[{"ddc":["572"],"related_material":{"record":[{"status":"public","id":"8340","relation":"dissertation_contains"}],"link":[{"description":"News on IST Website","relation":"press_release","url":"https://ist.ac.at/en/news/high-end-microscopy-reveals-structure-and-function-of-crucial-metabolic-enzyme/"}]},"isi":1,"title":"Structure and mechanism of mitochondrial proton-translocating transhydrogenase","external_id":{"pmid":["31462775"],"isi":["000485415400061"]},"ec_funded":1,"acknowledged_ssus":[{"_id":"ScienComp"}],"doi":"10.1038/s41586-019-1519-2","year":"2019","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","acknowledgement":" We thank R. Thompson, G. Effantin and V.-V. Hodirnau for their assistance with collecting NADP+, NADPH and apo datasets, respectively. Data processing was performed at the IST high-performance computing cluster.\r\nThis project has received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie Grant Agreement no. 665385.","project":[{"name":"International IST Doctoral Program","_id":"2564DBCA-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","grant_number":"665385"}],"quality_controlled":"1","oa_version":"Submitted Version","pmid":1,"_id":"6848","publication_identifier":{"eissn":["1476-4687"],"issn":["0028-0836"]},"oa":1,"volume":573,"date_updated":"2024-03-25T23:30:08Z","article_processing_charge":"No","author":[{"id":"37233050-F248-11E8-B48F-1D18A9856A87","first_name":"Domen","full_name":"Kampjut, Domen","last_name":"Kampjut"},{"id":"338D39FE-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0977-7989","full_name":"Sazanov, Leonid A","last_name":"Sazanov","first_name":"Leonid A"}],"abstract":[{"text":"Proton-translocating transhydrogenase (also known as nicotinamide nucleotide transhydrogenase (NNT)) is found in the plasma membranes of bacteria and the inner mitochondrial membranes of eukaryotes. NNT catalyses the transfer of a hydride between NADH and NADP+, coupled to the translocation of one proton across the membrane. Its main physiological function is the generation of NADPH, which is a substrate in anabolic reactions and a regulator of oxidative status; however, NNT may also fine-tune the Krebs cycle1,2. NNT deficiency causes familial glucocorticoid deficiency in humans and metabolic abnormalities in mice, similar to those observed in type II diabetes3,4. The catalytic mechanism of NNT has been proposed to involve a rotation of around 180° of the entire NADP(H)-binding domain that alternately participates in hydride transfer and proton-channel gating. However, owing to the lack of high-resolution structures of intact NNT, the details of this process remain unclear5,6. Here we present the cryo-electron microscopy structure of intact mammalian NNT in different conformational states. We show how the NADP(H)-binding domain opens the proton channel to the opposite sides of the membrane, and we provide structures of these two states. We also describe the catalytically important interfaces and linkers between the membrane and the soluble domains and their roles in nucleotide exchange. These structures enable us to propose a revised mechanism for a coupling process in NNT that is consistent with a large body of previous biochemical work. Our results are relevant to the development of currently unavailable NNT inhibitors, which may have therapeutic potential in ischaemia reperfusion injury, metabolic syndrome and some cancers7,8,9.","lang":"eng"}],"publication_status":"published","citation":{"ista":"Kampjut D, Sazanov LA. 2019. Structure and mechanism of mitochondrial proton-translocating transhydrogenase. Nature. 573(7773), 291–295.","short":"D. Kampjut, L.A. Sazanov, Nature 573 (2019) 291–295.","ama":"Kampjut D, Sazanov LA. Structure and mechanism of mitochondrial proton-translocating transhydrogenase. <i>Nature</i>. 2019;573(7773):291–295. doi:<a href=\"https://doi.org/10.1038/s41586-019-1519-2\">10.1038/s41586-019-1519-2</a>","mla":"Kampjut, Domen, and Leonid A. Sazanov. “Structure and Mechanism of Mitochondrial Proton-Translocating Transhydrogenase.” <i>Nature</i>, vol. 573, no. 7773, Springer Nature, 2019, pp. 291–295, doi:<a href=\"https://doi.org/10.1038/s41586-019-1519-2\">10.1038/s41586-019-1519-2</a>.","chicago":"Kampjut, Domen, and Leonid A Sazanov. “Structure and Mechanism of Mitochondrial Proton-Translocating Transhydrogenase.” <i>Nature</i>. Springer Nature, 2019. <a href=\"https://doi.org/10.1038/s41586-019-1519-2\">https://doi.org/10.1038/s41586-019-1519-2</a>.","apa":"Kampjut, D., &#38; Sazanov, L. A. (2019). Structure and mechanism of mitochondrial proton-translocating transhydrogenase. <i>Nature</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41586-019-1519-2\">https://doi.org/10.1038/s41586-019-1519-2</a>","ieee":"D. Kampjut and L. A. Sazanov, “Structure and mechanism of mitochondrial proton-translocating transhydrogenase,” <i>Nature</i>, vol. 573, no. 7773. Springer Nature, pp. 291–295, 2019."},"file":[{"relation":"main_file","content_type":"application/pdf","file_id":"8821","creator":"lsazanov","success":1,"access_level":"open_access","date_updated":"2020-11-26T16:33:44Z","file_size":3066206,"file_name":"Manuscript_final_acc_withFigs_SI_opt_red.pdf","checksum":"52728cda5210a3e9b74cc204e8aed3d5","date_created":"2020-11-26T16:33:44Z"}],"date_created":"2019-09-04T06:21:41Z","department":[{"_id":"LeSa"}],"has_accepted_license":"1","language":[{"iso":"eng"}],"publisher":"Springer Nature","scopus_import":"1","date_published":"2019-09-12T00:00:00Z","article_type":"letter_note","month":"09","file_date_updated":"2020-11-26T16:33:44Z","page":"291–295","issue":"7773","publication":"Nature","status":"public","intvolume":"       573","type":"journal_article","day":"12"},{"quality_controlled":"1","project":[{"grant_number":"742985","call_identifier":"H2020","name":"Tracing Evolution of Auxin Transport and Polarity in Plants","_id":"261099A6-B435-11E9-9278-68D0E5697425"}],"oa_version":"Submitted Version","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","publication_identifier":{"issn":["0028-0836"],"eissn":["1476-4687"]},"pmid":1,"_id":"6259","article_processing_charge":"No","volume":568,"oa":1,"date_updated":"2023-09-05T14:58:41Z","author":[{"full_name":"Cao, Min","last_name":"Cao","first_name":"Min"},{"full_name":"Chen, Rong","last_name":"Chen","first_name":"Rong"},{"full_name":"Li, Pan","last_name":"Li","first_name":"Pan"},{"first_name":"Yongqiang","last_name":"Yu","full_name":"Yu, Yongqiang"},{"first_name":"Rui","last_name":"Zheng","full_name":"Zheng, Rui"},{"first_name":"Danfeng","full_name":"Ge, Danfeng","last_name":"Ge"},{"first_name":"Wei","full_name":"Zheng, Wei","last_name":"Zheng"},{"first_name":"Xuhui","full_name":"Wang, Xuhui","last_name":"Wang"},{"first_name":"Yangtao","full_name":"Gu, Yangtao","last_name":"Gu"},{"orcid":"0000-0003-4783-1752","last_name":"Gelová","full_name":"Gelová, Zuzana","first_name":"Zuzana","id":"0AE74790-0E0B-11E9-ABC7-1ACFE5697425"},{"id":"4159519E-F248-11E8-B48F-1D18A9856A87","first_name":"Jiří","orcid":"0000-0002-8302-7596","full_name":"Friml, Jiří","last_name":"Friml"},{"first_name":"Heng","last_name":"Zhang","full_name":"Zhang, Heng"},{"full_name":"Liu, Renyi","last_name":"Liu","first_name":"Renyi"},{"last_name":"He","full_name":"He, Jun","first_name":"Jun"},{"last_name":"Xu","full_name":"Xu, Tongda","first_name":"Tongda"}],"abstract":[{"text":"The plant hormone auxin has crucial roles in almost all aspects of plant growth and development. Concentrations of auxin vary across different tissues, mediating distinct developmental outcomes and contributing to the functional diversity of auxin. However, the mechanisms that underlie these activities are poorly understood. Here we identify an auxin signalling mechanism, which acts in parallel to the canonical auxin pathway based on the transport inhibitor response1 (TIR1) and other auxin receptor F-box (AFB) family proteins (TIR1/AFB receptors)1,2, that translates levels of cellular auxin to mediate differential growth during apical-hook development. This signalling mechanism operates at the concave side of the apical hook, and involves auxin-mediated C-terminal cleavage of transmembrane kinase 1 (TMK1). The cytosolic and nucleus-translocated C terminus of TMK1 specifically interacts with and phosphorylates two non-canonical transcriptional repressors of the auxin or indole-3-acetic acid (Aux/IAA) family (IAA32 and IAA34), thereby regulating ARF transcription factors. In contrast to the degradation of Aux/IAA transcriptional repressors in the canonical pathway, the newly identified mechanism stabilizes the non-canonical IAA32 and IAA34 transcriptional repressors to regulate gene expression and ultimately inhibit growth. The auxin–TMK1 signalling pathway originates at the cell surface, is triggered by high levels of auxin and shares a partially overlapping set of transcription factors with the TIR1/AFB signalling pathway. This allows distinct interpretations of different concentrations of cellular auxin, and thus enables this versatile signalling molecule to mediate complex developmental outcomes.","lang":"eng"}],"citation":{"ama":"Cao M, Chen R, Li P, et al. TMK1-mediated auxin signalling regulates differential growth of the apical hook. <i>Nature</i>. 2019;568:240-243. doi:<a href=\"https://doi.org/10.1038/s41586-019-1069-7\">10.1038/s41586-019-1069-7</a>","mla":"Cao, Min, et al. “TMK1-Mediated Auxin Signalling Regulates Differential Growth of the Apical Hook.” <i>Nature</i>, vol. 568, Springer Nature, 2019, pp. 240–43, doi:<a href=\"https://doi.org/10.1038/s41586-019-1069-7\">10.1038/s41586-019-1069-7</a>.","short":"M. Cao, R. Chen, P. Li, Y. Yu, R. Zheng, D. Ge, W. Zheng, X. Wang, Y. Gu, Z. Gelová, J. Friml, H. Zhang, R. Liu, J. He, T. Xu, Nature 568 (2019) 240–243.","ista":"Cao M, Chen R, Li P, Yu Y, Zheng R, Ge D, Zheng W, Wang X, Gu Y, Gelová Z, Friml J, Zhang H, Liu R, He J, Xu T. 2019. TMK1-mediated auxin signalling regulates differential growth of the apical hook. Nature. 568, 240–243.","apa":"Cao, M., Chen, R., Li, P., Yu, Y., Zheng, R., Ge, D., … Xu, T. (2019). TMK1-mediated auxin signalling regulates differential growth of the apical hook. <i>Nature</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41586-019-1069-7\">https://doi.org/10.1038/s41586-019-1069-7</a>","ieee":"M. Cao <i>et al.</i>, “TMK1-mediated auxin signalling regulates differential growth of the apical hook,” <i>Nature</i>, vol. 568. Springer Nature, pp. 240–243, 2019.","chicago":"Cao, Min, Rong Chen, Pan Li, Yongqiang Yu, Rui Zheng, Danfeng Ge, Wei Zheng, et al. “TMK1-Mediated Auxin Signalling Regulates Differential Growth of the Apical Hook.” <i>Nature</i>. Springer Nature, 2019. <a href=\"https://doi.org/10.1038/s41586-019-1069-7\">https://doi.org/10.1038/s41586-019-1069-7</a>."