[{"publication":"Nano Letters","day":"08","year":"2020","isi":1,"date_created":"2019-12-10T15:36:05Z","doi":"10.1021/acs.nanolett.9b04445","date_published":"2020-01-08T00:00:00Z","page":"669-676","oa":1,"quality_controlled":"1","publisher":"American Chemical Society","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"apa":"Ucar, M. C., & Lipowsky, R. (2020). Collective force generation by molecular motors is determined by strain-induced unbinding. Nano Letters. American Chemical Society. https://doi.org/10.1021/acs.nanolett.9b04445","ama":"Ucar MC, Lipowsky R. Collective force generation by molecular motors is determined by strain-induced unbinding. Nano Letters. 2020;20(1):669-676. doi:10.1021/acs.nanolett.9b04445","ieee":"M. C. Ucar and R. Lipowsky, “Collective force generation by molecular motors is determined by strain-induced unbinding,” Nano Letters, vol. 20, no. 1. American Chemical Society, pp. 669–676, 2020.","short":"M.C. Ucar, R. Lipowsky, Nano Letters 20 (2020) 669–676.","mla":"Ucar, Mehmet C., and Reinhard Lipowsky. “Collective Force Generation by Molecular Motors Is Determined by Strain-Induced Unbinding.” Nano Letters, vol. 20, no. 1, American Chemical Society, 2020, pp. 669–76, doi:10.1021/acs.nanolett.9b04445.","ista":"Ucar MC, Lipowsky R. 2020. Collective force generation by molecular motors is determined by strain-induced unbinding. Nano Letters. 20(1), 669–676.","chicago":"Ucar, Mehmet C, and Reinhard Lipowsky. “Collective Force Generation by Molecular Motors Is Determined by Strain-Induced Unbinding.” Nano Letters. American Chemical Society, 2020. https://doi.org/10.1021/acs.nanolett.9b04445."},"title":"Collective force generation by molecular motors is determined by strain-induced unbinding","article_processing_charge":"No","external_id":{"pmid":["31797672"],"isi":["000507151600087"]},"author":[{"full_name":"Ucar, Mehmet C","orcid":"0000-0003-0506-4217","last_name":"Ucar","first_name":"Mehmet C","id":"50B2A802-6007-11E9-A42B-EB23E6697425"},{"full_name":"Lipowsky, Reinhard","last_name":"Lipowsky","first_name":"Reinhard"}],"language":[{"iso":"eng"}],"publication_status":"published","publication_identifier":{"eissn":["1530-6992"],"issn":["1530-6984"]},"volume":20,"issue":"1","related_material":{"record":[{"id":"9726","status":"public","relation":"research_data"},{"relation":"research_data","status":"public","id":"9885"}]},"oa_version":"Published Version","pmid":1,"abstract":[{"lang":"eng","text":"In the living cell, we encounter a large variety of motile processes such as organelle transport and cytoskeleton remodeling. These processes are driven by motor proteins that generate force by transducing chemical free energy into mechanical work. In many cases, the molecular motors work in teams to collectively generate larger forces. Recent optical trapping experiments on small teams of cytoskeletal motors indicated that the collectively generated force increases with the size of the motor team but that this increase depends on the motor type and on whether the motors are studied in vitro or in vivo. Here, we use the theory of stochastic processes to describe the motion of N motors in a stationary optical trap and to compute the N-dependence of the collectively generated forces. We consider six distinct motor types, two kinesins, two dyneins, and two myosins. We show that the force increases always linearly with N but with a prefactor that depends on the performance of the single motor. Surprisingly, this prefactor increases for weaker motors with a lower stall force. This counter-intuitive behavior reflects the increased probability with which stronger motors detach from the filament during strain generation. Our theoretical results are in quantitative agreement with experimental data on small teams of kinesin-1 motors."