[{"doi":"10.1242/jeb.246217","language":[{"iso":"eng"}],"external_id":{"pmid":["38054353"]},"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"oa":1,"quality_controlled":"1","month":"01","publication_identifier":{"issn":["1477-9145"],"eissn":["0022-0949"]},"author":[{"full_name":"Pal, Arka","first_name":"Arka","last_name":"Pal","id":"6AAB2240-CA9A-11E9-9C1A-D9D1E5697425","orcid":"0000-0002-4530-8469"},{"full_name":"Joshi, Mihir","first_name":"Mihir","last_name":"Joshi"},{"last_name":"Thaker","first_name":"Maria","full_name":"Thaker, Maria"}],"related_material":{"link":[{"relation":"software","url":"https://github.com/arka-pal/Cnemaspis-SexualSignaling"}]},"date_created":"2024-01-22T08:14:49Z","date_updated":"2024-01-23T12:13:08Z","volume":227,"acknowledgement":"We thank Anuradha Batabyal and Shakilur Kabir for scientific discussions, and help with sampling and colour analyses. We thank Muralidhar and the central LCMS facility of the IISc for their technical support with the GCMS.\r\nResearch funding was provided by the Department of Science and Technology Fund for Improvement of S&T Infrastructure (DST-FIST), the Department of Biotechnology-Indian Institute of Science (DBT-IISc) partnership program and a Science and Engineering Research Board (SERB) grant to M.T. (EMR/2017/002228). Open Access funding provided by Indian Institute of Science. Deposited in PMC for immediate release.","year":"2024","pmid":1,"publication_status":"published","publisher":"The Company of Biologists","department":[{"_id":"NiBa"}],"file_date_updated":"2024-01-23T12:08:24Z","article_number":"jeb246217","date_published":"2024-01-10T00:00:00Z","publication":"Journal of Experimental Biology","citation":{"ama":"Pal A, Joshi M, Thaker M. Too much information? Males convey parasite levels using more signal modalities than females utilise. Journal of Experimental Biology. 2024;227(1). doi:10.1242/jeb.246217","ista":"Pal A, Joshi M, Thaker M. 2024. Too much information? Males convey parasite levels using more signal modalities than females utilise. Journal of Experimental Biology. 227(1), jeb246217.","ieee":"A. Pal, M. Joshi, and M. Thaker, “Too much information? Males convey parasite levels using more signal modalities than females utilise,” Journal of Experimental Biology, vol. 227, no. 1. The Company of Biologists, 2024.","apa":"Pal, A., Joshi, M., & Thaker, M. (2024). Too much information? Males convey parasite levels using more signal modalities than females utilise. Journal of Experimental Biology. The Company of Biologists. https://doi.org/10.1242/jeb.246217","mla":"Pal, Arka, et al. “Too Much Information? Males Convey Parasite Levels Using More Signal Modalities than Females Utilise.” Journal of Experimental Biology, vol. 227, no. 1, jeb246217, The Company of Biologists, 2024, doi:10.1242/jeb.246217.","short":"A. Pal, M. Joshi, M. Thaker, Journal of Experimental Biology 227 (2024).","chicago":"Pal, Arka, Mihir Joshi, and Maria Thaker. “Too Much Information? Males Convey Parasite Levels Using More Signal Modalities than Females Utilise.” Journal of Experimental Biology. The Company of Biologists, 2024. https://doi.org/10.1242/jeb.246217."},"article_type":"original","day":"10","article_processing_charge":"Yes (via OA deal)","has_accepted_license":"1","keyword":["Insect Science","Molecular Biology","Animal Science and Zoology","Aquatic Science","Physiology","Ecology","Evolution","Behavior and Systematics"],"file":[{"access_level":"open_access","file_name":"2024_JourExperimBiology_Pal.pdf","creator":"dernst","content_type":"application/pdf","file_size":594128,"file_id":"14877","relation":"main_file","success":1,"checksum":"136325372f6f45abaa62a71e2d23bfb6","date_updated":"2024-01-23T12:08:24Z","date_created":"2024-01-23T12:08:24Z"}],"oa_version":"Published Version","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"14850","status":"public","ddc":["570"],"title":"Too much information? Males convey parasite levels using more signal modalities than females utilise","intvolume":" 227","abstract":[{"lang":"eng","text":"Elaborate sexual signals are thought to have evolved and be maintained to serve as honest indicators of signaller quality. One measure of quality is health, which can be affected by parasite infection. Cnemaspis mysoriensis is a diurnal gecko that is often infested with ectoparasites in the wild, and males of this species express visual (coloured gular patches) and chemical (femoral gland secretions) traits that receivers could assess during social interactions. In this paper, we tested whether ectoparasites affect individual health, and whether signal quality is an indicator of ectoparasite levels. In wild lizards, we found that ectoparasite level was negatively correlated with body condition in both sexes. Moreover, some characteristics of both visual and chemical traits in males were strongly associated with ectoparasite levels. Specifically, males with higher ectoparasite levels had yellow gular patches with lower brightness and chroma, and chemical secretions with a lower proportion of aromatic compounds. We then determined whether ectoparasite levels in males influence female behaviour. Using sequential choice trials, wherein females were provided with either the visual or the chemical signals of wild-caught males that varied in ectoparasite level, we found that only chemical secretions evoked an elevated female response towards less parasitised males. Simultaneous choice trials in which females were exposed to the chemical secretions from males that varied in parasite level further confirmed a preference for males with lower parasites loads. Overall, we find that although health (body condition) or ectoparasite load can be honestly advertised through multiple modalities, the parasite-mediated female response is exclusively driven by chemical signals."}],"issue":"1","type":"journal_article"},{"keyword":["Physiology","General Neuroscience"],"day":"01","article_processing_charge":"No","article_type":"original","page":"501-512","publication":"Journal of Neurophysiology","citation":{"short":"D.R. Ladle, S. Hippenmeyer, Journal of Neurophysiology 129 (2023) 501–512.","mla":"Ladle, David R., and Simon Hippenmeyer. “Loss of ETV1/ER81 in Motor Neurons Leads to Reduced Monosynaptic Inputs from Proprioceptive Sensory Neurons.” Journal of Neurophysiology, vol. 129, no. 3, American Physiological Society, 2023, pp. 501–12, doi:10.1152/jn.00172.2022.","chicago":"Ladle, David R., and Simon Hippenmeyer. “Loss of ETV1/ER81 in Motor Neurons Leads to Reduced Monosynaptic Inputs from Proprioceptive Sensory Neurons.” Journal of Neurophysiology. American Physiological Society, 2023. https://doi.org/10.1152/jn.00172.2022.","ama":"Ladle DR, Hippenmeyer S. Loss of ETV1/ER81 in motor neurons leads to reduced monosynaptic inputs from proprioceptive sensory neurons. Journal of Neurophysiology. 2023;129(3):501-512. doi:10.1152/jn.00172.2022","ieee":"D. R. Ladle and S. Hippenmeyer, “Loss of ETV1/ER81 in motor neurons leads to reduced monosynaptic inputs from proprioceptive sensory neurons,” Journal of Neurophysiology, vol. 129, no. 3. American Physiological Society, pp. 501–512, 2023.","apa":"Ladle, D. R., & Hippenmeyer, S. (2023). Loss of ETV1/ER81 in motor neurons leads to reduced monosynaptic inputs from proprioceptive sensory neurons. Journal of Neurophysiology. American Physiological Society. https://doi.org/10.1152/jn.00172.2022","ista":"Ladle DR, Hippenmeyer S. 2023. Loss of ETV1/ER81 in motor neurons leads to reduced monosynaptic inputs from proprioceptive sensory neurons. Journal of Neurophysiology. 