},"publication_status":"published","ddc":["580"],"related_material":{"link":[{"relation":"press_release","description":"News on IST Homepage","url":"https://ist.ac.at/en/news/newly-discovered-mechanism-of-plant-hormone-auxin-acts-the-opposite-way/"}]},"isi":1,"external_id":{"pmid":["30944466"],"isi":["000464412700050"]},"title":"TMK1-mediated auxin signalling regulates differential growth of the apical hook","ec_funded":1,"doi":"10.1038/s41586-019-1069-7","year":"2019","page":"240-243","file_date_updated":"2020-11-13T07:37:41Z","publication":"Nature","status":"public","intvolume":"       568","type":"journal_article","day":"11","file":[{"file_name":"2019_Nature _Cao_accepted.pdf","file_size":4321328,"date_created":"2020-11-13T07:37:41Z","checksum":"6b84ab602a34382cf0340a37a1378c75","date_updated":"2020-11-13T07:37:41Z","access_level":"open_access","success":1,"content_type":"application/pdf","relation":"main_file","creator":"dernst","file_id":"8751"}],"date_created":"2019-04-09T08:37:05Z","department":[{"_id":"JiFr"}],"has_accepted_license":"1","language":[{"iso":"eng"}],"scopus_import":"1","publisher":"Springer Nature","date_published":"2019-04-11T00:00:00Z","article_type":"original","month":"04"},{"date_created":"2019-03-19T14:06:41Z","date_published":"2017-02-02T00:00:00Z","month":"02","language":[{"iso":"eng"}],"publisher":"Springer Nature","page":"43-48","publication":"Nature","issue":"7639","type":"journal_article","day":"02","status":"public","intvolume":"       542","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pubmed/28099418"}],"year":"2017","doi":"10.1038/nature20818","external_id":{"pmid":["    28099418"]},"title":"IL-17 is a neuromodulator of Caenorhabditis elegans sensory responses","date_updated":"2021-01-12T08:06:12Z","volume":542,"oa":1,"oa_version":"Submitted Version","quality_controlled":"1","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","publication_identifier":{"issn":["0028-0836","1476-4687"]},"extern":"1","pmid":1,"_id":"6117","citation":{"apa":"Chen, C., Itakura, E., Nelson, G. M., Sheng, M., Laurent, P., Fenk, L. A., … de Bono, M. (2017). IL-17 is a neuromodulator of Caenorhabditis elegans sensory responses. <i>Nature</i>. Springer Nature. <a href=\"https://doi.org/10.1038/nature20818\">https://doi.org/10.1038/nature20818</a>","ieee":"C. Chen <i>et al.</i>, “IL-17 is a neuromodulator of Caenorhabditis elegans sensory responses,” <i>Nature</i>, vol. 542, no. 7639. Springer Nature, pp. 43–48, 2017.","chicago":"Chen, Changchun, Eisuke Itakura, Geoffrey M. Nelson, Ming Sheng, Patrick Laurent, Lorenz A. Fenk, Rebecca A. Butcher, Ramanujan S. Hegde, and Mario de Bono. “IL-17 Is a Neuromodulator of Caenorhabditis Elegans Sensory Responses.” <i>Nature</i>. Springer Nature, 2017. <a href=\"https://doi.org/10.1038/nature20818\">https://doi.org/10.1038/nature20818</a>.","mla":"Chen, Changchun, et al. “IL-17 Is a Neuromodulator of Caenorhabditis Elegans Sensory Responses.” <i>Nature</i>, vol. 542, no. 7639, Springer Nature, 2017, pp. 43–48, doi:<a href=\"https://doi.org/10.1038/nature20818\">10.1038/nature20818</a>.","ama":"Chen C, Itakura E, Nelson GM, et al. IL-17 is a neuromodulator of Caenorhabditis elegans sensory responses. <i>Nature</i>. 2017;542(7639):43-48. doi:<a href=\"https://doi.org/10.1038/nature20818\">10.1038/nature20818</a>","ista":"Chen C, Itakura E, Nelson GM, Sheng M, Laurent P, Fenk LA, Butcher RA, Hegde RS, de Bono M. 2017. IL-17 is a neuromodulator of Caenorhabditis elegans sensory responses. Nature. 542(7639), 43–48.","short":"C. Chen, E. Itakura, G.M. Nelson, M. Sheng, P. Laurent, L.A. Fenk, R.A. Butcher, R.S. Hegde, M. de Bono, Nature 542 (2017) 43–48."},"publication_status":"published","author":[{"first_name":"Changchun","last_name":"Chen","full_name":"Chen, Changchun"},{"first_name":"Eisuke","full_name":"Itakura, Eisuke","last_name":"Itakura"},{"last_name":"Nelson","full_name":"Nelson, Geoffrey M.","first_name":"Geoffrey M."},{"first_name":"Ming","full_name":"Sheng, Ming","last_name":"Sheng"},{"full_name":"Laurent, Patrick","last_name":"Laurent","first_name":"Patrick"},{"first_name":"Lorenz A.","last_name":"Fenk","full_name":"Fenk, Lorenz A."},{"full_name":"Butcher, Rebecca A.","last_name":"Butcher","first_name":"Rebecca A."},{"last_name":"Hegde","full_name":"Hegde, Ramanujan S.","first_name":"Ramanujan S."},{"first_name":"Mario","orcid":"0000-0001-8347-0443","last_name":"de Bono","full_name":"de Bono, Mario","id":"4E3FF80E-F248-11E8-B48F-1D18A9856A87"}],"abstract":[{"lang":"eng","text":"Interleukin-17 (IL-17) is a major pro-inflammatory cytokine: it mediates responses to pathogens or tissue damage, and drives autoimmune diseases. Little is known about its role in the nervous system. Here we show that IL-17 has neuromodulator-like properties in Caenorhabditis elegans. IL-17 can act directly on neurons to alter their response properties and contribution to behaviour. Using unbiased genetic screens, we delineate an IL-17 signalling pathway and show that it acts in the RMG hub interneurons. Disrupting IL-17 signalling reduces RMG responsiveness to input from oxygen sensors, and renders sustained escape from 21% oxygen transient and contingent on additional stimuli. Over-activating IL-17 receptors abnormally heightens responses to 21% oxygen in RMG neurons and whole animals. IL-17 deficiency can be bypassed by optogenetic stimulation of RMG. Inducing IL-17 expression in adults can rescue mutant defects within 6 h. These findings reveal a non-immunological role of IL-17 modulating circuit function and behaviour."}]},{"issue":"7683","publication":"Nature","page":"84-87","intvolume":"       552","status":"public","day":"07","type":"journal_article","date_created":"2023-09-06T12:14:20Z","publisher":"Springer Nature","scopus_import":"1","language":[{"iso":"eng"}],"month":"12","article_type":"original","date_published":"2017-12-07T00:00:00Z","_id":"14290","pmid":1,"publication_identifier":{"eissn":["1476-4687"],"issn":["0028-0836"]},"extern":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","oa_version":"None","quality_controlled":"1","volume":552,"date_updated":"2023-11-07T12:24:49Z","article_processing_charge":"No","abstract":[{"lang":"eng","text":"DNA nanotechnology, in particular DNA origami, enables the bottom-up self-assembly of micrometre-scale, three-dimensional structures with nanometre-precise features1,2,3,4,5,6,7,8,9,10,11,12. These structures are customizable in that they can be site-specifically functionalized13 or constructed to exhibit machine-like14,15 or logic-gating behaviour16. Their use has been limited to applications that require only small amounts of material (of the order of micrograms), owing to the limitations of current production methods. But many proposed applications, for example as therapeutic agents or in complex materials3,16,17,18,19,20,21,22, could be realized if more material could be used. In DNA origami, a nanostructure is assembled from a very long single-stranded scaffold molecule held in place by many short single-stranded staple oligonucleotides. Only the bacteriophage-derived scaffold molecules are amenable to scalable and efficient mass production23; the shorter staple strands are obtained through costly solid-phase synthesis24 or enzymatic processes25. Here we show that single strands of DNA of virtually arbitrary length and with virtually arbitrary sequences can be produced in a scalable and cost-efficient manner by using bacteriophages to generate single-stranded precursor DNA that contains target strand sequences interleaved with self-excising ‘cassettes’, with each cassette comprising two Zn2+-dependent DNA-cleaving DNA enzymes. We produce all of the necessary single strands of DNA for several DNA origami using shaker-flask cultures, and demonstrate end-to-end production of macroscopic amounts of a DNA origami nanorod in a litre-scale stirred-tank bioreactor. Our method is compatible with existing DNA origami design frameworks and retains the modularity and addressability of DNA origami objects that are necessary for implementing custom modifications using functional groups. With all of the production and purification steps amenable to scaling, we expect that our method will expand the scope of DNA nanotechnology in many areas of science and technology."}],"author":[{"id":"dfec9381-4341-11ee-8fd8-faa02bba7d62","first_name":"Florian M","full_name":"Praetorius, Florian M","last_name":"Praetorius"},{"full_name":"Kick, Benjamin","last_name":"Kick","first_name":"Benjamin"},{"first_name":"Karl L.","full_name":"Behler, Karl L.","last_name":"Behler"},{"last_name":"Honemann","full_name":"Honemann, Maximilian N.","first_name":"Maximilian N."},{"first_name":"Dirk","full_name":"Weuster-Botz, Dirk","last_name":"Weuster-Botz"},{"full_name":"Dietz, Hendrik","last_name":"Dietz","first_name":"Hendrik"}],"publication_status":"published","citation":{"ieee":"F. M. Praetorius, B. Kick, K. L. Behler, M. N. Honemann, D. Weuster-Botz, and H. Dietz, “Biotechnological mass production of DNA origami,” <i>Nature</i>, vol. 552, no. 7683. Springer Nature, pp. 84–87, 2017.","apa":"Praetorius, F. M., Kick, B., Behler, K. L., Honemann, M. N., Weuster-Botz, D., &#38; Dietz, H. (2017). Biotechnological mass production of DNA origami. <i>Nature</i>. Springer Nature. <a href=\"https://doi.org/10.1038/nature24650\">https://doi.org/10.1038/nature24650</a>","chicago":"Praetorius, Florian M, Benjamin Kick, Karl L. Behler, Maximilian N. Honemann, Dirk Weuster-Botz, and Hendrik Dietz. “Biotechnological Mass Production of DNA Origami.” <i>Nature</i>. Springer Nature, 2017. <a href=\"https://doi.org/10.1038/nature24650\">https://doi.org/10.1038/nature24650</a>.","ama":"Praetorius FM, Kick B, Behler KL, Honemann MN, Weuster-Botz D, Dietz H. Biotechnological mass production of DNA origami. <i>Nature</i>. 2017;552(7683):84-87. doi:<a href=\"https://doi.org/10.1038/nature24650\">10.1038/nature24650</a>","mla":"Praetorius, Florian M., et al. “Biotechnological Mass Production of DNA Origami.” <i>Nature</i>, vol. 552, no. 7683, Springer Nature, 2017, pp. 84–87, doi:<a href=\"https://doi.org/10.1038/nature24650\">10.1038/nature24650</a>.","ista":"Praetorius FM, Kick B, Behler KL, Honemann MN, Weuster-Botz D, Dietz H. 2017. Biotechnological mass production of DNA origami. Nature. 552(7683), 84–87.","short":"F.M. Praetorius, B. Kick, K.L. Behler, M.N. Honemann, D. Weuster-Botz, H. Dietz, Nature 552 (2017) 84–87."