}],"intvolume":" 20","month":"01","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1021/acs.nanolett.9b04445"}],"scopus_import":"1","date_updated":"2023-08-17T14:07:52Z","department":[{"_id":"EdHa"}],"_id":"7166","status":"public","type":"journal_article","article_type":"letter_note"},{"issue":"2","volume":98,"publication_status":"published","publication_identifier":{"issn":["08189641"],"eissn":["14401711"]},"language":[{"iso":"eng"}],"file":[{"file_size":8569945,"date_updated":"2020-11-19T11:22:33Z","creator":"dernst","file_name":"2020_ImmunologyCellBio_Obeidy.pdf","date_created":"2020-11-19T11:22:33Z","content_type":"application/pdf","relation":"main_file","access_level":"open_access","success":1,"file_id":"8775","checksum":"c389477b4b52172ef76afff8a06c6775"}],"scopus_import":"1","intvolume":" 98","month":"02","abstract":[{"lang":"eng","text":"T lymphocytes utilize amoeboid migration to navigate effectively within complex microenvironments. The precise rearrangement of the actin cytoskeleton required for cellular forward propulsion is mediated by actin regulators, including the actin‐related protein 2/3 (Arp2/3) complex, a macromolecular machine that nucleates branched actin filaments at the leading edge. The consequences of modulating Arp2/3 activity on the biophysical properties of the actomyosin cortex and downstream T cell function are incompletely understood. We report that even a moderate decrease of Arp3 levels in T cells profoundly affects actin cortex integrity. Reduction in total F‐actin content leads to reduced cortical tension and disrupted lamellipodia formation. Instead, in Arp3‐knockdown cells, the motility mode is dominated by blebbing migration characterized by transient, balloon‐like protrusions at the leading edge. Although this migration mode seems to be compatible with interstitial migration in three‐dimensional environments, diminished locomotion kinetics and impaired cytotoxicity interfere with optimal T cell function. These findings define the importance of finely tuned, Arp2/3‐dependent mechanophysical membrane integrity in cytotoxic effector T lymphocyte activities."}],"oa_version":"Published Version","pmid":1,"department":[{"_id":"MiSi"}],"file_date_updated":"2020-11-19T11:22:33Z","date_updated":"2023-08-17T14:21:12Z","ddc":["570"],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","article_type":"original","status":"public","_id":"7234","page":"93-113","date_created":"2020-01-05T23:00:48Z","date_published":"2020-02-01T00:00:00Z","doi":"10.1111/imcb.12304","year":"2020","isi":1,"has_accepted_license":"1","publication":"Immunology and Cell Biology","day":"01","oa":1,"quality_controlled":"1","publisher":"Wiley","external_id":{"pmid":["31698518"],"isi":["000503885600001"]},"article_processing_charge":"No","author":[{"first_name":"Peyman","last_name":"Obeidy","full_name":"Obeidy, Peyman"},{"first_name":"Lining A.","full_name":"Ju, Lining A.","last_name":"Ju"},{"full_name":"Oehlers, Stefan H.","last_name":"Oehlers","first_name":"Stefan H."},{"full_name":"Zulkhernain, Nursafwana S.","last_name":"Zulkhernain","first_name":"Nursafwana S."},{"first_name":"Quintin","last_name":"Lee","full_name":"Lee, Quintin"},{"first_name":"Jorge L.","full_name":"Galeano Niño, Jorge L.","last_name":"Galeano Niño"},{"full_name":"Kwan, Rain Y.Q.","last_name":"Kwan","first_name":"Rain Y.Q."},{"last_name":"Tikoo","full_name":"Tikoo, Shweta","first_name":"Shweta"},{"last_name":"Cavanagh","full_name":"Cavanagh, Lois L.","first_name":"Lois L."},{"first_name":"Paulus","last_name":"Mrass","full_name":"Mrass, Paulus"},{"first_name":"Adam J.L.","last_name":"Cook","full_name":"Cook, Adam J.L."},{"full_name":"Jackson, Shaun P.","last_name":"Jackson","first_name":"Shaun P."},{"last_name":"Biro","full_name":"Biro, Maté","first_name":"Maté"},{"first_name":"Ben","full_name":"Roediger, Ben","last_name":"Roediger"},{"full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"},{"last_name":"Weninger","full_name":"Weninger, Wolfgang","first_name":"Wolfgang"}],"title":"Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes","citation":{"mla":"Obeidy, Peyman, et al. “Partial Loss of Actin Nucleator Actin-Related Protein 2/3 Activity Triggers Blebbing in Primary T Lymphocytes.” Immunology and Cell Biology, vol. 98, no. 2, Wiley, 2020, pp. 93–113, doi:10.1111/imcb.12304.","ama":"Obeidy P, Ju LA, Oehlers SH, et al. Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes. Immunology and Cell Biology. 2020;98(2):93-113. doi:10.1111/imcb.12304","apa":"Obeidy, P., Ju, L. A., Oehlers, S. H., Zulkhernain, N. S., Lee, Q., Galeano Niño, J. L., … Weninger, W. (2020). Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes. Immunology and Cell Biology. Wiley. https://doi.org/10.1111/imcb.12304","ieee":"P. Obeidy et al., “Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes,” Immunology and Cell Biology, vol. 98, no. 2. Wiley, pp. 93–113, 2020.","short":"P. Obeidy, L.A. Ju, S.H. Oehlers, N.S. Zulkhernain, Q. Lee, J.L. Galeano Niño, R.Y.Q. Kwan, S. Tikoo, L.L. Cavanagh, P. Mrass, A.J.L. Cook, S.P. Jackson, M. Biro, B. Roediger, M.K. Sixt, W. Weninger, Immunology and Cell Biology 98 (2020) 93–113.","chicago":"Obeidy, Peyman, Lining A. Ju, Stefan H. Oehlers, Nursafwana S. Zulkhernain, Quintin Lee, Jorge L. Galeano Niño, Rain Y.Q. Kwan, et al. “Partial Loss of Actin Nucleator Actin-Related Protein 2/3 Activity Triggers Blebbing in Primary T Lymphocytes.” Immunology and Cell Biology. Wiley, 2020. https://doi.org/10.1111/imcb.12304.","ista":"Obeidy P, Ju LA, Oehlers SH, Zulkhernain NS, Lee Q, Galeano Niño JL, Kwan RYQ, Tikoo S, Cavanagh LL, Mrass P, Cook AJL, Jackson SP, Biro M, Roediger B, Sixt MK, Weninger W. 2020. Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes. Immunology and Cell Biology. 98(2), 93–113."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8"},{"oa":1,"publisher":"Springer Nature","quality_controlled":"1","year":"2020","has_accepted_license":"1","isi":1,"publication":"Nature Communications","day":"10","date_created":"2020-01-11T10:42:48Z","doi":"10.1038/s41467-019-14077-2","date_published":"2020-01-10T00:00:00Z","article_number":"195","project":[{"_id":"268F8446-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","grant_number":"T0101031","name":"Role of Eed in neural stem cell lineage progression"},{"grant_number":"M02416","name":"Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex","call_identifier":"FWF","_id":"264E56E2-B435-11E9-9278-68D0E5697425"},{"_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","grant_number":"725780","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"},{"grant_number":"LS13-002","name":"Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain","_id":"25D92700-B435-11E9-9278-68D0E5697425"}],"citation":{"chicago":"Laukoter, Susanne, Robert J Beattie, Florian Pauler, Nicole Amberg, Keiichi I. Nakayama, and Simon Hippenmeyer. “Imprinted Cdkn1c Genomic Locus Cell-Autonomously Promotes Cell Survival in Cerebral Cortex Development.” Nature Communications. Springer Nature, 2020. https://doi.org/10.1038/s41467-019-14077-2.","ista":"Laukoter S, Beattie RJ, Pauler F, Amberg N, Nakayama KI, Hippenmeyer S. 2020. Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development. Nature Communications. 11, 195.","mla":"Laukoter, Susanne, et al. “Imprinted Cdkn1c Genomic Locus Cell-Autonomously Promotes Cell Survival in Cerebral Cortex Development.” Nature Communications, vol. 11, 195, Springer Nature, 2020, doi:10.1038/s41467-019-14077-2.","ieee":"S. Laukoter, R. J. Beattie, F. Pauler, N. Amberg, K. I. Nakayama, and S. Hippenmeyer, “Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development,” Nature Communications, vol. 11. Springer Nature, 2020.","short":"S. Laukoter, R.J. Beattie, F. Pauler, N. Amberg, K.I. Nakayama, S. Hippenmeyer, Nature Communications 11 (2020).","apa":"Laukoter, S., Beattie, R. J., Pauler, F., Amberg, N., Nakayama, K. I., & Hippenmeyer, S. (2020). Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-019-14077-2","ama":"Laukoter S, Beattie RJ, Pauler F, Amberg N, Nakayama KI, Hippenmeyer S. Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development. Nature Communications. 2020;11. doi:10.1038/s41467-019-14077-2"},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","external_id":{"isi":["000551459000005"]},"article_processing_charge":"No","author":[{"last_name":"Laukoter","full_name":"Laukoter, Susanne","orcid":"0000-0002-7903-3010","id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87","first_name":"Susanne"},{"first_name":"Robert J","id":"2E26DF60-F248-11E8-B48F-1D18A9856A87","full_name":"Beattie, Robert J","orcid":"0000-0002-8483-8753","last_name":"Beattie"},{"id":"48EA0138-F248-11E8-B48F-1D18A9856A87","first_name":"Florian","last_name":"Pauler","full_name":"Pauler, Florian","orcid":"0000-0002-7462-0048"},{"orcid":"0000-0002-3183-8207","full_name":"Amberg, Nicole","last_name":"Amberg","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87","first_name":"Nicole"},{"full_name":"Nakayama, Keiichi I.","last_name":"Nakayama","first_name":"Keiichi I."