129(3), 501–512."},"date_published":"2023-03-01T00:00:00Z","type":"journal_article","abstract":[{"text":"Presynaptic inputs determine the pattern of activation of postsynaptic neurons in a neural circuit. Molecular and genetic pathways that regulate the selective formation of subsets of presynaptic inputs are largely unknown, despite significant understanding of the general process of synaptogenesis. In this study, we have begun to identify such factors using the spinal monosynaptic stretch reflex circuit as a model system. In this neuronal circuit, Ia proprioceptive afferents establish monosynaptic connections with spinal motor neurons that project to the same muscle (termed homonymous connections) or muscles with related or synergistic function. However, monosynaptic connections are not formed with motor neurons innervating muscles with antagonistic functions. The ETS transcription factor ER81 (also known as ETV1) is expressed by all proprioceptive afferents, but only a small set of motor neuron pools in the lumbar spinal cord of the mouse. Here we use conditional mouse genetic techniques to eliminate Er81 expression selectively from motor neurons. We find that ablation of Er81 in motor neurons reduces synaptic inputs from proprioceptive afferents conveying information from homonymous and synergistic muscles, with no change observed in the connectivity pattern from antagonistic proprioceptive afferents. In summary, these findings suggest a role for ER81 in defined motor neuron pools to control the assembly of specific presynaptic inputs and thereby influence the profile of activation of these motor neurons.","lang":"eng"}],"issue":"3","status":"public","title":"Loss of ETV1/ER81 in motor neurons leads to reduced monosynaptic inputs from proprioceptive sensory neurons","intvolume":" 129","_id":"12562","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","oa_version":"None","month":"03","publication_identifier":{"issn":["0022-3077"],"eissn":["1522-1598"]},"quality_controlled":"1","isi":1,"external_id":{"pmid":["36695533"],"isi":["000957721600001"]},"language":[{"iso":"eng"}],"doi":"10.1152/jn.00172.2022","publication_status":"published","department":[{"_id":"SiHi"}],"publisher":"American Physiological Society","year":"2023","acknowledgement":"The authors gratefully thank Dr. Silvia Arber, University of Basel and Friedrich Miescher Institute for Biomedical Research, for support and in whose lab the data were collected. For advice on statistical analysis, we thank Michael Bottomley from the Statistical Consulting Center, College of Science and Mathematics, Wright State University.","pmid":1,"date_created":"2023-02-15T14:46:14Z","date_updated":"2023-09-05T12:13:34Z","volume":129,"author":[{"full_name":"Ladle, David R.","last_name":"Ladle","first_name":"David R."},{"full_name":"Hippenmeyer, Simon","first_name":"Simon","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061"}]},{"quality_controlled":"1","isi":1,"main_file_link":[{"url":"https://doi.org/10.1101/2022.03.02.482658","open_access":"1"}],"external_id":{"isi":["000992064000002"],"pmid":["36941451"]},"oa":1,"language":[{"iso":"eng"}],"doi":"10.1038/s42255-023-00766-2","month":"03","publication_identifier":{"issn":["2522-5812"]},"publication_status":"published","publisher":"Springer Nature","department":[{"_id":"Bio"}],"year":"2023","acknowledgement":"The authors thank the participants and their families for participating in the study. We thank all members of our laboratories for helpful discussions. We are grateful to Vienna BioCenter Core Facilities: Mouse Phenotyping Unit, Histopathology Unit, Bioinformatics Unit, BioOptics Unit, Electron Microscopy Unit and Comparative Medicine Unit. We are grateful to the Lipidomics Facility, and K. Klavins and T. Hannich at the CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences for assistance with lipidomics analysis. We also thank T. Huan and A. Hui (UBC Vancouver) for mouse tissue and mitochondria lipidomics analysis. We thank A. Klymchenko (Laboratoire de Bioimagerie et Pathologies Université de Strasbourg, Strasbourg, France) for providing the NR12S probe. We are thankful to the Sen. Paul D. Wellstone Muscular Dystrophy Cooperative Specialized Research Center Viral Vector Core Facility for AAV6 production. We also thank K. P. Campbell and M. E. Anderson (University of Iowa, Carver College of Medicine) for advice on muscle tissue handling. We thank A. Al-Qassabi from the Sultan Qaboos University for the clinical assessment of the participants. D.C. and J.M.P. are supported by the Austrian Federal Ministry of Education, Science and Research, the Austrian Academy of Sciences, and the City of Vienna, and grants from the Austrian Science Fund (FWF) Wittgenstein award (Z 271-B19), the T. von Zastrow Foundation, and a Canada 150 Research Chairs Program (F18-01336). J.S.C. is supported by grants RO1AR44533 and P50AR065139 from the US National Institutes of Health. C.K. is supported by a grant from the Agence Nationale de la Recherche (ANR-18-CE14-0007-01). A.V.K. is supported by European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement no. 67544, and an Austrian Science Fund (FWF; no P-33799). A.W. is supported by Austrian Research Promotion Agency (FFG) project no 867674. E.S. is supported by a SciLifeLab fellowship and Karolinska Institutet Foundation Grants. Work in the laboratory of G.S.-F. is supported by the Austrian Academy of Sciences, the European Research Council (ERC AdG 695214 GameofGates) and the Innovative Medicines Initiative 2 Joint Undertaking (grant agreement no. 777372, ReSOLUTE). S.B., M.L. and R.Y. acknowledge the support of the Spastic Paraplegia Foundation.","pmid":1,"date_created":"2023-03-23T12:58:43Z","date_updated":"2023-11-28T07:31:33Z","volume":5,"author":[{"full_name":"Cikes, Domagoj","last_name":"Cikes","first_name":"Domagoj"},{"full_name":"Elsayad, Kareem","last_name":"Elsayad","first_name":"Kareem"},{"full_name":"Sezgin, Erdinc","last_name":"Sezgin","first_name":"Erdinc"},{"last_name":"Koitai","first_name":"Erika","full_name":"Koitai, Erika"},{"last_name":"Ferenc","first_name":"Torma","full_name":"Ferenc, Torma"},{"full_name":"Orthofer, Michael","first_name":"Michael","last_name":"Orthofer"},{"last_name":"Yarwood","first_name":"Rebecca","full_name":"Yarwood, Rebecca"},{"full_name":"Heinz, Leonhard X.","last_name":"Heinz","first_name":"Leonhard X."