date_updated":"2020-07-14T12:46:31Z","file_id":"5052","access_level":"open_access","content_type":"application/pdf","date_created":"2018-12-12T10:14:03Z","file_size":977192}]},{"date_published":"2017-06-28T00:00:00Z","article_number":"176","intvolume":"        11","year":"2017","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","ddc":["570"],"has_accepted_license":"1","day":"28","citation":{"chicago":"Hansen, Andi H, Christian F Düllberg, Christine Mieck, Martin Loose, and Simon Hippenmeyer. “Cell Polarity in Cerebral Cortex Development - Cellular Architecture Shaped by Biochemical Networks.” <i>Frontiers in Cellular Neuroscience</i>. Frontiers Research Foundation, 2017. <a href=\"https://doi.org/10.3389/fncel.2017.00176\">https://doi.org/10.3389/fncel.2017.00176</a>.","ama":"Hansen AH, Düllberg CF, Mieck C, Loose M, Hippenmeyer S. Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks. <i>Frontiers in Cellular Neuroscience</i>. 2017;11. doi:<a href=\"https://doi.org/10.3389/fncel.2017.00176\">10.3389/fncel.2017.00176</a>","ista":"Hansen AH, Düllberg CF, Mieck C, Loose M, Hippenmeyer S. 2017. Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks. Frontiers in Cellular Neuroscience. 11, 176.","apa":"Hansen, A. H., Düllberg, C. F., Mieck, C., Loose, M., &#38; Hippenmeyer, S. (2017). Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks. <i>Frontiers in Cellular Neuroscience</i>. Frontiers Research Foundation. <a href=\"https://doi.org/10.3389/fncel.2017.00176\">https://doi.org/10.3389/fncel.2017.00176</a>","mla":"Hansen, Andi H., et al. “Cell Polarity in Cerebral Cortex Development - Cellular Architecture Shaped by Biochemical Networks.” <i>Frontiers in Cellular Neuroscience</i>, vol. 11, 176, Frontiers Research Foundation, 2017, doi:<a href=\"https://doi.org/10.3389/fncel.2017.00176\">10.3389/fncel.2017.00176</a>.","short":"A.H. Hansen, C.F. Düllberg, C. Mieck, M. Loose, S. Hippenmeyer, Frontiers in Cellular Neuroscience 11 (2017).","ieee":"A. H. Hansen, C. F. Düllberg, C. Mieck, M. Loose, and S. Hippenmeyer, “Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks,” <i>Frontiers in Cellular Neuroscience</i>, vol. 11. Frontiers Research Foundation, 2017."},"_id":"960","language":[{"iso":"eng"}],"abstract":[{"lang":"eng","text":"The human cerebral cortex is the seat of our cognitive abilities and composed of an extraordinary number of neurons, organized in six distinct layers. The establishment of specific morphological and physiological features in individual neurons needs to be regulated with high precision. Impairments in the sequential developmental programs instructing corticogenesis lead to alterations in the cortical cytoarchitecture which is thought to represent the major underlying cause for several neurological disorders including neurodevelopmental and psychiatric diseases. In this review we discuss the role of cell polarity at sequential stages during cortex development. We first provide an overview of morphological cell polarity features in cortical neural stem cells and newly-born postmitotic neurons. We then synthesize a conceptual molecular and biochemical framework how cell polarity is established at the cellular level through a break in symmetry in nascent cortical projection neurons. Lastly we provide a perspective how the molecular mechanisms applying to single cells could be probed and integrated in an in vivo and tissue-wide context."}],"external_id":{"isi":["000404486700001"]},"type":"journal_article","quality_controlled":"1","ec_funded":1,"scopus_import":"1","status":"public","publication":"Frontiers in Cellular Neuroscience","date_updated":"2026-04-27T22:30:40Z","isi":1,"file_date_updated":"2020-07-14T12:48:16Z","title":"Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks","date_created":"2018-12-11T11:49:25Z","oa_version":"Published Version","publication_identifier":{"issn":["1662-5102"]},"file":[{"access_level":"open_access","date_created":"2018-12-12T10:09:40Z","file_size":2153858,"content_type":"application/pdf","file_name":"IST-2017-830-v1+1_2017_Hansen_CellPolarity.pdf","checksum":"dc1f5a475b918d09a0f9f587400b1626","date_updated":"2020-07-14T12:48:16Z","file_id":"4764","relation":"main_file","creator":"system"}],"publist_id":"6445","publication_status":"published","related_material":{"record":[{"id":"9962","status":"public","relation":"dissertation_contains"}]},"tmp":{"short":"CC BY (4.0)","image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"article_processing_charge":"Yes","publisher":"Frontiers Research Foundation","author":[{"full_name":"Hansen, Andi H","last_name":"Hansen","id":"38853E16-F248-11E8-B48F-1D18A9856A87","first_name":"Andi H"},{"orcid":"0000-0001-6335-9748","first_name":"Christian F","id":"459064DC-F248-11E8-B48F-1D18A9856A87","full_name":"Düllberg, Christian