},{"full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon"}],"title":"Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development","abstract":[{"text":"The cyclin-dependent kinase inhibitor p57KIP2 is encoded by the imprinted Cdkn1c locus, exhibits maternal expression, and is essential for cerebral cortex development. How Cdkn1c regulates corticogenesis is however not clear. To this end we employ Mosaic Analysis with Double Markers (MADM) technology to genetically dissect Cdkn1c gene function in corticogenesis at single cell resolution. We find that the previously described growth-inhibitory Cdkn1c function is a non-cell-autonomous one, acting on the whole organism. In contrast we reveal a growth-promoting cell-autonomous Cdkn1c function which at the mechanistic level mediates radial glial progenitor cell and nascent projection neuron survival. Strikingly, the growth-promoting function of Cdkn1c is highly dosage sensitive but not subject to genomic imprinting. Collectively, our results suggest that the Cdkn1c locus regulates cortical development through distinct cell-autonomous and non-cell-autonomous mechanisms. More generally, our study highlights the importance to probe the relative contributions of cell intrinsic gene function and tissue-wide mechanisms to the overall phenotype.","lang":"eng"}],"acknowledged_ssus":[{"_id":"PreCl"}],"oa_version":"Published Version","scopus_import":"1","intvolume":" 11","month":"01","publication_status":"published","publication_identifier":{"issn":["2041-1723"]},"language":[{"iso":"eng"}],"file":[{"file_size":8063333,"date_updated":"2020-07-14T12:47:54Z","creator":"dernst","file_name":"2020_NatureComm_Laukoter.pdf","date_created":"2020-01-13T07:42:31Z","content_type":"application/pdf","relation":"main_file","access_level":"open_access","file_id":"7261","checksum":"ebf1ed522f4e0be8d94c939c1806a709"}],"ec_funded":1,"volume":11,"related_material":{"link":[{"description":"News on IST Homepage","relation":"press_release","url":"https://ist.ac.at/en/news/new-function-for-potential-tumour-suppressor-in-brain-development/"}]},"_id":"7253","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"article_type":"original","type":"journal_article","status":"public","date_updated":"2023-08-17T14:23:41Z","ddc":["570"],"department":[{"_id":"SiHi"}],"file_date_updated":"2020-07-14T12:47:54Z"},{"article_processing_charge":"No","external_id":{"isi":["000505167600013"],"pmid":["31767677"]},"author":[{"last_name":"Piriya Ananda Babu","full_name":"Piriya Ananda Babu, Lashmi","first_name":"Lashmi"},{"full_name":"Wang, Han Ying","last_name":"Wang","first_name":"Han Ying"},{"id":"2B7846DC-F248-11E8-B48F-1D18A9856A87","first_name":"Kohgaku","full_name":"Eguchi, Kohgaku","orcid":"0000-0002-6170-2546","last_name":"Eguchi"},{"first_name":"Laurent","full_name":"Guillaud, Laurent","last_name":"Guillaud"},{"first_name":"Tomoyuki","full_name":"Takahashi, Tomoyuki","last_name":"Takahashi"}],"title":"Microtubule and actin differentially regulate synaptic vesicle cycling to maintain high-frequency neurotransmission","citation":{"ieee":"L. Piriya Ananda Babu, H. Y. Wang, K. Eguchi, L. Guillaud, and T. Takahashi, “Microtubule and actin differentially regulate synaptic vesicle cycling to maintain high-frequency neurotransmission,” Journal of neuroscience, vol. 40, no. 1. Society for Neuroscience, pp. 131–142, 2020.","short":"L. Piriya Ananda Babu, H.Y. Wang, K. Eguchi, L. Guillaud, T. Takahashi, Journal of Neuroscience 40 (2020) 131–142.","apa":"Piriya Ananda Babu, L., Wang, H. Y., Eguchi, K., Guillaud, L., & Takahashi, T. (2020). Microtubule and actin differentially regulate synaptic vesicle cycling to maintain high-frequency neurotransmission. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.1571-19.2019","ama":"Piriya Ananda Babu L, Wang HY, Eguchi K, Guillaud L, Takahashi T. Microtubule and actin differentially regulate synaptic vesicle cycling to maintain high-frequency neurotransmission. Journal of neuroscience. 2020;40(1):131-142. doi:10.1523/JNEUROSCI.1571-19.2019","mla":"Piriya Ananda Babu, Lashmi, et al. “Microtubule and Actin Differentially Regulate Synaptic Vesicle Cycling to Maintain High-Frequency Neurotransmission.” Journal of Neuroscience, vol. 40, no. 1, Society for Neuroscience, 2020, pp. 131–42, doi:10.1523/JNEUROSCI.1571-19.2019.","ista":"Piriya Ananda Babu L, Wang HY, Eguchi K, Guillaud L, Takahashi T. 2020. Microtubule and actin differentially regulate synaptic vesicle cycling to maintain high-frequency neurotransmission. Journal of neuroscience. 40(1), 131–142.","chicago":"Piriya Ananda Babu, Lashmi, Han Ying Wang, Kohgaku Eguchi, Laurent Guillaud, and Tomoyuki Takahashi. “Microtubule and Actin Differentially Regulate Synaptic Vesicle Cycling to Maintain High-Frequency Neurotransmission.” Journal of Neuroscience. Society for Neuroscience, 2020. https://doi.org/10.1523/JNEUROSCI.1571-19.2019."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","oa":1,"quality_controlled":"1","publisher":"Society for Neuroscience","page":"131-142","date_created":"2020-01-19T23:00:38Z","doi":"10.1523/JNEUROSCI.1571-19.2019","date_published":"2020-01-02T00:00:00Z","year":"2020","isi":1,"has_accepted_license":"1","publication":"Journal of neuroscience","day":"02","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"article_type":"original","type":"journal_article","status":"public","_id":"7339","department":[{"_id":"RySh"}],"file_date_updated":"2020-07-14T12:47:56Z","date_updated":"2023-08-17T14:25:23Z","ddc":["570"],"scopus_import":"1","intvolume":" 40","month":"01","abstract":[{"text":"Cytoskeletal filaments such as microtubules (MTs) and filamentous actin (F-actin) dynamically support cell structure and functions. In central presynaptic terminals, F-actin is expressed along the release edge and reportedly plays diverse functional roles, but whether axonal MTs extend deep into terminals and play any physiological role remains controversial. At the calyx of Held in rats of either sex, confocal and high-resolution microscopy revealed that MTs enter deep into presynaptic terminal swellings and partially colocalize with a subset of synaptic vesicles (SVs). Electrophysiological analysis demonstrated that depolymerization of MTs specifically prolonged the slow-recovery time component of EPSCs from short-term depression induced by a train of high-frequency stimulation, whereas depolymerization of F-actin specifically prolonged the fast-recovery component. In simultaneous presynaptic and postsynaptic action potential recordings, depolymerization of MTs or F-actin significantly impaired the fidelity of high-frequency neurotransmission. We conclude that MTs and F-actin differentially contribute to slow and fast SV replenishment, thereby maintaining high-frequency neurotransmission.","lang":"eng"}],"oa_version":"Published Version","pmid":1,"volume":40,"issue":"1","publication_status":"published","publication_identifier":{"eissn":["15292401"]},"language":[{"iso":"eng"}],"file":[{"checksum":"92f5e8a47f454fc131fb94cd7f106e60","file_id":"7345","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_name":"2020_JourNeuroscience_Piriya.pdf","date_created":"2020-01-20T14:44:10Z","creator":"dernst","file_size":4460781,"date_updated":"2020-07-14T12:47:56Z"}]},{"month":"01","intvolume":" 10","scopus_import":"1","oa_version":"Published Version","abstract":[{"lang":"eng","text":"The ability to sense environmental temperature and to coordinate growth and development accordingly, is critical to the reproductive success of plants. Flowering time is regulated at the level of gene expression by a complex network of factors that integrate environmental and developmental cues. One of the main players, involved in modulating flowering time in response to changes in ambient temperature is FLOWERING LOCUS M (FLM). FLM transcripts can undergo extensive alternative splicing producing multiple variants, of which FLM-β and FLM-δ are the most representative. While FLM-β codes for the flowering repressor FLM