},{"first_name":"Vitaly","last_name":"Sedlyarov","full_name":"Sedlyarov, Vitaly"},{"full_name":"Darwish-Miranda, Nasser","last_name":"Darwish-Miranda","first_name":"Nasser","orcid":"0000-0002-8821-8236","id":"39CD9926-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Taylor, Adrian","last_name":"Taylor","first_name":"Adrian"},{"first_name":"Sophie","last_name":"Grapentine","full_name":"Grapentine, Sophie"},{"full_name":"al-Murshedi, Fathiya","last_name":"al-Murshedi","first_name":"Fathiya"},{"first_name":"Anne","last_name":"Abot","full_name":"Abot, Anne"},{"full_name":"Weidinger, Adelheid","last_name":"Weidinger","first_name":"Adelheid"},{"first_name":"Candice","last_name":"Kutchukian","full_name":"Kutchukian, Candice"},{"full_name":"Sanchez, Colline","first_name":"Colline","last_name":"Sanchez"},{"full_name":"Cronin, Shane J. F.","first_name":"Shane J. F.","last_name":"Cronin"},{"full_name":"Novatchkova, Maria","first_name":"Maria","last_name":"Novatchkova"},{"full_name":"Kavirayani, Anoop","last_name":"Kavirayani","first_name":"Anoop"},{"first_name":"Thomas","last_name":"Schuetz","full_name":"Schuetz, Thomas"},{"first_name":"Bernhard","last_name":"Haubner","full_name":"Haubner, Bernhard"},{"first_name":"Lisa","last_name":"Haas","full_name":"Haas, Lisa"},{"full_name":"Hagelkruys, Astrid","last_name":"Hagelkruys","first_name":"Astrid"},{"full_name":"Jackowski, Suzanne","first_name":"Suzanne","last_name":"Jackowski"},{"full_name":"Kozlov, Andrey","last_name":"Kozlov","first_name":"Andrey"},{"last_name":"Jacquemond","first_name":"Vincent","full_name":"Jacquemond, Vincent"},{"last_name":"Knauf","first_name":"Claude","full_name":"Knauf, Claude"},{"full_name":"Superti-Furga, Giulio","first_name":"Giulio","last_name":"Superti-Furga"},{"last_name":"Rullman","first_name":"Eric","full_name":"Rullman, Eric"},{"first_name":"Thomas","last_name":"Gustafsson","full_name":"Gustafsson, Thomas"},{"full_name":"McDermot, John","last_name":"McDermot","first_name":"John"},{"full_name":"Lowe, Martin","last_name":"Lowe","first_name":"Martin"},{"last_name":"Radak","first_name":"Zsolt","full_name":"Radak, Zsolt"},{"full_name":"Chamberlain, Jeffrey S.","first_name":"Jeffrey S.","last_name":"Chamberlain"},{"full_name":"Bakovic, Marica","first_name":"Marica","last_name":"Bakovic"},{"full_name":"Banka, Siddharth","first_name":"Siddharth","last_name":"Banka"},{"first_name":"Josef M.","last_name":"Penninger","full_name":"Penninger, Josef M."}],"related_material":{"link":[{"url":"https://doi.org/10.1038/s42255-023-00791-1","relation":"erratum"}]},"article_type":"original","page":"495-515","publication":"Nature Metabolism","citation":{"ama":"Cikes D, Elsayad K, Sezgin E, et al. PCYT2-regulated lipid biosynthesis is critical to muscle health and ageing. Nature Metabolism. 2023;5:495-515. doi:10.1038/s42255-023-00766-2","apa":"Cikes, D., Elsayad, K., Sezgin, E., Koitai, E., Ferenc, T., Orthofer, M., … Penninger, J. M. (2023). PCYT2-regulated lipid biosynthesis is critical to muscle health and ageing. Nature Metabolism. Springer Nature. https://doi.org/10.1038/s42255-023-00766-2","ieee":"D. Cikes et al., “PCYT2-regulated lipid biosynthesis is critical to muscle health and ageing,” Nature Metabolism, vol. 5. Springer Nature, pp. 495–515, 2023.","ista":"Cikes D, Elsayad K, Sezgin E, Koitai E, Ferenc T, Orthofer M, Yarwood R, Heinz LX, Sedlyarov V, Darwish-Miranda N, Taylor A, Grapentine S, al-Murshedi F, Abot A, Weidinger A, Kutchukian C, Sanchez C, Cronin SJF, Novatchkova M, Kavirayani A, Schuetz T, Haubner B, Haas L, Hagelkruys A, Jackowski S, Kozlov A, Jacquemond V, Knauf C, Superti-Furga G, Rullman E, Gustafsson T, McDermot J, Lowe M, Radak Z, Chamberlain JS, Bakovic M, Banka S, Penninger JM. 2023. PCYT2-regulated lipid biosynthesis is critical to muscle health and ageing. Nature Metabolism. 5, 495–515.","short":"D. Cikes, K. Elsayad, E. Sezgin, E. Koitai, T. Ferenc, M. Orthofer, R. Yarwood, L.X. Heinz, V. Sedlyarov, N. Darwish-Miranda, A. Taylor, S. Grapentine, F. al-Murshedi, A. Abot, A. Weidinger, C. Kutchukian, C. Sanchez, S.J.F. Cronin, M. Novatchkova, A. Kavirayani, T. Schuetz, B. Haubner, L. Haas, A. Hagelkruys, S. Jackowski, A. Kozlov, V. Jacquemond, C. Knauf, G. Superti-Furga, E. Rullman, T. Gustafsson, J. McDermot, M. Lowe, Z. Radak, J.S. Chamberlain, M. Bakovic, S. Banka, J.M. Penninger, Nature Metabolism 5 (2023) 495–515.","mla":"Cikes, Domagoj, et al. “PCYT2-Regulated Lipid Biosynthesis Is Critical to Muscle Health and Ageing.” Nature Metabolism, vol. 5, Springer Nature, 2023, pp. 495–515, doi:10.1038/s42255-023-00766-2.","chicago":"Cikes, Domagoj, Kareem Elsayad, Erdinc Sezgin, Erika Koitai, Torma Ferenc, Michael Orthofer, Rebecca Yarwood, et al. “PCYT2-Regulated Lipid Biosynthesis Is Critical to Muscle Health and Ageing.” Nature Metabolism. Springer Nature, 2023. https://doi.org/10.1038/s42255-023-00766-2."},"date_published":"2023-03-20T00:00:00Z","keyword":["Cell Biology","Physiology (medical)","Endocrinology","Diabetes and Metabolism","Internal Medicine"],"scopus_import":"1","day":"20","article_processing_charge":"No","title":"PCYT2-regulated lipid biosynthesis is critical to muscle health and ageing","status":"public","intvolume":" 5","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"12747","oa_version":"Preprint","type":"journal_article","abstract":[{"lang":"eng","text":"Muscle degeneration is the most prevalent cause for frailty and dependency in inherited diseases and ageing. Elucidation of pathophysiological mechanisms, as well as effective treatments for muscle diseases, represents an important goal in improving human health. Here, we show that the lipid synthesis enzyme phosphatidylethanolamine cytidyltransferase (PCYT2/ECT) is critical to muscle health. Human deficiency in PCYT2 causes a severe disease with failure to thrive and progressive weakness. pcyt2-mutant zebrafish and muscle-specific Pcyt2-knockout mice recapitulate the participant phenotypes, with failure to thrive, progressive muscle weakness and accelerated ageing. Mechanistically, muscle Pcyt2 deficiency affects cellular bioenergetics and membrane lipid bilayer structure and stability. PCYT2 activity declines in ageing muscles of mice and humans, and adeno-associated virus-based delivery of PCYT2 ameliorates muscle weakness in Pcyt2-knockout and old mice, offering a therapy for individuals with a rare disease and muscle ageing. Thus, PCYT2 plays a fundamental and conserved role in vertebrate muscle health, linking PCYT2 and PCYT2-synthesized lipids to severe muscle dystrophy and ageing."}]},{"extern":"1","pmid":1,"acknowledgement":"We thank the Gatsby Foundation (UK) for funding to the JDGJ laboratory. PD acknowledges support from the European Union’s Horizon 2020 Research and Innovation Program under Marie Skłodowska Curie Actions (grant agreement: 656243) and a Future Leader Fellowship from the Biotechnology and Biological Sciences Research Council (BBSRC) (grant agreement: BB/R012172/1). TS, RKS, DM, and JDGJ were supported by the Gatsby Foundation funding to the\r\nSainsbury Laboratory. NMP and KV were supported by a BOF grant from Ghent University (grant agreement: BOF24Y2019001901). WG and RZ were supported by the Scottish Government Rural and Environment Science and Analytical Services division (RESAS), and RZ also acknowledges the support from a BBSRC Bioinformatics and Biological Resources Fund (grant agreement: BB/S020160/1).BPMN was supported by the Norwich Research Park (NRP) Biosciences Doctoral Training Partnership (DTP) funded by the BBSRC (grant agreement: BB/M011216/1). SH and XF were supported by a BBSRC Responsive Mode grant (grant agreement: BB/S009620/1) and a European Research Council Starting grant ‘SexMeth’ (grant agreement: 804981). CL was supported by Deutsche Forschungsgemeinschaft (grant agreement: LI 2862/4). ","year":"2021","department":[{"_id":"XiFe"}],"publisher":"Oxford University Press","publication_status":"published","author":[{"full_name":"Ding, Pingtao","last_name":"Ding","first_name":"Pingtao"},{"last_name":"Sakai","first_name":"Toshiyuki","full_name":"Sakai, Toshiyuki"},{"last_name":"Krishna Shrestha","first_name":"Ram","full_name":"Krishna Shrestha, Ram"},{"full_name":"Manosalva Perez, Nicolas","first_name":"Nicolas","last_name":"Manosalva Perez"},{"last_name":"Guo","first_name":"Wenbin","full_name":"Guo, Wenbin"},{"first_name":"Bruno Pok Man","last_name":"Ngou","full_name":"Ngou, Bruno Pok