},"title":"Biotechnological mass production of DNA origami","external_id":{"pmid":["29219963"]},"year":"2017","doi":"10.1038/nature24650"},{"year":"2016","doi":"10.1038/nature20110","external_id":{"pmid":["27760113"]},"title":"Mechanism for DNA transposons to generate introns on genomic scales","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5684705/"}],"citation":{"ieee":"J. T. Huff, D. Zilberman, and S. W. Roy, “Mechanism for DNA transposons to generate introns on genomic scales,” <i>Nature</i>, vol. 538, no. 7626. Springer Nature , pp. 533–536, 2016.","apa":"Huff, J. T., Zilberman, D., &#38; Roy, S. W. (2016). Mechanism for DNA transposons to generate introns on genomic scales. <i>Nature</i>. Springer Nature . <a href=\"https://doi.org/10.1038/nature20110\">https://doi.org/10.1038/nature20110</a>","chicago":"Huff, Jason T., Daniel Zilberman, and Scott W. Roy. “Mechanism for DNA Transposons to Generate Introns on Genomic Scales.” <i>Nature</i>. Springer Nature , 2016. <a href=\"https://doi.org/10.1038/nature20110\">https://doi.org/10.1038/nature20110</a>.","mla":"Huff, Jason T., et al. “Mechanism for DNA Transposons to Generate Introns on Genomic Scales.” <i>Nature</i>, vol. 538, no. 7626, Springer Nature , 2016, pp. 533–36, doi:<a href=\"https://doi.org/10.1038/nature20110\">10.1038/nature20110</a>.","ama":"Huff JT, Zilberman D, Roy SW. Mechanism for DNA transposons to generate introns on genomic scales. <i>Nature</i>. 2016;538(7626):533-536. doi:<a href=\"https://doi.org/10.1038/nature20110\">10.1038/nature20110</a>","ista":"Huff JT, Zilberman D, Roy SW. 2016. Mechanism for DNA transposons to generate introns on genomic scales. Nature. 538(7626), 533–536.","short":"J.T. Huff, D. Zilberman, S.W. Roy, Nature 538 (2016) 533–536."},"publication_status":"published","abstract":[{"lang":"eng","text":"The discovery of introns four decades ago was one of the most unexpected findings in molecular biology. Introns are sequences interrupting genes that must be removed as part of messenger RNA production. Genome sequencing projects have shown that most eukaryotic genes contain at least one intron, and frequently many. Comparison of these genomes reveals a history of long evolutionary periods during which few introns were gained, punctuated by episodes of rapid, extensive gain. However, although several detailed mechanisms for such episodic intron generation have been proposed, none has been empirically supported on a genomic scale. Here we show how short, non-autonomous DNA transposons independently generated hundreds to thousands of introns in the prasinophyte Micromonas pusilla and the pelagophyte Aureococcus anophagefferens. Each transposon carries one splice site. The other splice site is co-opted from the gene sequence that is duplicated upon transposon insertion, allowing perfect splicing out of the RNA. The distributions of sequences that can be co-opted are biased with respect to codons, and phasing of transposon-generated introns is similarly biased. These transposons insert between pre-existing nucleosomes, so that multiple nearby insertions generate nucleosome-sized intervening segments. Thus, transposon insertion and sequence co-option may explain the intron phase biases and prevalence of nucleosome-sized exons observed in eukaryotes. Overall, the two independent examples of proliferating elements illustrate a general DNA transposon mechanism that can plausibly account for episodes of rapid, extensive intron gain during eukaryotic evolution."}],"author":[{"first_name":"Jason T.","full_name":"Huff, Jason T.","last_name":"Huff"},{"id":"6973db13-dd5f-11ea-814e-b3e5455e9ed1","first_name":"Daniel","full_name":"Zilberman, Daniel","last_name":"Zilberman","orcid":"0000-0002-0123-8649"},{"full_name":"Roy, Scott W.","last_name":"Roy","first_name":"Scott W."}],"article_processing_charge":"No","oa":1,"date_updated":"2021-12-14T07:55:30Z","volume":538,"publication_identifier":{"issn":["0028-0836"],"eissn":["1476-4687"]},"extern":"1","pmid":1,"_id":"9456","oa_version":"Submitted Version","quality_controlled":"1","user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","month":"10","date_published":"2016-10-27T00:00:00Z","article_type":"letter_note","scopus_import":"1","publisher":"Springer Nature ","language":[{"iso":"eng"}],"department":[{"_id":"DaZi"}],"date_created":"2021-06-04T11:34:55Z","day":"27","type":"journal_article","intvolume":"       538","status":"public","publication":"Nature","issue":"7626","page":"533-536"},{"extern":"1","publication_identifier":{"eissn":["1476-4687"],"issn":["0028-0836"]},"_id":"9654","pmid":1,"oa_version":"None","quality_controlled":"1","user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","article_processing_charge":"No","date_updated":"2021-07-22T09:22:20Z","volume":540,"abstract":[{"text":"RNA polymerase I (Pol I) is a highly processive enzyme that transcribes ribosomal DNA (rDNA) and regulates growth of eukaryotic cells. Crystal structures of free Pol I from the yeast Saccharomyces cerevisiae have revealed dimers of the enzyme stabilized by a 'connector' element and an expanded cleft containing the active centre in an inactive conformation. The central bridge helix was unfolded and a Pol-I-specific 'expander' element occupied the DNA-template-binding site. The structure of Pol I in its active transcribing conformation has yet to be determined, whereas structures of Pol II and Pol III have been solved with bound DNA template and RNA transcript. Here we report structures of active transcribing Pol I from yeast solved by two different cryo-electron microscopy approaches. A single-particle structure at 3.8 Å resolution reveals a contracted active centre cleft with bound DNA and RNA, and a narrowed pore beneath the active site that no longer holds the RNA-cleavage-stimulating domain of subunit A12.2. A structure at 29 Å resolution that was determined from cryo-electron tomograms of Pol I enzymes transcribing cellular rDNA confirms contraction of the cleft and reveals that incoming and exiting rDNA enclose an angle of around 150°. The structures suggest a model for the regulation of transcription elongation in which contracted and expanded polymerase conformations are associated with active and inactive states, respectively.","lang":"eng"}],"author":[{"full_name":"Neyer, Simon","last_name":"Neyer","first_name":"Simon"},{"last_name":"Kunz","full_name":"Kunz, Michael","first_name":"Michael"},{"first_name":"Christian","last_name":"Geiss","full_name":"Geiss, Christian"},{"last_name":"Hantsche","full_name":"Hantsche, Merle","first_name":"Merle"},{"id":"3661B498-F248-11E8-B48F-1D18A9856A87","first_name":"Victor-Valentin","last_name":"Hodirnau","full_name":"Hodirnau, Victor-Valentin"},{"first_name":"Anja","last_name":"Seybert","full_name":"Seybert, Anja"},{"first_name":"Christoph","full_name":"Engel, Christoph","last_name":"Engel"},{"first_name":"Margot P.","full_name":"Scheffer, Margot P.","last_name":"Scheffer"},{"full_name":"Cramer, Patrick","last_name":"Cramer","first_name":"Patrick"},{"first_name":"Achilleas S.","last_name":"Frangakis","full_name":"Frangakis, Achilleas S."}],"citation":{"ama":"Neyer S, Kunz M, Geiss C, et al. Structure of RNA polymerase I transcribing ribosomal DNA genes. <i>Nature</i>. 2016;540(7634):607-610. doi:<a href=\"https://doi.org/10.1038/nature20561\">10.1038/nature20561</a>","mla":"Neyer, Simon, et al. “Structure of RNA Polymerase I Transcribing Ribosomal DNA Genes.” <i>Nature</i>, vol. 540, no. 7634, Springer Nature, 2016, pp. 607–10, doi:<a href=\"https://doi.org/10.1038/nature20561\">10.1038/nature20561</a>.","ista":"Neyer S, Kunz M, Geiss C, Hantsche M, Hodirnau V-V, Seybert A, Engel C, Scheffer MP, Cramer P, Frangakis AS. 2016. Structure of RNA polymerase I transcribing ribosomal DNA genes. Nature. 540(7634), 607–610.","short":"S. Neyer, M. Kunz, C. Geiss, M. Hantsche, V.-V. Hodirnau, A. Seybert, C. Engel, M.P. Scheffer, P. Cramer, A.S. Frangakis, Nature 540 (2016) 607–610.","apa":"Neyer, S., Kunz, M., Geiss, C., Hantsche, M., Hodirnau, V.-V., Seybert, A., … Frangakis, A. S. (2016). Structure of RNA polymerase I transcribing ribosomal DNA genes. <i>Nature</i>. Springer Nature. <a href=\"https://doi.org/10.1038/nature20561\">https://doi.org/10.1038/nature20561</a>","ieee":"S. Neyer <i>et al.</i>, “Structure of RNA polymerase I transcribing ribosomal DNA genes,” <i>Nature</i>, vol. 540, no. 7634. Springer Nature, pp. 607–610, 2016.","chicago":"Neyer, Simon, Michael Kunz, Christian Geiss, Merle Hantsche, Victor-Valentin Hodirnau, Anja Seybert, Christoph Engel, Margot P. Scheffer, Patrick Cramer, and Achilleas S. Frangakis. “Structure of RNA Polymerase I Transcribing Ribosomal DNA Genes.” <i>Nature</i>. Springer Nature, 2016. <a href=\"https://doi.org/10.1038/nature20561\">https://doi.org/10.1038/nature20561</a>."},"publication_status":"published","title":"Structure of RNA polymerase I transcribing ribosomal DNA genes","external_id":{"pmid":["27842382"]},"year":"2016","doi":"10.1038/nature20561","publication":"Nature","issue":"7634","page":"607-610","intvolume":"       540","status":"public","day":"22","type":"journal_article","date_created":"2021-07-14T09:04:24Z","scopus_import":"1","publisher":"Springer Nature","language":[{"iso":"eng"}],"month":"12","article_type":"letter_note","date_published":"2016-12-22T00:00:00Z"},{"date_created":"2018-12-11T11:54:25Z","department":[{"_id":"JiFr"},{"_id":"Bio"},{"_id":"EvBe"}],"language":[{"iso":"eng"}],"publisher":"Nature Publishing Group","scopus_import":"1","article_type":"original","date_published":"2014-12-04T00:00:00Z","month":"12","page":"90 - 93","issue":"729","publication":"Nature","status":"public","intvolume":"       516","type":"journal_article","day":"04","main_file_link":[{"url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4257754/","open_access":"1"}],"title":"Inhibition of cell expansion by rapid ABP1-mediated auxin effect on microtubules","external_id":{"pmid":["25409144"]},"ec_funded":1,"year":"2014","doi":"10.1038/nature13889","acknowledgement":"We thank R. Dixit for performing complementary experiments, D. W. Ehrhardt and T. Hashimoto for providing the seeds of TUB6–RFP and EB1b–GFP respectively, E. Zazimalova, J. Petrasek and M. Fendrych for discussing the manuscript and J. Leung for text optimization. This work was supported by the European Research Council (project ERC-2011-StG-20101109-PSDP, to J.F.), ANR blanc AuxiWall project (ANR-11-BSV5-0007, to C.P.