protein, translation of FLM-δ has the opposite effect on flowering. Here we show that the cyclin-dependent kinase G2 (CDKG2), together with its cognate cyclin, CYCLYN L1 (CYCL1) affects the alternative splicing of FLM, balancing the levels of FLM-β and FLM-δ across the ambient temperature range. In the absence of the CDKG2/CYCL1 complex, FLM-β expression is reduced while FLM-δ is increased in a temperature dependent manner and these changes are associated with an early flowering phenotype in the cdkg2 mutant lines. In addition, we found that transcript variants retaining the full FLM intron 1 are sequestered in the cell nucleus. Strikingly, FLM intron 1 splicing is also regulated by CDKG2/CYCL1. Our results provide evidence that temperature and CDKs regulate the alternative splicing of FLM, contributing to flowering time definition."}],"volume":10,"file":[{"access_level":"open_access","relation":"main_file","content_type":"application/pdf","file_id":"7366","checksum":"d1f92e60a713fbd15097ce895e5c7ccb","creator":"dernst","date_updated":"2020-07-14T12:47:56Z","file_size":1951438,"date_created":"2020-01-27T09:07:02Z","file_name":"2020_FrontiersPlantScience_Nibau.pdf"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["1664-462X"]},"publication_status":"published","status":"public","type":"journal_article","article_type":"original","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"_id":"7350","file_date_updated":"2020-07-14T12:47:56Z","department":[{"_id":"EvBe"}],"ddc":["580"],"date_updated":"2023-08-17T14:21:45Z","publisher":"Frontiers Media","quality_controlled":"1","oa":1,"doi":"10.3389/fpls.2019.01680","date_published":"2020-01-22T00:00:00Z","date_created":"2020-01-22T15:23:57Z","day":"22","publication":"Frontiers in Plant Science","isi":1,"has_accepted_license":"1","year":"2020","article_number":"1680","title":"Thermo-sensitive alternative splicing of FLOWERING LOCUS M is modulated by cyclin-dependent kinase G2","author":[{"full_name":"Nibau, Candida","last_name":"Nibau","first_name":"Candida"},{"id":"460C6802-F248-11E8-B48F-1D18A9856A87","first_name":"Marçal","full_name":"Gallemi, Marçal","orcid":"0000-0003-4675-6893","last_name":"Gallemi"},{"first_name":"Despoina","last_name":"Dadarou","full_name":"Dadarou, Despoina"},{"first_name":"John H.","full_name":"Doonan, John H.","last_name":"Doonan"},{"last_name":"Cavallari","full_name":"Cavallari, Nicola","first_name":"Nicola","id":"457160E6-F248-11E8-B48F-1D18A9856A87"}],"article_processing_charge":"No","external_id":{"isi":["000511376000001"]},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"ista":"Nibau C, Gallemi M, Dadarou D, Doonan JH, Cavallari N. 2020. Thermo-sensitive alternative splicing of FLOWERING LOCUS M is modulated by cyclin-dependent kinase G2. Frontiers in Plant Science. 10, 1680.","chicago":"Nibau, Candida, Marçal Gallemi, Despoina Dadarou, John H. Doonan, and Nicola Cavallari. “Thermo-Sensitive Alternative Splicing of FLOWERING LOCUS M Is Modulated by Cyclin-Dependent Kinase G2.” Frontiers in Plant Science. Frontiers Media, 2020. https://doi.org/10.3389/fpls.2019.01680.","short":"C. Nibau, M. Gallemi, D. Dadarou, J.H. Doonan, N. Cavallari, Frontiers in Plant Science 10 (2020).","ieee":"C. Nibau, M. Gallemi, D. Dadarou, J. H. Doonan, and N. Cavallari, “Thermo-sensitive alternative splicing of FLOWERING LOCUS M is modulated by cyclin-dependent kinase G2,” Frontiers in Plant Science, vol. 10. Frontiers Media, 2020.","apa":"Nibau, C., Gallemi, M., Dadarou, D., Doonan, J. H., & Cavallari, N. (2020). Thermo-sensitive alternative splicing of FLOWERING LOCUS M is modulated by cyclin-dependent kinase G2. Frontiers in Plant Science. Frontiers Media. https://doi.org/10.3389/fpls.2019.01680","ama":"Nibau C, Gallemi M, Dadarou D, Doonan JH, Cavallari N. Thermo-sensitive alternative splicing of FLOWERING LOCUS M is modulated by cyclin-dependent kinase G2. Frontiers in Plant Science. 2020;10. doi:10.3389/fpls.2019.01680","mla":"Nibau, Candida, et al. “Thermo-Sensitive Alternative Splicing of FLOWERING LOCUS M Is Modulated by Cyclin-Dependent Kinase G2.” Frontiers in Plant Science, vol. 10, 1680, Frontiers Media, 2020, doi:10.3389/fpls.2019.01680."}}]