Man"},{"last_name":"He","first_name":"Shengbo","full_name":"He, Shengbo"},{"last_name":"Liu","first_name":"Chang","full_name":"Liu, Chang"},{"first_name":"Xiaoqi","last_name":"Feng","id":"e0164712-22ee-11ed-b12a-d80fcdf35958","orcid":"0000-0002-4008-1234","full_name":"Feng, Xiaoqi"},{"last_name":"Zhang","first_name":"Runxuan","full_name":"Zhang, Runxuan"},{"full_name":"Vandepoele, Klaas","first_name":"Klaas","last_name":"Vandepoele"},{"first_name":"Dan","last_name":"MacLean","full_name":"MacLean, Dan"},{"full_name":"Jones, Jonathan D G","first_name":"Jonathan D G","last_name":"Jones"}],"volume":72,"date_created":"2023-01-16T09:14:35Z","date_updated":"2023-05-08T11:01:18Z","publication_identifier":{"issn":["0022-0957","1460-2431"]},"month":"08","external_id":{"pmid":["34387350"]},"quality_controlled":"1","doi":"10.1093/jxb/erab373","language":[{"iso":"eng"}],"type":"journal_article","issue":"22","abstract":[{"text":"Activation of cell-surface and intracellular receptor-mediated immunity results in rapid transcriptional reprogramming that underpins disease resistance. However, the mechanisms by which co-activation of both immune systems lead to transcriptional changes are not clear. Here, we combine RNA-seq and ATAC-seq to define changes in gene expression and chromatin accessibility. Activation of cell-surface or intracellular receptor-mediated immunity, or both, increases chromatin accessibility at induced defence genes. Analysis of ATAC-seq and RNA-seq data combined with publicly available information on transcription factor DNA-binding motifs enabled comparison of individual gene regulatory networks activated by cell-surface or intracellular receptor-mediated immunity, or by both. These results and analyses reveal overlapping and conserved transcriptional regulatory mechanisms between the two immune systems.","lang":"eng"}],"_id":"12186","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","intvolume":" 72","status":"public","title":"Chromatin accessibility landscapes activated by cell-surface and intracellular immune receptors","oa_version":"None","scopus_import":"1","keyword":["Plant Science","Physiology"],"article_processing_charge":"No","day":"13","citation":{"short":"P. Ding, T. Sakai, R. Krishna Shrestha, N. Manosalva Perez, W. Guo, B.P.M. Ngou, S. He, C. Liu, X. Feng, R. Zhang, K. Vandepoele, D. MacLean, J.D.G. Jones, Journal of Experimental Botany 72 (2021) 7927–7941.","mla":"Ding, Pingtao, et al. “Chromatin Accessibility Landscapes Activated by Cell-Surface and Intracellular Immune Receptors.” Journal of Experimental Botany, vol. 72, no. 22, Oxford University Press, 2021, pp. 7927–41, doi:10.1093/jxb/erab373.","chicago":"Ding, Pingtao, Toshiyuki Sakai, Ram Krishna Shrestha, Nicolas Manosalva Perez, Wenbin Guo, Bruno Pok Man Ngou, Shengbo He, et al. “Chromatin Accessibility Landscapes Activated by Cell-Surface and Intracellular Immune Receptors.” Journal of Experimental Botany. Oxford University Press, 2021. https://doi.org/10.1093/jxb/erab373.","ama":"Ding P, Sakai T, Krishna Shrestha R, et al. Chromatin accessibility landscapes activated by cell-surface and intracellular immune receptors. Journal of Experimental Botany. 2021;72(22):7927-7941. doi:10.1093/jxb/erab373","apa":"Ding, P., Sakai, T., Krishna Shrestha, R., Manosalva Perez, N., Guo, W., Ngou, B. P. M., … Jones, J. D. G. (2021). Chromatin accessibility landscapes activated by cell-surface and intracellular immune receptors. Journal of Experimental Botany. Oxford University Press. https://doi.org/10.1093/jxb/erab373","ieee":"P. Ding et al., “Chromatin accessibility landscapes activated by cell-surface and intracellular immune receptors,” Journal of Experimental Botany, vol. 72, no. 22. Oxford University Press, pp. 7927–7941, 2021.","ista":"Ding P, Sakai T, Krishna Shrestha R, Manosalva Perez N, Guo W, Ngou BPM, He S, Liu C, Feng X, Zhang R, Vandepoele K, MacLean D, Jones JDG. 2021. Chromatin accessibility landscapes activated by cell-surface and intracellular immune receptors. Journal of Experimental Botany. 72(22), 7927–7941."},"publication":"Journal of Experimental Botany","page":"7927-7941","article_type":"original","date_published":"2021-08-13T00:00:00Z"},{"month":"01","publication_identifier":{"issn":["1741-7007"]},"main_file_link":[{"url":"https://doi.org/10.1186/s12915-019-0733-6","open_access":"1"}],"external_id":{"pmid":["31907035"]},"oa":1,"quality_controlled":"1","doi":"10.1186/s12915-019-0733-6","language":[{"iso":"eng"}],"article_number":"2","extern":"1","year":"2020","pmid":1,"publication_status":"published","publisher":"Springer Nature","author":[{"last_name":"Rampelt","first_name":"Heike","full_name":"Rampelt, Heike"},{"full_name":"Sucec, Iva","first_name":"Iva","last_name":"Sucec"},{"full_name":"Bersch, Beate","first_name":"Beate","last_name":"Bersch"},{"full_name":"Horten, Patrick","first_name":"Patrick","last_name":"Horten"},{"last_name":"Perschil","first_name":"Inge","full_name":"Perschil, Inge"},{"full_name":"Martinou, Jean-Claude","first_name":"Jean-Claude","last_name":"Martinou"},{"full_name":"van der Laan, Martin","first_name":"Martin","last_name":"van der Laan"},{"full_name":"Wiedemann, Nils","first_name":"Nils","last_name":"Wiedemann"},{"full_name":"Schanda, Paul","last_name":"Schanda","first_name":"Paul","orcid":"0000-0002-9350-7606","id":"7B541462-FAF6-11E9-A490-E8DFE5697425"},{"full_name":"Pfanner, Nikolaus","last_name":"Pfanner","first_name":"Nikolaus"}],"date_created":"2020-09-17T10:26:53Z","date_updated":"2021-01-12T08:19:02Z","volume":18,"keyword":["Biotechnology","Plant Science","General Biochemistry","Genetics and Molecular Biology","Developmental Biology","Cell Biology","Physiology","Ecology","Evolution","Behavior and Systematics","Structural Biology","General Agricultural and Biological Sciences"],"day":"06","article_processing_charge":"No","publication":"BMC Biology","citation":{"ama":"Rampelt H, Sucec I, Bersch B, et al. The mitochondrial carrier pathway transports non-canonical substrates with an odd number of transmembrane segments. BMC Biology. 2020;18. doi:10.1186/s12915-019-0733-6","ista":"Rampelt H, Sucec I, Bersch B, Horten P, Perschil I, Martinou J-C, van der Laan M, Wiedemann N, Schanda P, Pfanner N. 2020. The mitochondrial carrier pathway transports non-canonical substrates with an odd number of transmembrane segments. BMC Biology. 18, 2.","apa":"Rampelt, H., Sucec, I., Bersch, B., Horten, P., Perschil, I., Martinou, J.-C., … Pfanner, N. (2020). The mitochondrial carrier pathway transports non-canonical substrates with an odd number of transmembrane segments. BMC Biology. Springer Nature. https://doi.org/10.1186/s12915-019-0733-6","ieee":"H. Rampelt et al., “The mitochondrial carrier pathway transports non-canonical substrates with an odd number of transmembrane segments,” BMC Biology, vol. 18. Springer Nature, 2020.","mla":"Rampelt, Heike, et al. “The Mitochondrial Carrier Pathway Transports Non-Canonical Substrates with an Odd Number of Transmembrane Segments.” BMC Biology, vol. 18, 2, Springer Nature, 2020, doi:10.1186/s12915-019-0733-6.","short":"H. Rampelt, I. Sucec, B. Bersch, P. Horten, I. Perschil, J.-C. Martinou, M. van der Laan, N. Wiedemann, P. Schanda, N. Pfanner, BMC Biology 18 (2020).","chicago":"Rampelt, Heike, Iva Sucec, Beate Bersch, Patrick Horten, Inge Perschil, Jean-Claude Martinou, Martin van der Laan, Nils Wiedemann, Paul Schanda, and Nikolaus Pfanner. “The Mitochondrial Carrier Pathway Transports Non-Canonical Substrates with an Odd Number of Transmembrane Segments.” BMC Biology. Springer Nature, 2020. https://doi.org/10.1186/s12915-019-0733-6."