-R. and L.G.) and the Agency for Innovation by Science and Technology (IWT) (to H.R.). This work benefited from the facilities and expertise of the Imagif Cell Biology platform (http://www.imagif.cnrs.fr), which is supported by the Conseil Général de l’Essonne.","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","project":[{"grant_number":"282300","call_identifier":"FP7","_id":"25716A02-B435-11E9-9278-68D0E5697425","name":"Polarity and subcellular dynamics in plants"}],"oa_version":"Submitted Version","quality_controlled":"1","pmid":1,"_id":"1862","publication_identifier":{"eissn":["1476-4687"],"issn":["0028-0836"]},"date_updated":"2025-05-07T11:12:31Z","oa":1,"publist_id":"5237","volume":516,"article_processing_charge":"No","author":[{"first_name":"Xu","full_name":"Chen, Xu","last_name":"Chen","id":"4E5ADCAA-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Laurie","full_name":"Grandont, Laurie","last_name":"Grandont"},{"id":"33CA54A6-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5039-9660","last_name":"Li","full_name":"Li, Hongjiang","first_name":"Hongjiang"},{"orcid":"0000-0001-9843-3522","full_name":"Hauschild, Robert","last_name":"Hauschild","first_name":"Robert","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Sébastien","last_name":"Paque","full_name":"Paque, Sébastien"},{"last_name":"Abuzeineh","full_name":"Abuzeineh, Anas","first_name":"Anas"},{"first_name":"Hana","last_name":"Rakusova","full_name":"Rakusova, Hana","id":"4CAAA450-78D2-11EA-8E57-B40A396E08BA"},{"id":"38F4F166-F248-11E8-B48F-1D18A9856A87","last_name":"Benková","full_name":"Benková, Eva","orcid":"0000-0002-8510-9739","first_name":"Eva"},{"last_name":"Perrot Rechenmann","full_name":"Perrot Rechenmann, Catherine","first_name":"Catherine"},{"id":"4159519E-F248-11E8-B48F-1D18A9856A87","first_name":"Jirí","orcid":"0000-0002-8302-7596","last_name":"Friml","full_name":"Friml, Jirí"}],"abstract":[{"text":"The prominent and evolutionarily ancient role of the plant hormone auxin is the regulation of cell expansion. Cell expansion requires ordered arrangement of the cytoskeleton but molecular mechanisms underlying its regulation by signalling molecules including auxin are unknown. Here we show in the model plant Arabidopsis thaliana that in elongating cells exogenous application of auxin or redistribution of endogenous auxin induces very rapid microtubule re-orientation from transverse to longitudinal, coherent with the inhibition of cell expansion. This fast auxin effect requires auxin binding protein 1 (ABP1) and involves a contribution of downstream signalling components such as ROP6 GTPase, ROP-interactive protein RIC1 and the microtubule-severing protein katanin. These components are required for rapid auxin-and ABP1-mediated re-orientation of microtubules to regulate cell elongation in roots and dark-grown hypocotyls as well as asymmetric growth during gravitropic responses.","lang":"eng"}],"publication_status":"published","citation":{"apa":"Chen, X., Grandont, L., Li, H., Hauschild, R., Paque, S., Abuzeineh, A., … Friml, J. (2014). Inhibition of cell expansion by rapid ABP1-mediated auxin effect on microtubules. <i>Nature</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/nature13889\">https://doi.org/10.1038/nature13889</a>","ieee":"X. Chen <i>et al.</i>, “Inhibition of cell expansion by rapid ABP1-mediated auxin effect on microtubules,” <i>Nature</i>, vol. 516, no. 729. Nature Publishing Group, pp. 90–93, 2014.","chicago":"Chen, Xu, Laurie Grandont, Hongjiang Li, Robert Hauschild, Sébastien Paque, Anas Abuzeineh, Hana Rakusova, Eva Benková, Catherine Perrot Rechenmann, and Jiří Friml. “Inhibition of Cell Expansion by Rapid ABP1-Mediated Auxin Effect on Microtubules.” <i>Nature</i>. Nature Publishing Group, 2014. <a href=\"https://doi.org/10.1038/nature13889\">https://doi.org/10.1038/nature13889</a>.","ama":"Chen X, Grandont L, Li H, et al. Inhibition of cell expansion by rapid ABP1-mediated auxin effect on microtubules. <i>Nature</i>. 2014;516(729):90-93. doi:<a href=\"https://doi.org/10.1038/nature13889\">10.1038/nature13889</a>","mla":"Chen, Xu, et al. “Inhibition of Cell Expansion by Rapid ABP1-Mediated Auxin Effect on Microtubules.” <i>Nature</i>, vol. 516, no. 729, Nature Publishing Group, 2014, pp. 90–93, doi:<a href=\"https://doi.org/10.1038/nature13889\">10.1038/nature13889</a>.","ista":"Chen X, Grandont L, Li H, Hauschild R, Paque S, Abuzeineh A, Rakusova H, Benková E, Perrot Rechenmann C, Friml J. 2014. Inhibition of cell expansion by rapid ABP1-mediated auxin effect on microtubules. Nature. 516(729), 90–93.","short":"X. Chen, L. Grandont, H. Li, R. Hauschild, S. Paque, A. Abuzeineh, H. Rakusova, E. Benková, C. Perrot Rechenmann, J. Friml, Nature 516 (2014) 90–93."}},{"publication_status":"published","day":"23","citation":{"chicago":"Persson, Annelie, Einav Gross, Patrick Laurent, Karl Emanuel Busch, Hugo Bretes, and Mario de Bono. “Natural Variation in a Neural Globin Tunes Oxygen Sensing in Wild Caenorhabditis Elegans.” <i>Nature</i>. Springer Nature, 2009. <a href=\"https://doi.org/10.1038/nature07820\">https://doi.org/10.1038/nature07820</a>.","apa":"Persson, A., Gross, E., Laurent, P., Busch, K. E., Bretes, H., &#38; de Bono, M. (2009). Natural variation in a neural globin tunes oxygen sensing in wild Caenorhabditis elegans. <i>Nature</i>. Springer Nature. <a href=\"https://doi.org/10.1038/nature07820\">https://doi.org/10.1038/nature07820</a>","ieee":"A. Persson, E. Gross, P. Laurent, K. E. Busch, H. Bretes, and M. de Bono, “Natural variation in a neural globin tunes oxygen sensing in wild Caenorhabditis elegans,” <i>Nature</i>, vol. 458, no. 7241. Springer Nature, pp. 1030–1033, 2009.","short":"A. Persson, E. Gross, P. Laurent, K.E. Busch, H. Bretes, M. de Bono, Nature 458 (2009) 1030–1033.","ista":"Persson A, Gross E, Laurent P, Busch KE, Bretes H, de Bono M. 2009. Natural variation in a neural globin tunes oxygen sensing in wild Caenorhabditis elegans. Nature. 458(7241), 1030–1033.","mla":"Persson, Annelie, et al. “Natural Variation in a Neural Globin Tunes Oxygen Sensing in Wild Caenorhabditis Elegans.” <i>Nature</i>, vol. 458, no. 7241, Springer Nature, 2009, pp. 1030–33, doi:<a href=\"https://doi.org/10.1038/nature07820\">10.1038/nature07820</a>.","ama":"Persson A, Gross E, Laurent P, Busch KE, Bretes H, de Bono M. Natural variation in a neural globin tunes oxygen sensing in wild Caenorhabditis elegans. <i>Nature</i>. 2009;458(7241):1030-1033. doi:<a href=\"https://doi.org/10.1038/nature07820\">10.1038/nature07820</a>"},"type":"journal_article","intvolume":"       458","abstract":[{"text":"Behaviours evolve by iterations of natural selection, but we have few insights into the molecular and neural mechanisms involved. Here we show that some Caenorhabditis elegans wild strains switch between two foraging behaviours in response to subtle changes in ambient oxygen. This finely tuned switch is conferred by a naturally variable hexacoordinated globin, GLB-5. GLB-5 acts with the atypical soluble guanylate cyclases1,2,3, which are a different type of oxygen binding protein, to tune the dynamic range of oxygen-sensing neurons close to atmospheric (21%) concentrations. Calcium imaging indicates that one group of these neurons is activated when oxygen rises towards 21%, and is inhibited as oxygen drops below 21%. The soluble guanylate cyclase GCY-35 is required for high oxygen to activate the neurons; GLB-5 provides inhibitory input when oxygen decreases below 21%. Together, these oxygen binding proteins tune neuronal and behavioural responses to a narrow oxygen concentration range close to atmospheric levels. The effect of the glb-5 gene on oxygen sensing and foraging is modified by the naturally variable neuropeptide receptor npr-1 (refs 4, 5), providing insights into how polygenic variation reshapes neural circuit function.","lang":"eng"}],"author":[{"first_name":"Annelie","last_name":"Persson","full_name":"Persson, Annelie"},{"last_name":"Gross","full_name":"Gross, Einav","first_name":"Einav"},{"last_name":"Laurent","full_name":"Laurent, Patrick","first_name":"Patrick"},{"last_name":"Busch","full_name":"Busch, Karl Emanuel","first_name":"Karl Emanuel"},{"first_name":"Hugo","last_name":"Bretes","full_name":"Bretes, Hugo"},{"id":"4E3FF80E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8347-0443","last_name":"de Bono","full_name":"de Bono, Mario","first_name":"Mario"}],"status":"public","issue":"7241","publication":"Nature","date_updated":"2021-01-12T08:06:20Z","volume":458,"page":"1030-1033","_id":"6144","pmid":1,"publication_identifier":{"issn":["0028-0836","1476-4687"]},"extern":"1","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","quality_controlled":"1","oa_version":"None","doi":"10.1038/nature07820","month":"04","year":"2009","date_published":"2009-04-23T00:00:00Z","publisher":"Springer Nature","title":"Natural variation in a neural globin tunes oxygen sensing in wild Caenorhabditis elegans","external_id":{"pmid":["19262507"]},"language":[{"iso":"eng"}],"date_created":"2019-03-21T07:48:44Z"},{"year":"2009","doi":"10.1038/nature08131","title":"Photoconductance and inverse photoconductance in films of functionalized metal nanoparticles","external_id":{"pmid":["19606145"]},"citation":{"mla":"Nakanishi, Hideyuki, et al. “Photoconductance and Inverse Photoconductance in Films of Functionalized Metal Nanoparticles.” <i>Nature</i>, vol. 460, no. 7253, Springer Nature, 2009, pp. 371–75, doi:<a href=\"https://doi.org/10.1038/nature08131\">10.1038/nature08131</a>.","ama":"Nakanishi H, Bishop KJM, Kowalczyk B, et al. Photoconductance and inverse photoconductance in films of functionalized metal nanoparticles. <i>Nature</i>. 2009;460(7253):371-375. doi:<a href=\"https://doi.org/10.1038/nature08131\">10.1038/nature08131</a>","ista":"Nakanishi H, Bishop KJM, Kowalczyk B, Nitzan A, Weiss EA, Tretiakov KV, Apodaca MM, Klajn R, Stoddart JF, Grzybowski BA. 2009. Photoconductance and inverse photoconductance in films of functionalized metal nanoparticles. Nature. 460(7253), 371–375.","short":"H. Nakanishi, K.J.M. Bishop, B. Kowalczyk, A. Nitzan, E.A. Weiss, K.V. Tretiakov, M.M. Apodaca, R. Klajn, J.F. Stoddart, B.A. Grzybowski, Nature 460 (2009) 371–375.","ieee":"H. Nakanishi <i>et al.</i>, “Photoconductance and inverse photoconductance in films of functionalized metal nanoparticles,” <i>Nature</i>, vol. 460, no. 7253. Springer Nature, pp. 371–375, 2009.","apa":"Nakanishi, H., Bishop, K. J. M., Kowalczyk, B., Nitzan, A., Weiss, E. A., Tretiakov, K. V., … Grzybowski, B. A. (2009). Photoconductance and inverse photoconductance in films of functionalized metal nanoparticles. <i>Nature</i>. Springer Nature. <a href=\"https://doi.org/10.1038/nature08131\">https://doi.org/10.1038/nature08131</a>","chicago":"Nakanishi, Hideyuki, Kyle J. M. Bishop, Bartlomiej Kowalczyk, Abraham Nitzan, Emily A. Weiss, Konstantin V. Tretiakov, Mario M. Apodaca, Rafal Klajn, J. Fraser Stoddart, and Bartosz A. Grzybowski. “Photoconductance and Inverse Photoconductance in Films of Functionalized Metal Nanoparticles.” <i>Nature</i>. Springer Nature, 2009. <a href=\"https://doi.org/10.1038/nature08131\">https://doi.org/10.1038/nature08131</a>."