F","last_name":"Düllberg"},{"last_name":"Mieck","full_name":"Mieck, Christine","orcid":"0000-0003-1919-7416","first_name":"Christine","id":"34CAE85C-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Loose","full_name":"Loose, Martin","first_name":"Martin","id":"462D4284-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-7309-9724"},{"first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer"}],"volume":11,"project":[{"grant_number":"618444","call_identifier":"FP7","_id":"25D61E48-B435-11E9-9278-68D0E5697425","name":"Molecular Mechanisms of Cerebral Cortex Development"},{"name":"Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal Level","_id":"25D7962E-B435-11E9-9278-68D0E5697425","grant_number":"RGP0053/2014"},{"name":"International IST Postdoc Fellowship Programme","grant_number":"291734","_id":"25681D80-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"},{"call_identifier":"FWF","_id":"25985A36-B435-11E9-9278-68D0E5697425","grant_number":"T00817-B21","name":"The biochemical basis of PAR polarization"}],"department":[{"_id":"SiHi"},{"_id":"MaLo"}],"month":"06","oa":1,"doi":"10.3389/fncel.2017.00176","pubrep_id":"830"},{"publisher":"Oxford University Press","status":"public","page":"3563 - 3573","article_processing_charge":"No","issue":"22","extern":"1","doi":"10.1091/mbc.E16-07-0548","month":"11","date_updated":"2021-01-12T06:48:34Z","publication":"Molecular Biology and Evolution","author":[{"full_name":"Düllberg, Christian F","last_name":"Düllberg","first_name":"Christian F","id":"459064DC-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6335-9748"},{"last_name":"Cade","full_name":"Cade, Nicholas","first_name":"Nicholas"},{"first_name":"Thomas","full_name":"Surrey, Thomas","last_name":"Surrey"}],"volume":27,"year":"2016","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","intvolume":"        27","oa_version":"None","date_published":"2016-11-07T00:00:00Z","title":"Microtubule aging probed by microfluidics assisted tubulin washout","date_created":"2018-12-11T11:50:21Z","type":"journal_article","publist_id":"6218","publication_status":"published","language":[{"iso":"eng"}],"_id":"1139","abstract":[{"lang":"eng","text":"Microtubules switch stochastically between phases of growth and shrinkage. The molecular mechanism responsible for the end of a growth phase, an event called catastrophe, is still not understood. The probability for a catastrophe to occur increases with microtubule age, putting constraints on the possible molecular mechanism of catastrophe induction. Here we used microfluidics-Assisted fast tubulin washout experiments to induce microtubule depolymerization in a controlled manner at different times after the start of growth. We found that aging can also be observed in this assay, providing valuable new constraints against which theoretical models of catastrophe induction can be tested. We found that the data can be quantitatively well explained by a simple kinetic threshold model that assumes an age-dependent broadening of the protective cap at the microtubule end as a result of an evolving tapered end structure; this leads to a decrease of the cap density and its stability. This analysis suggests an intuitive picture of the role of morphological changes of the protective cap for the age dependence of microtubule stability."}],"citation":{"apa":"Düllberg, C. F., Cade, N., &#38; Surrey, T. (2016). Microtubule aging probed by microfluidics assisted tubulin washout. <i>Molecular Biology and Evolution</i>. Oxford University Press. <a href=\"https://doi.org/10.1091/mbc.E16-07-0548\">https://doi.org/10.1091/mbc.E16-07-0548</a>","mla":"Düllberg, Christian F., et al. “Microtubule Aging Probed by Microfluidics Assisted Tubulin Washout.” <i>Molecular Biology and Evolution</i>, vol. 27, no. 22, Oxford University Press, 2016, pp. 3563–73, doi:<a href=\"https://doi.org/10.1091/mbc.E16-07-0548\">10.1091/mbc.E16-07-0548</a>.","ieee":"C. F. Düllberg, N. Cade, and T. Surrey, “Microtubule aging probed by microfluidics assisted tubulin washout,” <i>Molecular Biology and Evolution</i>, vol. 27, no. 22. Oxford University Press, pp. 3563–3573, 2016.","short":"C.F. Düllberg, N. Cade, T. Surrey, Molecular Biology and Evolution 27 (2016) 3563–3573.","chicago":"Düllberg, Christian F, Nicholas Cade, and Thomas Surrey. “Microtubule Aging Probed by Microfluidics Assisted Tubulin Washout.” <i>Molecular Biology and Evolution</i>. Oxford University Press, 2016. <a href=\"https://doi.org/10.1091/mbc.E16-07-0548\">https://doi.org/10.1091/mbc.E16-07-0548</a>.","ama":"Düllberg CF, Cade N, Surrey T. Microtubule aging probed by microfluidics assisted tubulin washout. <i>Molecular Biology and Evolution</i>. 2016;27(22):3563-3573. doi:<a href=\"https://doi.org/10.1091/mbc.E16-07-0548\">10.1091/mbc.E16-07-0548</a>","ista":"Düllberg CF, Cade N, Surrey T. 2016. Microtubule aging probed by microfluidics assisted tubulin washout. Molecular Biology and Evolution. 27(22), 3563–3573."},"day":"07"}]