},"article_type":"original","date_published":"2020-01-06T00:00:00Z","type":"journal_article","abstract":[{"text":"Background: The mitochondrial pyruvate carrier (MPC) plays a central role in energy metabolism by transporting pyruvate across the inner mitochondrial membrane. Its heterodimeric composition and homology to SWEET and semiSWEET transporters set the MPC apart from the canonical mitochondrial carrier family (named MCF or SLC25). The import of the canonical carriers is mediated by the carrier translocase of the inner membrane (TIM22) pathway and is dependent on their structure, which features an even number of transmembrane segments and both termini in the intermembrane space. The import pathway of MPC proteins has not been elucidated. The odd number of transmembrane segments and positioning of the N-terminus in the matrix argues against an import via the TIM22 carrier pathway but favors an import via the flexible presequence pathway.\r\nResults: Here, we systematically analyzed the import pathways of Mpc2 and Mpc3 and report that, contrary to an expected import via the flexible presequence pathway, yeast MPC proteins with an odd number of transmembrane segments and matrix-exposed N-terminus are imported by the carrier pathway, using the receptor Tom70, small TIM chaperones, and the TIM22 complex. The TIM9·10 complex chaperones MPC proteins through the mitochondrial intermembrane space using conserved hydrophobic motifs that are also required for the interaction with canonical carrier proteins.\r\nConclusions: The carrier pathway can import paired and non-paired transmembrane helices and translocate N-termini to either side of the mitochondrial inner membrane, revealing an unexpected versatility of the mitochondrial import pathway for non-cleavable inner membrane proteins.","lang":"eng"}],"_id":"8402","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","status":"public","title":"The mitochondrial carrier pathway transports non-canonical substrates with an odd number of transmembrane segments","intvolume":" 18","oa_version":"Published Version"},{"keyword":["Escherichia coli","antibiotic combinations","translation","growth laws","drug interactions","bacterial physiology","translation inhibitors"],"month":"07","day":"15","has_accepted_license":"1","article_processing_charge":"No","tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"oa":1,"citation":{"ista":"Kavcic B. 2020. Analysis scripts and research data for the paper ‘Mechanisms of drug interactions between translation-inhibiting antibiotics’, Institute of Science and Technology Austria, 10.15479/AT:ISTA:8097.","ieee":"B. Kavcic, “Analysis scripts and research data for the paper ‘Mechanisms of drug interactions between translation-inhibiting antibiotics.’” Institute of Science and Technology Austria, 2020.","apa":"Kavcic, B. (2020). Analysis scripts and research data for the paper “Mechanisms of drug interactions between translation-inhibiting antibiotics.” Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:8097","ama":"Kavcic B. Analysis scripts and research data for the paper “Mechanisms of drug interactions between translation-inhibiting antibiotics.” 2020. doi:10.15479/AT:ISTA:8097","chicago":"Kavcic, Bor. “Analysis Scripts and Research Data for the Paper ‘Mechanisms of Drug Interactions between Translation-Inhibiting Antibiotics.’” Institute of Science and Technology Austria, 2020. https://doi.org/10.15479/AT:ISTA:8097.","mla":"Kavcic, Bor. Analysis Scripts and Research Data for the Paper “Mechanisms of Drug Interactions between Translation-Inhibiting Antibiotics.” Institute of Science and Technology Austria, 2020, doi:10.15479/AT:ISTA:8097.","short":"B. Kavcic, (2020)."},"acknowledged_ssus":[{"_id":"LifeSc"}],"date_published":"2020-07-15T00:00:00Z","doi":"10.15479/AT:ISTA:8097","type":"research_data","file_date_updated":"2020-07-14T12:48:09Z","abstract":[{"text":"Antibiotics that interfere with translation, when combined, interact in diverse and difficult-to-predict ways. Here, we explain these interactions by \"translation bottlenecks\": points in the translation cycle where antibiotics block ribosomal progression. To elucidate the underlying mechanisms of drug interactions between translation inhibitors, we generate translation bottlenecks genetically using inducible control of translation factors that regulate well-defined translation cycle steps. These perturbations accurately mimic antibiotic action and drug interactions, supporting that the interplay of different translation bottlenecks causes these interactions. We further show that growth laws, combined with drug uptake and binding kinetics, enable the direct prediction of a large fraction of observed interactions, yet fail to predict suppression. However, varying two translation bottlenecks simultaneously supports that dense traffic of ribosomes and competition for translation factors account for the previously unexplained suppression. These results highlight the importance of \"continuous epistasis\" in bacterial physiology.","lang":"eng"}],"title":"Analysis scripts and research data for the paper \"Mechanisms of drug interactions between translation-inhibiting antibiotics\"","status":"public","publisher":"Institute of Science and Technology Austria","department":[{"_id":"GaTk"}],"year":"2020","_id":"8097","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2024-02-21T12:40:51Z","date_created":"2020-07-06T20:40:19Z","oa_version":"Published Version","file":[{"creator":"bkavcic","file_size":255770756,"content_type":"application/zip","file_name":"natComm_2020_scripts.zip","access_level":"open_access","date_created":"2020-07-06T20:38:27Z","date_updated":"2020-07-14T12:48:09Z","checksum":"5c321dbbb6d4b3c85da786fd3ebbdc98","file_id":"8098","relation":"main_file"}],"author":[{"full_name":"Kavcic, Bor","id":"350F91D2-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6041-254X","first_name":"Bor","last_name":"Kavcic"}],"contributor":[{"id":"3D494DCA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6699-1455","first_name":"Gašper","contributor_type":"research_group","last_name":"Tkačik"},{"id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","contributor_type":"research_group","last_name":"Bollenbach","first_name":"Tobias"}]},{"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"oa":1,"citation":{"short":"B. Kavcic, (2020).","mla":"Kavcic, Bor. Analysis Scripts and Research Data for the Paper “Minimal Biophysical Model of Combined Antibiotic Action.” Institute of Science and Technology Austria, 2020, doi:10.15479/AT:ISTA:8930.","chicago":"Kavcic, Bor. “Analysis Scripts and Research Data for the Paper ‘Minimal Biophysical Model of Combined Antibiotic Action.’” Institute of Science and Technology Austria, 2020. https://doi.org/10.15479/AT:ISTA:8930.","ama":"Kavcic B. Analysis scripts and research data for the paper “Minimal biophysical model of combined antibiotic action.” 2020. doi:10.15479/AT:ISTA:8930","apa":"Kavcic, B. (2020). Analysis scripts and research data for the paper “Minimal biophysical model of combined antibiotic action.” Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:8930","ieee":"B. Kavcic, “Analysis scripts and research data for the paper ‘Minimal biophysical model of combined antibiotic action.’” Institute of Science and Technology Austria, 2020.","ista":"Kavcic B. 2020. Analysis scripts and research data for the paper ‘Minimal biophysical model of combined antibiotic action’, Institute of Science and Technology Austria, 10.15479/AT:ISTA:8930."