},"publication_status":"published","abstract":[{"lang":"eng","text":"In traditional photoconductors1,2,3, the impinging light generates mobile charge carriers in the valence and/or conduction bands, causing the material’s conductivity to increase4. Such positive photoconductance is observed in both bulk and nanostructured5,6 photoconductors. Here we describe a class of nanoparticle-based materials whose conductivity can either increase or decrease on irradiation with visible light of wavelengths close to the particles’ surface plasmon resonance. The remarkable feature of these plasmonic materials is that the sign of the conductivity change and the nature of the electron transport between the nanoparticles depend on the molecules comprising the self-assembled monolayers (SAMs)7,8 stabilizing the nanoparticles. For SAMs made of electrically neutral (polar and non-polar) molecules, conductivity increases on irradiation. If, however, the SAMs contain electrically charged (either negatively or positively) groups, conductivity decreases. The optical and electrical characteristics of these previously undescribed inverse photoconductors can be engineered flexibly by adjusting the material properties of the nanoparticles and of the coating SAMs. In particular, in films comprising mixtures of different nanoparticles or nanoparticles coated with mixed SAMs, the overall photoconductance is a weighted average of the changes induced by the individual components. These and other observations can be rationalized in terms of light-induced creation of mobile charge carriers whose transport through the charged SAMs is inhibited by carrier trapping in transient polaron-like states9,10. The nanoparticle-based photoconductors we describe could have uses in chemical sensors and/or in conjunction with flexible substrates."}],"keyword":["Multidisciplinary"],"author":[{"full_name":"Nakanishi, Hideyuki","last_name":"Nakanishi","first_name":"Hideyuki"},{"first_name":"Kyle J. M.","full_name":"Bishop, Kyle J. M.","last_name":"Bishop"},{"last_name":"Kowalczyk","full_name":"Kowalczyk, Bartlomiej","first_name":"Bartlomiej"},{"first_name":"Abraham","last_name":"Nitzan","full_name":"Nitzan, Abraham"},{"full_name":"Weiss, Emily A.","last_name":"Weiss","first_name":"Emily A."},{"last_name":"Tretiakov","full_name":"Tretiakov, Konstantin V.","first_name":"Konstantin V."},{"first_name":"Mario M.","last_name":"Apodaca","full_name":"Apodaca, Mario M."},{"id":"8e84690e-1e48-11ed-a02b-a1e6fb8bb53b","last_name":"Klajn","full_name":"Klajn, Rafal","first_name":"Rafal"},{"full_name":"Stoddart, J. Fraser","last_name":"Stoddart","first_name":"J. Fraser"},{"full_name":"Grzybowski, Bartosz A.","last_name":"Grzybowski","first_name":"Bartosz A."}],"article_processing_charge":"No","volume":460,"date_updated":"2023-08-08T09:00:59Z","publication_identifier":{"issn":["0028-0836"],"eissn":["1476-4687"]},"extern":"1","_id":"13418","pmid":1,"oa_version":"None","quality_controlled":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","month":"07","date_published":"2009-07-16T00:00:00Z","article_type":"original","scopus_import":"1","publisher":"Springer Nature","language":[{"iso":"eng"}],"date_created":"2023-08-01T10:29:50Z","day":"16","type":"journal_article","intvolume":"       460","status":"public","publication":"Nature","issue":"7253","page":"371-375"},{"day":"06","type":"journal_article","intvolume":"       456","status":"public","publication":"Nature","issue":"7218","page":"125-129","month":"11","article_type":"letter_note","date_published":"2008-11-06T00:00:00Z","scopus_import":"1","publisher":"Springer Nature","language":[{"iso":"eng"}],"department":[{"_id":"DaZi"}],"date_created":"2021-06-04T11:49:32Z","citation":{"short":"D. Zilberman, D. Coleman-Derr, T. Ballinger, S. Henikoff, Nature 456 (2008) 125–129.","ista":"Zilberman D, Coleman-Derr D, Ballinger T, Henikoff S. 2008. Histone H2A.Z and DNA methylation are mutually antagonistic chromatin marks. Nature. 456(7218), 125–129.","ama":"Zilberman D, Coleman-Derr D, Ballinger T, Henikoff S. Histone H2A.Z and DNA methylation are mutually antagonistic chromatin marks. <i>Nature</i>. 2008;456(7218):125-129. doi:<a href=\"https://doi.org/10.1038/nature07324\">10.1038/nature07324</a>","mla":"Zilberman, Daniel, et al. “Histone H2A.Z and DNA Methylation Are Mutually Antagonistic Chromatin Marks.” <i>Nature</i>, vol. 456, no. 7218, Springer Nature, 2008, pp. 125–29, doi:<a href=\"https://doi.org/10.1038/nature07324\">10.1038/nature07324</a>.","chicago":"Zilberman, Daniel, Devin Coleman-Derr, Tracy Ballinger, and Steven Henikoff. “Histone H2A.Z and DNA Methylation Are Mutually Antagonistic Chromatin Marks.” <i>Nature</i>. Springer Nature, 2008. <a href=\"https://doi.org/10.1038/nature07324\">https://doi.org/10.1038/nature07324</a>.","ieee":"D. Zilberman, D. Coleman-Derr, T. Ballinger, and S. Henikoff, “Histone H2A.Z and DNA methylation are mutually antagonistic chromatin marks,” <i>Nature</i>, vol. 456, no. 7218. Springer Nature, pp. 125–129, 2008.","apa":"Zilberman, D., Coleman-Derr, D., Ballinger, T., &#38; Henikoff, S. (2008). Histone H2A.Z and DNA methylation are mutually antagonistic chromatin marks. <i>Nature</i>. Springer Nature. <a href=\"https://doi.org/10.1038/nature07324\">https://doi.org/10.1038/nature07324</a>"},"publication_status":"published","abstract":[{"lang":"eng","text":"Eukaryotic chromatin is separated into functional domains differentiated by posttranslational histone modifications, histone variants, and DNA methylation1–6. Methylation is associated with repression of transcriptional initiation in plants and animals, and is frequently found in transposable elements. Proper methylation patterns are critical for eukaryotic development4,5, and aberrant methylation-induced silencing of tumor suppressor genes is a common feature of human cancer7. In contrast to methylation, the histone variant H2A.Z is preferentially deposited by the Swr1 ATPase complex near 5′ ends of genes where it promotes transcriptional competence8–20. How DNA methylation and H2A.Z influence transcription remains largely unknown. Here we show that in the plant Arabidopsis thaliana, regions of DNA methylation are quantitatively deficient in H2A.Z. Exclusion of H2A.Z is seen at sites of DNA methylation in the bodies of actively transcribed genes and in methylated transposons. Mutation of the MET1 DNA methyltransferase, which causes both losses and gains of DNA methylation4,5, engenders opposite changes in H2A.Z deposition, while mutation of the PIE1 subunit of the Swr1 complex that deposits H2A.Z17 leads to genome-wide hypermethylation. Our findings indicate that DNA methylation can influence chromatin structure and effect gene silencing by excluding H2A.Z, and that H2A.Z protects genes from DNA methylation."}],"author":[{"id":"6973db13-dd5f-11ea-814e-b3e5455e9ed1","first_name":"Daniel","orcid":"0000-0002-0123-8649","full_name":"Zilberman, Daniel","last_name":"Zilberman"},{"first_name":"Devin","last_name":"Coleman-Derr","full_name":"Coleman-Derr, Devin"},{"first_name":"Tracy","full_name":"Ballinger, Tracy","last_name":"Ballinger"},{"last_name":"Henikoff","full_name":"Henikoff, Steven","first_name":"Steven"}],"keyword":["Multidisciplinary"],"article_processing_charge":"No","volume":456,"oa":1,"date_updated":"2021-12-14T08:54:36Z","publication_identifier":{"issn":["0028-0836"],"eissn":["1476-4687"]},"extern":"1","_id":"9457","pmid":1,"quality_controlled":"1","oa_version":"Submitted Version","user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","year":"2008","doi":"10.1038/nature07324","title":"Histone H2A.Z and DNA methylation are mutually antagonistic chromatin marks","external_id":{"pmid":["18815594"]},"main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2877514/"}]},{"volume":424,"date_updated":"2022-07-18T08:57:40Z","article_processing_charge":"No","_id":"11121","pmid":1,"extern":"1","publication_identifier":{"issn":["0028-0836"],"eissn":["1476-4687"]},"user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","oa_version":"None","quality_controlled":"1","publication_status":"published","citation":{"apa":"Walther, T. C., Askjaer, P., Gentzel, M., Habermann, A., Griffiths, G., Wilm, M., … Hetzer, M. (2003). RanGTP mediates nuclear pore complex assembly. <i>Nature</i>. Springer Nature. <a href=\"https://doi.org/10.1038/nature01898\">https://doi.org/10.1038/nature01898</a>","ieee":"T. C. Walther <i>et al.</i>, “RanGTP mediates nuclear pore complex assembly,” <i>Nature</i>, vol. 424, no. 6949. Springer Nature, pp. 689–694, 2003.","chicago":"Walther, Tobias C., Peter Askjaer, Marc Gentzel, Anja Habermann, Gareth Griffiths, Matthias Wilm, Iain W. Mattaj, and Martin Hetzer. “RanGTP Mediates Nuclear Pore Complex Assembly.” <i>Nature</i>. Springer Nature, 2003. <a href=\"https://doi.org/10.1038/nature01898\">https://doi.org/10.1038/nature01898</a>.","ama":"Walther TC, Askjaer P, Gentzel M, et al. RanGTP mediates nuclear pore complex assembly. <i>Nature</i>. 2003;424(6949):689-694. doi:<a href=\"https://doi.org/10.1038/nature01898\">10.1038/nature01898</a>","mla":"Walther, Tobias C., et al. “RanGTP Mediates Nuclear Pore Complex Assembly.” <i>Nature</i>, vol. 424, no. 6949, Springer Nature, 2003, pp. 689–94, doi:<a href=\"https://doi.org/10.1038/nature01898\">10.1038/nature01898</a>.","ista":"Walther TC, Askjaer P, Gentzel M, Habermann A, Griffiths G, Wilm M, Mattaj IW, Hetzer M. 2003. RanGTP mediates nuclear pore complex assembly. Nature. 424(6949), 689–694.","short":"T.C. Walther, P. Askjaer, M. Gentzel, A. Habermann, G. Griffiths, M. Wilm, I.W. Mattaj, M. Hetzer, Nature 424 (2003) 689–694."},"abstract":[{"text":"In metazoa, the nuclear envelope breaks down and reforms during each cell cycle. Nuclear pore complexes (NPCs), which serve as channels for transport between the nucleus and cytoplasm1, assemble into the reforming nuclear envelope in a sequential process involving association of a subset of NPC proteins, nucleoporins, with chromatin followed by the formation of a closed nuclear envelope fenestrated by NPCs2,3,4,5,6,7. How chromatin recruitment of nucleoporins and NPC assembly are regulated is unknown. Here we demonstrate that RanGTP production is required to dissociate nucleoporins Nup107, Nup153 and Nup358 from Importin β, to target them to chromatin and to induce association between separate NPC subcomplexes. Additionally, either an excess of RanGTP or removal of Importin β induces formation of NPC-containing membrane structures—annulate lamellae—both in vitro in the absence of chromatin and in vivo. Annulate lamellae formation is strongly and specifically inhibited by an excess of Importin β. The data demonstrate that RanGTP triggers distinct steps of NPC assembly, and suggest a mechanism for the spatial restriction of NPC assembly to the surface of chromatin.","lang":"eng"}],"keyword":["Multidisciplinary"],"author":[{"full_name":"Walther, Tobias C.","last_name":"Walther","first_name":"Tobias C."},{"full_name":"Askjaer, Peter","last_name":"Askjaer","first_name":"Peter"},{"last_name":"Gentzel","full_name":"Gentzel, Marc","first_name":"Marc"},{"full_name":"Habermann, Anja","last_name":"Habermann","first_name":"Anja"},{"first_name":"Gareth","last_name":"Griffiths","full_name":"Griffiths, Gareth"},{"first_name":"Matthias","last_name":"Wilm","full_name":"Wilm, Matthias"},{"first_name":"Iain W.","full_name":"Mattaj, Iain W.","last_name":"Mattaj"},{"id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","first_name":"Martin W","last_name":"HETZER","full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X"}],"doi":"10.1038/nature01898","year":"2003","external_id":{"pmid":["12894213"]},"title":"RanGTP mediates nuclear pore complex assembly","issue":"6949","publication":"Nature","page":"689-694","day":"30","type":"journal_article","intvolume":"       424","status":"public","date_created":"2022-04-07T07:57:02Z","month":"07","article_type":"original","date_published":"2003-07-30T00:00:00Z","publisher":"Springer Nature","scopus_import":"1","language":[{"iso":"eng"}]},{"year":"2002","doi":"10.1038/415806a","title":"Lateral relocation of auxin efflux regulator PIN3 mediates tropism in Arabidopsis","external_id":{"pmid":["11845211 "]},"citation":{"mla":"Friml, Jiří, et al. “Lateral Relocation of Auxin Efflux Regulator PIN3 Mediates Tropism in Arabidopsis.” <i>Nature</i>, vol. 415, no. 6873, Nature Publishing Group, 2002, pp. 806–09, doi:<a href=\"https://doi.org/10.1038/415806a\">10.1038/415806a</a>.","ama":"Friml J, Wiśniewska J, Benková E, Mendgen K, Palme K. Lateral relocation of auxin efflux regulator PIN3 mediates tropism in Arabidopsis. <i>Nature</i>. 2002;415(6873):806-809. doi:<a href=\"https://doi.org/10.1038/415806a\">10.1038/415806a</a>","ista":"Friml J, Wiśniewska J, Benková E, Mendgen K, Palme K. 2002. Lateral relocation of auxin efflux regulator PIN3 mediates tropism in Arabidopsis. Nature. 415(6873), 806–809.","short":"J. Friml, J. Wiśniewska, E. Benková, K. Mendgen, K. Palme, Nature 415 (2002) 806–809.","ieee":"J. Friml, J. Wiśniewska, E. Benková, K. Mendgen, and K. Palme, “Lateral relocation of auxin efflux regulator PIN3 mediates tropism in Arabidopsis,” <i>Nature</i>, vol. 415, no. 6873. Nature Publishing Group, pp. 806–809, 2002.","apa":"Friml, J., Wiśniewska, J., Benková, E., Mendgen, K., &#38; Palme, K. (2002). Lateral relocation of auxin efflux regulator PIN3 mediates tropism in Arabidopsis. <i>Nature</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/415806a\">https://doi.org/10.1038/415806a</a>","chicago":"Friml, Jiří, Justyna Wiśniewska, Eva Benková, Kurt Mendgen, and Klaus Palme. “Lateral Relocation of Auxin Efflux Regulator PIN3 Mediates Tropism in Arabidopsis.” <i>Nature</i>. Nature Publishing Group, 2002. <a href=\"https://doi.org/10.1038/415806a\">https://doi.org/10.1038/415806a</a>."},"publication_status":"published","abstract":[{"text":"Long-standing models propose that plant growth responses to light or gravity are mediated by asymmetric distribution of the phytohormone auxin. Physiological studies implicated a specific transport system that relocates auxin laterally, thereby effecting differential growth; however, neither the molecular components of this system nor the cellular mechanism of auxin redistribution on light or gravity perception have been identified. Here, we show that auxin accumulates asymmetrically during differential growth in an efflux-dependent manner. Mutations in the Arabidopsis gene PIN3, a regulator of auxin efflux, alter differential growth. PIN3 is expressed in gravity-sensing tissues, with PIN3 protein accumulating predominantly at the lateral cell surface. PIN3 localizes to the plasma membrane and to vesicles that cycle in an actin-dependent manner. In the root columella, PIN3 is positioned symmetrically at the plasma membrane but rapidly relocalizes laterally on gravity stimulation. Our data indicate that PIN3 is a component of the lateral auxin transport system regulating tropic growth. In addition, actin-dependent relocalization of PIN3 in response to gravity provides a mechanism for redirecting auxin flux to trigger asymmetric growth.","lang":"eng"}],"author":[{"id":"4159519E-F248-11E8-B48F-1D18A9856A87","full_name":"Friml, Jirí","last_name":"Friml","orcid":"0000-0002-8302-7596","first_name":"Jirí"},{"first_name":"Justyna","full_name":"Wiśniewska, Justyna","last_name":"Wiśniewska"},{"first_name":"Eva","last_name":"Benková","full_name":"Benková, Eva","orcid":"0000-0002-8510-9739","id":"38F4F166-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Kurt","last_name":"Mendgen","full_name":"Mendgen, Kurt"},{"full_name":"Palme, Klaus","last_name":"Palme","first_name":"Klaus"}],"article_processing_charge":"No","date_updated":"2023-07-18T07:30:27Z","publist_id":"3715","volume":415,"publication_identifier":{"issn":["0028-0836"]},"extern":"1","_id":"2986","pmid":1,"quality_controlled":"1","oa_version":"None","acknowledgement":"We thank G. Jürgens for enabling J.F. to accomplish part of this work in his laboratory; P. Tänzler and M. Sauer for technical assistance; H. Vahlenkamp for technical assistance in immunocytochemistry; M. Estelle for providing material and suggestions; T. Altman for BAC filter sets; the ADIS (Automated DNA Isolation and Sequencing) service group for DNA sequencing; ZIGIA (Center for Functional Genomics in Arabidopsis) for the En lines; and N. Geldner, T. Hamann, G. Jürgens, K. Schrick and C. Schwechheimer for comments and critical reading of the manuscript. This work was supported by a fellowship of the DAAD (J.F.), the DFG (Schwerpunktprogramm Phytohormone), the Fonds der chemischen Industrie, the European Communities Biotechnology Programs, the INCO-Copernicus Program and the European Space Agency MAP-Biotechnology Programme","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","month":"02","date_published":"2002-02-14T00:00:00Z","article_type":"original","scopus_import":"1","publisher":"Nature Publishing Group","language":[{"iso":"eng"}],"date_created":"2018-12-11T12:00:42Z","day":"14","type":"journal_article","intvolume":"       415","status":"public","publication":"Nature","issue":"6873","page":"806 - 809"},{"volume":419,"date_updated":"2021-01-12T08:06:26Z","page":"925-929","issue":"6910","publication":"Nature","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","oa_version":"None","quality_controlled":"1","pmid":1,"_id":"6158","extern":"1","publication_identifier":{"issn":["0028-0836"]},"type":"journal_article","publication_status":"published","day":"31","citation":{"apa":"Coates, J. C., &#38; de Bono, M. (2002). Antagonistic pathways in neurons exposed to body fluid regulate social feeding in Caenorhabditis elegans. <i>Nature</i>. Springer Nature. <a href=\"https://doi.org/10.1038/nature01170\">https://doi.org/10.1038/nature01170</a>","ieee":"J. C. Coates and M. de Bono, “Antagonistic pathways in neurons exposed to body fluid regulate social feeding in Caenorhabditis elegans,” <i>Nature</i>, vol. 419, no. 6910. Springer Nature, pp. 925–929, 2002.","chicago":"Coates, Juliet C., and Mario de Bono. “Antagonistic Pathways in Neurons Exposed to Body Fluid Regulate Social Feeding in Caenorhabditis Elegans.” <i>Nature</i>. Springer Nature, 2002. <a href=\"https://doi.org/10.1038/nature01170\">https://doi.org/10.1038/nature01170</a>.","ama":"Coates JC, de Bono M. Antagonistic pathways in neurons exposed to body fluid regulate social feeding in Caenorhabditis elegans. <i>Nature</i>. 2002;419(6910):925-929. doi:<a href=\"https://doi.org/10.1038/nature01170\">10.1038/nature01170</a>","mla":"Coates, Juliet C., and Mario de Bono. “Antagonistic Pathways in Neurons Exposed to Body Fluid Regulate Social Feeding in Caenorhabditis Elegans.” <i>Nature</i>, vol. 419, no. 6910, Springer Nature, 2002, pp. 925–29, doi:<a href=\"https://doi.org/10.1038/nature01170\">10.1038/nature01170</a>.","ista":"Coates JC, de Bono M. 2002. Antagonistic pathways in neurons exposed to body fluid regulate social feeding in Caenorhabditis elegans. Nature. 419(6910), 925–929.","short":"J.C. Coates, M. de Bono, Nature 419 (2002) 925–929."},"status":"public","author":[{"full_name":"Coates, Juliet C.","last_name":"Coates","first_name":"Juliet C."},{"id":"4E3FF80E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8347-0443","full_name":"de Bono, Mario","last_name":"de Bono","first_name":"Mario"}],"abstract":[{"text":"Wild isolates of Caenorhabditis elegans can feed either alone or in groups1,2. This natural variation in behaviour is associated with a single residue difference in NPR-1, a predicted G-protein-coupled neuropeptide receptor related to Neuropeptide Y receptors2. Here we show that the NPR-1 isoform associated with solitary feeding acts in neurons exposed to the body fluid to inhibit social feeding. Furthermore, suppressing the activity of these neurons, called AQR, PQR and URX, using an activated K+ channel, inhibits social feeding. NPR-1 activity in AQR, PQR and URX neurons seems to suppress social feeding by antagonizing signalling through a cyclic GMP-gated ion channel encoded by tax-2 and tax-4. We show that mutations in tax-2 or tax-4 disrupt social feeding, and that tax-4 is required in several neurons for social feeding, including one or more of AQR, PQR and URX. The AQR, PQR and URX neurons are unusual in C. elegans because they are directly exposed to the pseudocoelomic body fluid3. Our data suggest a model in which these neurons integrate antagonistic signals to control the choice between social and solitary feeding behaviour.","lang":"eng"}],"intvolume":"       419","date_created":"2019-03-21T10:09:20Z","date_published":"2002-10-31T00:00:00Z","doi":"10.1038/nature01170","month":"10","year":"2002","language":[{"iso":"eng"}],"publisher":"Springer Nature","title":"Antagonistic pathways in neurons exposed to body fluid regulate social feeding in Caenorhabditis elegans","external_id":{"pmid":["12410311"]}},{"date_created":"2019-03-21T10:27:04Z","title":"Social feeding in Caenorhabditis elegans is induced by neurons that detect aversive stimuli","external_id":{"pmid":["12410303"]},"publisher":"Springer Nature","language":[{"iso":"eng"}],"year":"2002","month":"10","doi":"10.1038/nature01169","date_published":"2002-10-31T00:00:00Z","extern":"1","publication_identifier":{"issn":["0028-0836"]},"pmid":1,"_id":"6159","quality_controlled":"1","oa_version":"None","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","publication":"Nature","issue":"6910","page":"899-903","volume":419,"date_updated":"2021-01-12T08:06:27Z","intvolume":"       419","abstract":[{"lang":"eng","text":"Natural Caenorhabditis elegans isolates exhibit either social or solitary feeding on bacteria. We show here that social feeding is induced by nociceptive neurons that detect adverse or stressful conditions. Ablation of the nociceptive neurons ASH and ADL transforms social animals into solitary feeders. Social feeding is probably due to the sensation of noxious chemicals by ASH and ADL neurons; it requires the genes ocr-2 and osm-9, which encode TRP-related transduction channels, and odr-4 and odr-8, which are required to localize sensory chemoreceptors to cilia. Other sensory neurons may suppress social feeding, as social feeding in ocr-2 and odr-4 mutants is restored by mutations in osm-3, a gene required for the development of 26 ciliated sensory neurons. Our data suggest a model for regulation of social feeding by opposing sensory inputs: aversive inputs to nociceptive neurons promote social feeding, whereas antagonistic inputs from neurons that express osm-3 inhibit aggregation."