},"date_published":"2020-12-10T00:00:00Z","doi":"10.15479/AT:ISTA:8930","keyword":["Escherichia coli","antibiotic combinations","translation","growth laws","drug interactions","bacterial physiology","translation inhibitors"],"day":"10","month":"12","article_processing_charge":"No","has_accepted_license":"1","title":"Analysis scripts and research data for the paper \"Minimal biophysical model of combined antibiotic action\"","status":"public","ddc":["570"],"department":[{"_id":"GaTk"}],"publisher":"Institute of Science and Technology Austria","_id":"8930","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","year":"2020","date_updated":"2024-02-21T12:41:42Z","date_created":"2020-12-09T15:04:02Z","oa_version":"Published Version","file":[{"relation":"main_file","file_id":"8932","date_created":"2020-12-09T15:00:19Z","date_updated":"2020-12-09T15:00:19Z","checksum":"60a818edeffaa7da1ebf5f8fbea9ba18","success":1,"file_name":"PLoSCompBiol2020_datarep.zip","access_level":"open_access","content_type":"application/zip","file_size":315494370,"creator":"bkavcic"}],"author":[{"first_name":"Bor","last_name":"Kavcic","id":"350F91D2-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6041-254X","full_name":"Kavcic, Bor"}],"related_material":{"record":[{"relation":"used_in_publication","status":"public","id":"8997"}]},"contributor":[{"first_name":"Gašper","last_name":"Tkačik","contributor_type":"supervisor","id":"3D494DCA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6699-1455"},{"last_name":"Bollenbach","contributor_type":"supervisor","first_name":"Tobias","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87"}],"type":"research_data","file_date_updated":"2020-12-09T15:00:19Z","abstract":[{"lang":"eng","text":"Phenomenological relations such as Ohm’s or Fourier’s law have a venerable history in physics but are still scarce in biology. This situation restrains predictive theory. Here, we build on bacterial “growth laws,” which capture physiological feedback between translation and cell growth, to construct a minimal biophysical model for the combined action of ribosome-targeting antibiotics. Our model predicts drug interactions like antagonism or synergy solely from responses to individual drugs. We provide analytical results for limiting cases, which agree well with numerical results. We systematically refine the model by including direct physical interactions of different antibiotics on the ribosome. In a limiting case, our model provides a mechanistic underpinning for recent predictions of higher-order interactions that were derived using entropy maximization. We further refine the model to include the effects of antibiotics that mimic starvation and the presence of resistance genes. We describe the impact of a starvation-mimicking antibiotic on drug interactions analytically and verify it experimentally. Our extended model suggests a change in the type of drug interaction that depends on the strength of resistance, which challenges established rescaling paradigms. We experimentally show that the presence of unregulated resistance genes can lead to altered drug interaction, which agrees with the prediction of the model. While minimal, the model is readily adaptable and opens the door to predicting interactions of second and higher-order in a broad range of biological systems."}]},{"date_published":"2019-08-06T00:00:00Z","citation":{"short":"R. Arrojo e Drigo, V. Lev-Ram, S. Tyagi, R. Ramachandra, T. Deerinck, E. Bushong, S. Phan, V. Orphan, C. Lechene, M.H. Ellisman, M. Hetzer, Cell Metabolism 30 (2019) 343–351.e3.","mla":"Arrojo e Drigo, Rafael, et al. “Age Mosaicism across Multiple Scales in Adult Tissues.” Cell Metabolism, vol. 30, no. 2, Elsevier, 2019, p. 343–351.e3, doi:10.1016/j.cmet.2019.05.010.","chicago":"Arrojo e Drigo, Rafael, Varda Lev-Ram, Swati Tyagi, Ranjan Ramachandra, Thomas Deerinck, Eric Bushong, Sebastien Phan, et al. “Age Mosaicism across Multiple Scales in Adult Tissues.” Cell Metabolism. Elsevier, 2019. https://doi.org/10.1016/j.cmet.2019.05.010.","ama":"Arrojo e Drigo R, Lev-Ram V, Tyagi S, et al. Age mosaicism across multiple scales in adult tissues. Cell Metabolism. 2019;30(2):343-351.e3. doi:10.1016/j.cmet.2019.05.010","apa":"Arrojo e Drigo, R., Lev-Ram, V., Tyagi, S., Ramachandra, R., Deerinck, T., Bushong, E., … Hetzer, M. (2019). Age mosaicism across multiple scales in adult tissues. Cell Metabolism. Elsevier. https://doi.org/10.1016/j.cmet.2019.05.010","ieee":"R. Arrojo e Drigo et al., “Age mosaicism across multiple scales in adult tissues,” Cell Metabolism, vol. 30, no. 2. Elsevier, p. 343–351.e3, 2019.","ista":"Arrojo e Drigo R, Lev-Ram V, Tyagi S, Ramachandra R, Deerinck T, Bushong E, Phan S, Orphan V, Lechene C, Ellisman MH, Hetzer M. 2019. Age mosaicism across multiple scales in adult tissues. Cell Metabolism. 30(2), 343–351.e3."},"publication":"Cell Metabolism","page":"343-351.e3","article_type":"original","article_processing_charge":"No","day":"06","scopus_import":"1","keyword":["Cell Biology","Molecular Biology","Physiology"],"oa_version":"Published Version","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","_id":"11062","intvolume":" 30","status":"public","title":"Age mosaicism across multiple scales in adult tissues","issue":"2","abstract":[{"lang":"eng","text":"Most neurons are not replaced during an animal’s lifetime. This nondividing state is characterized by extreme longevity and age-dependent decline of key regulatory proteins. To study the lifespans of cells and proteins in adult tissues, we combined isotope labeling of mice with a hybrid imaging method (MIMS-EM). Using 15N mapping, we show that liver and pancreas are composed of cells with vastly different ages, many as old as the animal. Strikingly, we also found that a subset of fibroblasts and endothelial cells, both known for their replicative potential, are characterized by the absence of cell division during adulthood. In addition, we show that the primary cilia of beta cells and neurons contains different structural regions with vastly different lifespans. Based on these results, we propose that age mosaicism across multiple scales is a fundamental principle of adult tissue, cell, and protein complex organization."}],"type":"journal_article","doi":"10.1016/j.cmet.2019.05.010","language":[{"iso":"eng"}],"external_id":{"pmid":["31178361"]},"oa":1,"main_file_link":[{"url":"https://doi.org/10.1016/j.cmet.2019.05.010","open_access":"1"}],"quality_controlled":"1","publication_identifier":{"issn":["1550-4131"]},"month":"08","author":[{"last_name":"Arrojo e Drigo","first_name":"Rafael","full_name":"Arrojo e Drigo, Rafael"},{"first_name":"Varda","last_name":"Lev-Ram","full_name":"Lev-Ram, Varda"},{"full_name":"Tyagi, Swati","first_name":"Swati","last_name":"Tyagi"},{"last_name":"Ramachandra","first_name":"Ranjan","full_name":"Ramachandra, Ranjan"},{"full_name":"Deerinck, Thomas","first_name":"Thomas","last_name":"Deerinck"},{"full_name":"Bushong, Eric","first_name":"Eric","last_name":"Bushong"},{"full_name":"Phan, Sebastien","last_name":"Phan","first_name":"Sebastien"},{"full_name":"Orphan, Victoria","first_name":"Victoria","last_name":"Orphan"},{"last_name":"Lechene","first_name":"Claude","full_name":"Lechene, Claude"},{"full_name":"Ellisman, Mark H.","first_name":"Mark H.","last_name":"Ellisman"},{"full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","last_name":"HETZER","first_name":"Martin W"}],"volume":30,"date_updated":"2022-07-18T08:32:30Z","date_created":"2022-04-07T07:45:21Z","pmid":1,"year":"2019","publisher":"Elsevier","publication_status":"published","extern":"1"},{"date_published":"2018-04-13T00:00:00Z","publication":"Journal of Experimental Botany","citation":{"ista":"Moturu TR, Thula S, Singh RK, Nodzyński T, Vařeková RS, Friml J, Simon S. 2018. Molecular evolution and diversification of the SMXL gene family. Journal of Experimental Botany. 