}],"status":"public","author":[{"id":"4E3FF80E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8347-0443","last_name":"de Bono","full_name":"de Bono, Mario","first_name":"Mario"},{"first_name":"David M.","last_name":"Tobin","full_name":"Tobin, David M."},{"first_name":"M. Wayne","last_name":"Davis","full_name":"Davis, M. Wayne"},{"first_name":"Leon","last_name":"Avery","full_name":"Avery, Leon"},{"first_name":"Cornelia I.","full_name":"Bargmann, Cornelia I.","last_name":"Bargmann"}],"citation":{"mla":"de Bono, Mario, et al. “Social Feeding in Caenorhabditis Elegans Is Induced by Neurons That Detect Aversive Stimuli.” <i>Nature</i>, vol. 419, no. 6910, Springer Nature, 2002, pp. 899–903, doi:<a href=\"https://doi.org/10.1038/nature01169\">10.1038/nature01169</a>.","ama":"de Bono M, Tobin DM, Davis MW, Avery L, Bargmann CI. Social feeding in Caenorhabditis elegans is induced by neurons that detect aversive stimuli. <i>Nature</i>. 2002;419(6910):899-903. doi:<a href=\"https://doi.org/10.1038/nature01169\">10.1038/nature01169</a>","ista":"de Bono M, Tobin DM, Davis MW, Avery L, Bargmann CI. 2002. Social feeding in Caenorhabditis elegans is induced by neurons that detect aversive stimuli. Nature. 419(6910), 899–903.","short":"M. de Bono, D.M. Tobin, M.W. Davis, L. Avery, C.I. Bargmann, Nature 419 (2002) 899–903.","ieee":"M. de Bono, D. M. Tobin, M. W. Davis, L. Avery, and C. I. Bargmann, “Social feeding in Caenorhabditis elegans is induced by neurons that detect aversive stimuli,” <i>Nature</i>, vol. 419, no. 6910. Springer Nature, pp. 899–903, 2002.","apa":"de Bono, M., Tobin, D. M., Davis, M. W., Avery, L., &#38; Bargmann, C. I. (2002). Social feeding in Caenorhabditis elegans is induced by neurons that detect aversive stimuli. <i>Nature</i>. Springer Nature. <a href=\"https://doi.org/10.1038/nature01169\">https://doi.org/10.1038/nature01169</a>","chicago":"Bono, Mario de, David M. Tobin, M. Wayne Davis, Leon Avery, and Cornelia I. Bargmann. “Social Feeding in Caenorhabditis Elegans Is Induced by Neurons That Detect Aversive Stimuli.” <i>Nature</i>. Springer Nature, 2002. <a href=\"https://doi.org/10.1038/nature01169\">https://doi.org/10.1038/nature01169</a>."},"day":"31","publication_status":"published","type":"journal_article"},{"citation":{"ista":"Cremer S, Sledge M, Heinze J. 2002. Chemical mimicry: Male ants disguised by the queen’s bouquet. Nature. 419, 897–897.","short":"S. Cremer, M. Sledge, J. Heinze, Nature 419 (2002) 897–897.","mla":"Cremer, Sylvia, et al. “Chemical Mimicry: Male Ants Disguised by the Queen’s Bouquet.” <i>Nature</i>, vol. 419, Nature Publishing Group, 2002, pp. 897–897, doi:<a href=\"https://doi.org/10.1038/419897a\">10.1038/419897a</a>.","ama":"Cremer S, Sledge M, Heinze J. Chemical mimicry: Male ants disguised by the queen’s bouquet. <i>Nature</i>. 2002;419:897-897. doi:<a href=\"https://doi.org/10.1038/419897a\">10.1038/419897a</a>","chicago":"Cremer, Sylvia, Matthew Sledge, and Jürgen Heinze. “Chemical Mimicry: Male Ants Disguised by the Queen’s Bouquet.” <i>Nature</i>. Nature Publishing Group, 2002. <a href=\"https://doi.org/10.1038/419897a\">https://doi.org/10.1038/419897a</a>.","ieee":"S. Cremer, M. Sledge, and J. Heinze, “Chemical mimicry: Male ants disguised by the queen’s bouquet,” <i>Nature</i>, vol. 419. Nature Publishing Group, pp. 897–897, 2002.","apa":"Cremer, S., Sledge, M., &#38; Heinze, J. (2002). Chemical mimicry: Male ants disguised by the queen’s bouquet. <i>Nature</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/419897a\">https://doi.org/10.1038/419897a</a>"},"publication_status":"published","author":[{"id":"2F64EC8C-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-2193-3868","last_name":"Cremer","full_name":"Cremer, Sylvia","first_name":"Sylvia"},{"last_name":"Sledge","full_name":"Sledge, Matthew","first_name":"Matthew"},{"last_name":"Heinze","full_name":"Heinze, Jürgen","first_name":"Jürgen"}],"abstract":[{"lang":"eng","text":"Males of the tropical ant Cardiocondyla obscurior are either wingless and aggressive or winged and docile, and both compete for access to virgin queens in the nest1, 2. Although the fighter males (ergatoids) attack and kill other ergatoids, they tolerate and even attempt to mate with their winged rivals. Here we show that the winged males avoid the aggression of wingless males by mimicking the chemical bouquet of virgin queens, but that their mating success is not reduced as a result. This example of female mimicry by vigorous males is surprising, as in other species it is typically used as a protective strategy by weaker males, and may explain the coexistence and equal mating success of two male morphs."}],"article_processing_charge":"No","publist_id":"2230","date_updated":"2023-06-13T11:47:19Z","volume":419,"quality_controlled":"1","oa_version":"None","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","extern":"1","publication_identifier":{"issn":["0028-0836"]},"_id":"3925","pmid":1,"year":"2002","doi":"10.1038/419897a","external_id":{"pmid":["12410300"]},"title":"Chemical mimicry: Male ants disguised by the queen's bouquet","type":"journal_article","day":"31","status":"public","intvolume":"       419","page":"897 - 897","publication":"Nature","date_published":"2002-10-31T00:00:00Z","article_type":"original","month":"10","language":[{"iso":"eng"}],"scopus_import":"1","publisher":"Nature Publishing Group","date_created":"2018-12-11T12:05:55Z"},{"year":"2001","doi":"10.1038/35096571","external_id":{"pmid":["11574889"]},"title":"Auxin transport inhibitors block PIN1 cycling and vesicle trafficking","volume":413,"date_updated":"2023-05-16T11:51:44Z","publist_id":"3719","article_processing_charge":"No","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","quality_controlled":"1","oa_version":"None","pmid":1,"_id":"2983","extern":"1","publication_identifier":{"issn":["0028-0836"]},"publication_status":"published","citation":{"chicago":"Geldner, Niko, Jiří Friml, York Stierhof, Gerd Jürgens, and Klaus Palme. “Auxin Transport Inhibitors Block PIN1 Cycling and Vesicle Trafficking.” <i>Nature</i>. Nature Publishing Group, 2001. <a href=\"https://doi.org/10.1038/35096571\">https://doi.org/10.1038/35096571</a>.","ieee":"N. Geldner, J. Friml, Y. Stierhof, G. Jürgens, and K. Palme, “Auxin transport inhibitors block PIN1 cycling and vesicle trafficking,” <i>Nature</i>, vol. 413, no. 6854. Nature Publishing Group, pp. 425–428, 2001.","apa":"Geldner, N., Friml, J., Stierhof, Y., Jürgens, G., &#38; Palme, K. (2001). Auxin transport inhibitors block PIN1 cycling and vesicle trafficking. <i>Nature</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/35096571\">https://doi.org/10.1038/35096571</a>","ista":"Geldner N, Friml J, Stierhof Y, Jürgens G, Palme K. 2001. Auxin transport inhibitors block PIN1 cycling and vesicle trafficking. Nature. 413(6854), 425–428.","short":"N. Geldner, J. Friml, Y. Stierhof, G. Jürgens, K. Palme, Nature 413 (2001) 425–428.","ama":"Geldner N, Friml J, Stierhof Y, Jürgens G, Palme K. Auxin transport inhibitors block PIN1 cycling and vesicle trafficking. <i>Nature</i>. 2001;413(6854):425-428. doi:<a href=\"https://doi.org/10.1038/35096571\">10.1038/35096571</a>","mla":"Geldner, Niko, et al. “Auxin Transport Inhibitors Block PIN1 Cycling and Vesicle Trafficking.” <i>Nature</i>, vol. 413, no. 6854, Nature Publishing Group, 2001, pp. 425–28, doi:<a href=\"https://doi.org/10.1038/35096571\">10.1038/35096571</a>."},"author":[{"first_name":"Niko","full_name":"Geldner, Niko","last_name":"Geldner"},{"first_name":"Jirí","orcid":"0000-0002-8302-7596","full_name":"Friml, Jirí","last_name":"Friml","id":"4159519E-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Stierhof, York","last_name":"Stierhof","first_name":"York"},{"last_name":"Jürgens","full_name":"Jürgens, Gerd","first_name":"Gerd"},{"full_name":"Palme, Klaus","last_name":"Palme","first_name":"Klaus"}],"abstract":[{"text":"Polar transport of the phytohormone auxin mediates various processes in plant growth and development, such as apical dominance, tropisms, vascular patterning and axis formation. This view is based largely on the effects of polar auxin transport inhibitors. These compounds disrupt auxin efflux from the cell but their mode of action is unknown. It is thought that polar auxin flux is caused by the asymmetric distribution of efflux carriers acting at the plasma membrane. The polar localization of efflux carrier candidate PIN1 supports this model. Here we show that the seemingly static localization of PIN1 results from rapid actin-dependent cycling between the plasma membrane and endosomal compartments. Auxin transport inhibitors block PIN1 cycling and inhibit trafficking of membrane proteins that are unrelated to auxin transport. Our data suggest that PIN1 cycling is of central importance for auxin transport and that auxin transport inhibitors affect efflux by generally interfering with membrane-trafficking processes. In support of our conclusion, the vesicle-trafficking inhibitor brefeldin A mimics physiological effects of auxin transport inhibitors.","lang":"eng"}],"date_created":"2018-12-11T12:00:41Z","article_type":"letter_note","date_published":"2001-09-27T00:00:00Z","month":"09","language":[{"iso":"eng"}],"publisher":"Nature Publishing Group","scopus_import":"1","page":"425 - 428","issue":"6854","publication":"Nature","type":"journal_article","day":"27","status":"public","intvolume":"       413"},{"title":"Silberblick/Wnt11 mediates convergent extension movements during zebrafish gastrulation","external_id":{"pmid":["10811221 "]},"doi":"10.1038/35011068","year":"2000","abstract":[{"text":"Vertebrate gastrulation involves the specification and coordinated