69(9), 2367–2378.","ieee":"T. R. Moturu et al., “Molecular evolution and diversification of the SMXL gene family,” Journal of Experimental Botany, vol. 69, no. 9. Oxford University Press, pp. 2367–2378, 2018.","apa":"Moturu, T. R., Thula, S., Singh, R. K., Nodzyński, T., Vařeková, R. S., Friml, J., & Simon, S. (2018). Molecular evolution and diversification of the SMXL gene family. Journal of Experimental Botany. Oxford University Press. https://doi.org/10.1093/jxb/ery097","ama":"Moturu TR, Thula S, Singh RK, et al. Molecular evolution and diversification of the SMXL gene family. Journal of Experimental Botany. 2018;69(9):2367-2378. doi:10.1093/jxb/ery097","chicago":"Moturu, Taraka Ramji, Sravankumar Thula, Ravi Kumar Singh, Tomasz Nodzyński, Radka Svobodová Vařeková, Jiří Friml, and Sibu Simon. “Molecular Evolution and Diversification of the SMXL Gene Family.” Journal of Experimental Botany. Oxford University Press, 2018. https://doi.org/10.1093/jxb/ery097.","mla":"Moturu, Taraka Ramji, et al. “Molecular Evolution and Diversification of the SMXL Gene Family.” Journal of Experimental Botany, vol. 69, no. 9, Oxford University Press, 2018, pp. 2367–78, doi:10.1093/jxb/ery097.","short":"T.R. Moturu, S. Thula, R.K. Singh, T. Nodzyński, R.S. Vařeková, J. Friml, S. Simon, Journal of Experimental Botany 69 (2018) 2367–2378."},"article_type":"original","page":"2367-2378","day":"13","article_processing_charge":"No","scopus_import":"1","keyword":["Plant Science","Physiology"],"oa_version":"None","_id":"10881","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","title":"Molecular evolution and diversification of the SMXL gene family","status":"public","intvolume":" 69","abstract":[{"lang":"eng","text":"Strigolactones (SLs) are a relatively recent addition to the list of plant hormones that control different aspects of plant development. SL signalling is perceived by an α/β hydrolase, DWARF 14 (D14). A close homolog of D14, KARRIKIN INSENSTIVE2 (KAI2), is involved in perception of an uncharacterized molecule called karrikin (KAR). Recent studies in Arabidopsis identified the SUPPRESSOR OF MAX2 1 (SMAX1) and SMAX1-LIKE 7 (SMXL7) to be potential SCF–MAX2 complex-mediated proteasome targets of KAI2 and D14, respectively. Genetic studies on SMXL7 and SMAX1 demonstrated distinct developmental roles for each, but very little is known about these repressors in terms of their sequence features. In this study, we performed an extensive comparative analysis of SMXLs and determined their phylogenetic and evolutionary history in the plant lineage. Our results show that SMXL family members can be sub-divided into four distinct phylogenetic clades/classes, with an ancient SMAX1. Further, we identified the clade-specific motifs that have evolved and that might act as determinants of SL-KAR signalling specificity. These specificities resulted from functional diversities among the clades. Our results suggest that a gradual co-evolution of SMXL members with their upstream receptors D14/KAI2 provided an increased specificity to both the SL perception and response in land plants."}],"issue":"9","type":"journal_article","doi":"10.1093/jxb/ery097","language":[{"iso":"eng"}],"external_id":{"isi":["000430727000016"],"pmid":["29538714"]},"quality_controlled":"1","isi":1,"project":[{"grant_number":"282300","_id":"25716A02-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Polarity and subcellular dynamics in plants"}],"month":"04","publication_identifier":{"eissn":["1460-2431"],"issn":["0022-0957"]},"author":[{"first_name":"Taraka Ramji","last_name":"Moturu","full_name":"Moturu, Taraka Ramji"},{"first_name":"Sravankumar","last_name":"Thula","full_name":"Thula, Sravankumar"},{"first_name":"Ravi Kumar","last_name":"Singh","full_name":"Singh, Ravi Kumar"},{"full_name":"Nodzyński, Tomasz","first_name":"Tomasz","last_name":"Nodzyński"},{"full_name":"Vařeková, Radka Svobodová","first_name":"Radka Svobodová","last_name":"Vařeková"},{"orcid":"0000-0002-8302-7596","id":"4159519E-F248-11E8-B48F-1D18A9856A87","last_name":"Friml","first_name":"Jiří","full_name":"Friml, Jiří"},{"last_name":"Simon","first_name":"Sibu","full_name":"Simon, Sibu"}],"date_created":"2022-03-18T12:43:22Z","date_updated":"2023-09-19T15:10:43Z","volume":69,"year":"2018","acknowledgement":"This project received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie Actions and it is co-financed by the South Moravian Region under grant agreement No. 665860 (SS). Access to computing and storage facilities owned by parties and projects contributing to the national grid infrastructure, MetaCentrum, provided under the program ‘Projects of Large Infrastructure for Research, Development, and Innovations’ (LM2010005) was greatly appreciated (RSV). The project was funded by The Ministry of Education, Youth and Sports/MES of the Czech Republic under the project CEITEC 2020 (LQ1601) (TN, TRM). JF was supported by the European Research Council (project ERC-2011-StG 20101109-PSDP) and the Czech Science Foundation GAČR (GA13-40637S). We thank Dr Kamel Chibani for active discussions on the evolutionary analysis and Nandan Mysore Vardarajan for his critical comments on the manuscript. This article reflects\r\nonly the authors’ views, and the EU is not responsible for any use that may be made of the information it contains. ","pmid":1,"publication_status":"published","department":[{"_id":"JiFr"}],"publisher":"Oxford University Press","ec_funded":1},{"extern":"1","year":"2015","acknowledgement":"This work was supported by the National Sciences and Engineering Research Council of Canada [Canada Graduate\r\nScholarship–Doctoral to K.J.; Discovery Grant to X.L.]; the department of Botany at the University of f British Columbia\r\n[the Dewar Cooper Memorial Fund to X.L.].The authors would like to thank Dr. Yuelin Zhang and Ms. Yan Li for their assistance with next-generation sequencing, and Mr. Charles Copeland for critical reading of the manuscript.","pmid":1,"publication_status":"published","publisher":"Oxford University Press","department":[{"_id":"XiFe"}],"author":[{"full_name":"Johnson, Kaeli C.M.","last_name":"Johnson","first_name":"Kaeli C.M."},{"full_name":"Xia, Shitou","first_name":"Shitou","last_name":"Xia"},{"id":"e0164712-22ee-11ed-b12a-d80fcdf35958","orcid":"0000-0002-4008-1234","first_name":"Xiaoqi","last_name":"Feng","full_name":"Feng, Xiaoqi"},{"full_name":"Li, Xin","last_name":"Li","first_name":"Xin"}],"date_created":"2023-01-16T09:20:22Z","date_updated":"2023-05-08T11:03:23Z","volume":56,"month":"08","publication_identifier":{"issn":["0032-0781","1471-9053"]},"external_id":{"pmid":["26063389"]},"quality_controlled":"1","doi":"10.1093/pcp/pcv087","language":[{"iso":"eng"}],"type":"journal_article","abstract":[{"lang":"eng","text":"SNC1 (SUPPRESSOR OF NPR1, CONSTITUTIVE 1) is one of a suite of intracellular Arabidopsis NOD-like receptor (NLR) proteins which, upon activation, result in the induction of defense responses. However, the molecular mechanisms underlying NLR activation and the subsequent provocation of immune responses are only partially characterized. To identify negative regulators of NLR-mediated immunity, a forward genetic screen was undertaken to search for enhancers of the dwarf, autoimmune gain-of-function snc1 mutant. To avoid lethality resulting from severe dwarfism, the screen was conducted using mos4 (modifier of snc1, 4) snc1 plants, which display wild-type-like morphology and resistance. M2 progeny were screened for mutant, snc1-enhancing (muse) mutants displaying a reversion to snc1-like phenotypes. The muse9 mos4 snc1 triple mutant was found to exhibit dwarf morphology, elevated expression of the pPR2-GUS defense marker reporter gene and enhanced resistance to the oomycete pathogen Hyaloperonospora arabidopsidis Noco2. Via map-based cloning and Illumina sequencing, it was determined that the muse9 mutation is in the gene encoding the SWI/SNF chromatin remodeler SYD (SPLAYED), and was thus renamed syd-10. The syd-10 single mutant has no observable alteration from wild-type-like resistance, although the syd-4 T-DNA insertion allele displays enhanced resistance to the bacterial pathogen Pseudomonas syringae pv. maculicola ES4326. Transcription of SNC1 is increased in both syd-4 and syd-10. These data suggest that SYD plays a subtle, specific role in the regulation of SNC1 expression and SNC1-mediated immunity. SYD may work with other proteins at the chromatin level to repress SNC1 transcription; such regulation is important for fine-tuning the expression of NLR-encoding genes to prevent unpropitious autoimmunity."}],"issue":"8","_id":"12196","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","title":"The chromatin remodeler SPLAYED negatively regulates SNC1-mediated immunity","status":"public","intvolume":" 56","oa_version":"None","scopus_import":"1","keyword":["Cell Biology","Plant Science","Physiology","General Medicine"],"article_processing_charge":"No","publication":"Plant and Cell Physiology","citation":{"mla":"Johnson, Kaeli C. M., et al. “The Chromatin Remodeler SPLAYED Negatively Regulates SNC1-Mediated Immunity.” Plant and Cell Physiology, vol. 56, no. 8, Oxford University Press, 2015, pp. 1616–23, doi:10.1093/pcp/pcv087.","short":"K.C.M. Johnson, S. Xia, X. Feng, X. Li, Plant and Cell Physiology 56 (2015) 1616–1623.","chicago":"Johnson, Kaeli C.M., Shitou Xia, Xiaoqi Feng, and Xin Li. “The Chromatin Remodeler SPLAYED Negatively Regulates SNC1-Mediated Immunity.” Plant and Cell Physiology. Oxford University Press, 2015. https://doi.org/10.1093/pcp/pcv087.","ama":"Johnson KCM, Xia S, Feng X, Li X. The chromatin remodeler SPLAYED negatively regulates SNC1-mediated immunity. Plant and Cell Physiology. 2015;56(8):1616-1623. doi:10.1093/pcp/pcv087","ista":"Johnson KCM, Xia S, Feng X, Li X. 2015. The chromatin remodeler SPLAYED negatively regulates SNC1-mediated immunity. Plant and Cell Physiology. 56(8), 1616–1623.","apa":"Johnson, K. C. M., Xia, S., Feng, X., & Li, X. (2015). The chromatin remodeler SPLAYED negatively regulates SNC1-mediated immunity. Plant and Cell Physiology. Oxford University Press. https://doi.org/10.1093/pcp/pcv087","ieee":"K. C. M. Johnson, S. Xia, X. Feng, and X. Li, “The chromatin remodeler SPLAYED negatively regulates SNC1-mediated immunity,” Plant and Cell Physiology, vol. 56, no. 8. Oxford University Press, pp. 1616–1623, 2015."},"article_type":"original","page":"1616-1623","date_published":"2015-08-01T00:00:00Z"},{"date_published":"2000-01-01T00:00:00Z","article_type":"original","page":"329-334","publication":"Cellular Physiology and Biochemistry","citation":{"mla":"Fürst, Johannes, et al. “Structure and Function of the Ion Channel ICln.” Cellular Physiology and Biochemistry, vol. 10, no. 5–6, S. Karger AG, 2000, pp. 329–34, doi:10.1159/000016374.","short":"J. Fürst, M. Jakab, M. König, M. Ritter, M. Gschwentner, J. Rudzki, J.G. Danzl, M. Mayer, C.M. Burtscher, J. Schirmer, B. Maier, M. Nairz, S. Chwatal, M. Paulmichl, Cellular Physiology and Biochemistry 10 (2000) 329–334.","chicago":"Fürst, Johannes, Martin Jakab, Matthias König, Markus Ritter, Martin Gschwentner, Jakob Rudzki, Johann G Danzl, et al. “Structure and Function of the Ion Channel ICln.” Cellular Physiology and Biochemistry. S. Karger AG, 2000. https://doi.org/10.1159/000016374.","ama":"Fürst J, Jakab M, König M, et al. Structure and Function of the Ion Channel ICln. Cellular Physiology and Biochemistry. 2000;10(5-6):329-334. doi:10.1159/000016374","ista":"Fürst J, Jakab M, König M, Ritter M, Gschwentner M, Rudzki J, Danzl JG, Mayer M, Burtscher CM, Schirmer J, Maier B, Nairz M, Chwatal S, Paulmichl M. 2000. Structure and Function of the Ion Channel ICln. Cellular Physiology and Biochemistry. 10(5–6), 329–334.","ieee":"J. Fürst et al., “Structure and Function of the Ion Channel ICln,” Cellular Physiology and Biochemistry, vol. 10, no. 5–6. S. Karger AG, pp. 329–334, 2000.","apa":"Fürst, J., Jakab, M., König, M., Ritter, M., Gschwentner, M., Rudzki, J., … Paulmichl, M. (2000). Structure and Function of the Ion Channel ICln. Cellular Physiology and Biochemistry. S. Karger AG. https://doi.org/10.1159/000016374"},"article_processing_charge":"No","keyword":["Physiology"],"scopus_import":"1","oa_version":"None","title":"Structure and Function of the Ion Channel ICln","status":"public","intvolume":" 10","_id":"12925","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","abstract":[{"lang":"eng","text":"Normal function of organs and cells is tightly linked to the cytoarchitecture. Control of the cell volume is therefore vital for the organism. A widely established strategy of cells to counteract swelling is the activation of chloride and potassium channels, which leads to a net efflux of salt followed by water - a process termed regulatory volume decrease. Since there is evidence for swelling-dependent chloride channels (IClswell) being activated also during pathological processes, the identification of the molecular entity underlying IClswell is of utmost importance. Several proteins are discussed as the channel forming IClswell, i.e. phospholemman, p-glycoprotein, CLC-3 and ICln. In this review we would like to focus on the properties of ICln, a protein cloned from a Madin Darby canine kidney (MDCK) cell library whose expression in Xenopus laevis oocytes resulted in a nucleotide sensitive outwardly rectifying chloride current closely resembling the biophysical properties of IClswell."}],"issue":"5-6","type":"journal_article","language":[{"iso":"eng"}],"doi":"10.1159/000016374","quality_controlled":"1","external_id":{"pmid":["11125213"]},"publication_identifier":{"issn":["1015-8987","1421-9778"]},"date_updated":"2023-05-08T10:07:10Z","date_created":"2023-05-08T09:04:58Z","volume":10,"author":[{"first_name":"Johannes","last_name":"Fürst","full_name":"Fürst, Johannes"},{"full_name":"Jakab, Martin","last_name":"Jakab","first_name":"Martin"},{"full_name":"König, Matthias","last_name":"König","first_name":"Matthias"},{"first_name":"Markus","last_name":"Ritter","full_name":"Ritter, Markus"},{"full_name":"Gschwentner, Martin","last_name":"Gschwentner","first_name":"Martin"},{"last_name":"Rudzki","first_name":"Jakob","full_name":"Rudzki, Jakob"},{"full_name":"Danzl, Johann G","last_name":"Danzl","first_name":"Johann G","orcid":"0000-0001-8559-3973","id":"42EFD3B6-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Mayer, Michael","last_name":"Mayer","first_name":"Michael"},{"last_name":"Burtscher","first_name":"Carmen M.","full_name":"Burtscher, Carmen M."},{"full_name":"Schirmer, Julia","last_name":"Schirmer","first_name":"Julia"},{"last_name":"Maier","first_name":"Brigitte","full_name":"Maier, Brigitte"},{"full_name":"Nairz, Manfred","first_name":"Manfred","last_name":"Nairz"},{"full_name":"Chwatal, Sabine","last_name":"Chwatal","first_name":"Sabine"},{"full_name":"Paulmichl, Markus","first_name":"Markus","last_name":"Paulmichl"}],"publication_status":"published","publisher":"S. Karger AG","year":"2000","pmid":1,"extern":"1"}]