movement of large populations of cells that give rise to the ectodermal, mesodermal and endodermal germ layers. Although many of the genes involved in the specification of cell identity during this process have been identified, little is known of the genes that coordinate cell movement. Here we show that the zebrafish silberblick (slb) locus(1) encodes Wnt11 and that Slb/Wnt11 activity is required for cells to undergo correct convergent extension movements during gastrulation. In the absence of Slb/Wnt11 function, abnormal extension of axial tissue results in cyclopia and other midline defects in the head(2). The requirement for Slb/Wnt11 is cell non-autonomous, and our results indicate that the correct extension of axial tissue is at least partly dependent on medio-lateral cell intercalation in paraxial tissue. We also show that the slb phenotype is rescued by a truncated form of Dishevelled that does not signal through the canonical Wnt pathway(3), suggesting that, as in flies(4), Wnt signalling might mediate morphogenetic events through a divergent signal transduction cascade. Our results provide genetic and experimental evidence that Wnt activity in lateral tissues has a crucial role in driving the convergent extension movements underlying vertebrate gastrulation.","lang":"eng"}],"author":[{"orcid":"0000-0002-0912-4566","full_name":"Heisenberg, Carl-Philipp J","last_name":"Heisenberg","first_name":"Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Masazumi","last_name":"Tada","full_name":"Tada, Masazumi"},{"last_name":"Rauch","full_name":"Rauch, Gerd","first_name":"Gerd"},{"first_name":"Leonor","last_name":"Saúde","full_name":"Saúde, Leonor"},{"first_name":"Miguel","last_name":"Concha","full_name":"Concha, Miguel"},{"first_name":"Robert","last_name":"Geisler","full_name":"Geisler, Robert"},{"first_name":"Derek","last_name":"Stemple","full_name":"Stemple, Derek"},{"first_name":"James","full_name":"Smith, James","last_name":"Smith"},{"first_name":"Stephen","last_name":"Wilson","full_name":"Wilson, Stephen"}],"citation":{"chicago":"Heisenberg, Carl-Philipp J, Masazumi Tada, Gerd Rauch, Leonor Saúde, Miguel Concha, Robert Geisler, Derek Stemple, James Smith, and Stephen Wilson. “Silberblick/Wnt11 Mediates Convergent Extension Movements during Zebrafish Gastrulation.” <i>Nature</i>. Nature Publishing Group, 2000. <a href=\"https://doi.org/10.1038/35011068\">https://doi.org/10.1038/35011068</a>.","ieee":"C.-P. J. Heisenberg <i>et al.</i>, “Silberblick/Wnt11 mediates convergent extension movements during zebrafish gastrulation,” <i>Nature</i>, vol. 405, no. 6782. Nature Publishing Group, pp. 76–81, 2000.","apa":"Heisenberg, C.-P. J., Tada, M., Rauch, G., Saúde, L., Concha, M., Geisler, R., … Wilson, S. (2000). Silberblick/Wnt11 mediates convergent extension movements during zebrafish gastrulation. <i>Nature</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/35011068\">https://doi.org/10.1038/35011068</a>","short":"C.-P.J. Heisenberg, M. Tada, G. Rauch, L. Saúde, M. Concha, R. Geisler, D. Stemple, J. Smith, S. Wilson, Nature 405 (2000) 76–81.","ista":"Heisenberg C-PJ, Tada M, Rauch G, Saúde L, Concha M, Geisler R, Stemple D, Smith J, Wilson S. 2000. Silberblick/Wnt11 mediates convergent extension movements during zebrafish gastrulation. Nature. 405(6782), 76–81.","mla":"Heisenberg, Carl-Philipp J., et al. “Silberblick/Wnt11 Mediates Convergent Extension Movements during Zebrafish Gastrulation.” <i>Nature</i>, vol. 405, no. 6782, Nature Publishing Group, 2000, pp. 76–81, doi:<a href=\"https://doi.org/10.1038/35011068\">10.1038/35011068</a>.","ama":"Heisenberg C-PJ, Tada M, Rauch G, et al. Silberblick/Wnt11 mediates convergent extension movements during zebrafish gastrulation. <i>Nature</i>. 2000;405(6782):76-81. doi:<a href=\"https://doi.org/10.1038/35011068\">10.1038/35011068</a>"},"publication_status":"published","publication_identifier":{"issn":["0028-0836"]},"extern":"1","_id":"4197","pmid":1,"oa_version":"None","quality_controlled":"1","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","article_processing_charge":"No","publist_id":"1921","volume":405,"date_updated":"2023-04-19T14:40:45Z","scopus_import":"1","publisher":"Nature Publishing Group","language":[{"iso":"eng"}],"month":"05","article_type":"original","date_published":"2000-05-04T00:00:00Z","date_created":"2018-12-11T12:07:32Z","intvolume":"       405","status":"public","day":"04","type":"journal_article","publication":"Nature","issue":"6782","page":"76 - 81"},{"publication_status":"published","citation":{"ama":"Partridge L, Barton NH. Evolving evolvability. <i>Nature</i>. 2000;407(6803):457-458. doi:<a href=\"https://doi.org/10.1038/35035173\">10.1038/35035173</a>","mla":"Partridge, Linda, and Nicholas H. Barton. “Evolving Evolvability.” <i>Nature</i>, vol. 407, no. 6803, Nature Publishing Group, 2000, pp. 457–58, doi:<a href=\"https://doi.org/10.1038/35035173\">10.1038/35035173</a>.","short":"L. Partridge, N.H. Barton, Nature 407 (2000) 457–458.","ista":"Partridge L, Barton NH. 2000. Evolving evolvability. Nature. 407(6803), 457–458.","apa":"Partridge, L., &#38; Barton, N. H. (2000). Evolving evolvability. <i>Nature</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/35035173\">https://doi.org/10.1038/35035173</a>","ieee":"L. Partridge and N. H. Barton, “Evolving evolvability,” <i>Nature</i>, vol. 407, no. 6803. Nature Publishing Group, pp. 457–458, 2000.","chicago":"Partridge, Linda, and Nicholas H Barton. “Evolving Evolvability.” <i>Nature</i>. Nature Publishing Group, 2000. <a href=\"https://doi.org/10.1038/35035173\">https://doi.org/10.1038/35035173</a>."},"day":"01","type":"review","intvolume":"       407","author":[{"full_name":"Partridge, Linda","last_name":"Partridge","first_name":"Linda"},{"first_name":"Nicholas H","orcid":"0000-0002-8548-5240","last_name":"Barton","full_name":"Barton, Nicholas H","id":"4880FE40-F248-11E8-B48F-1D18A9856A87"}],"status":"public","issue":"6803","publication":"Nature","publist_id":"1823","volume":407,"date_updated":"2023-04-19T14:37:19Z","page":"457 - 458","article_processing_charge":"No","_id":"4268","publication_identifier":{"issn":["0028-0836"]},"extern":"1","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","quality_controlled":"1","oa_version":"None","month":"09","doi":"10.1038/35035173","year":"2000","date_published":"2000-09-01T00:00:00Z","publisher":"Nature Publishing Group","scopus_import":"1","title":"Evolving evolvability","language":[{"iso":"eng"}],"date_created":"2018-12-11T12:07:57Z"},{"day":"01","type":"journal_article","intvolume":"       400","status":"public","publication":"Nature","issue":"6742","page":"351 - 354","month":"07","date_published":"1999-07-01T00:00:00Z","article_type":"original","scopus_import":"1","publisher":"Nature Publishing Group","language":[{"iso":"eng"}],"date_created":"2018-12-11T11:49:00Z","citation":{"apa":"Kondrashov, A., &#38; Kondrashov, F. (1999). Interactions among quantitative traits in the course of sympatric speciation. <i>Nature</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/22514\">https://doi.org/10.1038/22514</a>","ieee":"A. Kondrashov and F. Kondrashov, “Interactions among quantitative traits in the course of sympatric speciation,” <i>Nature</i>, vol. 400, no. 6742. Nature Publishing Group, pp. 351–354, 1999.","chicago":"Kondrashov, Alexey, and Fyodor Kondrashov. “Interactions among Quantitative Traits in the Course of Sympatric Speciation.” <i>Nature</i>. Nature Publishing Group, 1999. <a href=\"https://doi.org/10.1038/22514\">https://doi.org/10.1038/22514</a>.","mla":"Kondrashov, Alexey, and Fyodor Kondrashov. “Interactions among Quantitative Traits in the Course of Sympatric Speciation.” <i>Nature</i>, vol. 400, no. 6742, Nature Publishing Group, 1999, pp. 351–54, doi:<a href=\"https://doi.org/10.1038/22514\">10.1038/22514</a>.","ama":"Kondrashov A, Kondrashov F. Interactions among quantitative traits in the course of sympatric speciation. <i>Nature</i>. 1999;400(6742):351-354. doi:<a href=\"https://doi.org/10.1038/22514\">10.1038/22514</a>","ista":"Kondrashov A, Kondrashov F. 1999. Interactions among quantitative traits in the course of sympatric speciation. Nature. 400(6742), 351–354.","short":"A. Kondrashov, F. Kondrashov, Nature 400 (1999) 351–354."},"publication_status":"published","abstract":[{"text":"Sympatric speciation, the origin of two or more species from a single local population, has almost certainly been involved in formation of several species flocks, and may be fairly common in nature. The most straightforward scenario for sympatric speciation requires disruptive selection favouring two substantially different phenotypes, and consists of the evolution of reproductive isolation between them followed by the elimination of all intermediate phenotypes. Here we use the hypergeometric phenotypic model to show that sympatric speciation is possible even when fitness and mate choice depend on different quantitative traits, so that speciation must involve formation of covariance between these traits. The increase in the number of variable loci affecting fitness facilitates sympatric speciation, whereas the increase in the number of variable loci affecting mate choice has the opposite effect. These predictions may enable more cases of sympatric speciation to be identified.","lang":"eng"}],"author":[{"first_name":"Alexey","last_name":"Kondrashov","full_name":"Kondrashov, Alexey"},{"id":"44FDEF62-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8243-4694","last_name":"Kondrashov","full_name":"Kondrashov, Fyodor","first_name":"Fyodor"}],"article_processing_charge":"No","date_updated":"2023-04-13T10:33:44Z","publist_id":"6761","volume":400,"extern":"1","publication_identifier":{"issn":["0028-0836"]},"pmid":1,"_id":"883","quality_controlled":"1","oa_version":"None","acknowledgement":"This study was supported by a grant from the NSF.","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","year":"1999","doi":"10.1038/22514","external_id":{"pmid":["10432111"]},"title":"Interactions among quantitative traits in the course of sympatric speciation"},{"intvolume":"       396","status":"public","day":"17","type":"journal_article","issue":"6712","publication":"Nature","page":"683 - 687","publisher":"Nature Publishing Group","scopus_import":"1","language":[{"iso":"eng"}],"month":"12","article_type":"original","date_published":"1998-12-17T00:00:00Z","date_created":"2018-12-11T11:58:32Z","abstract":[{"text":"B-type receptors for the neurotransmitter GABA (γ-aminobutyric acid) inhibit neuronal activity through G-protein-coupled second-messenger systems, which regulate the release of neurotransmitters and the activity of ion channels and adenylyl cyclase. Physiological and biochemical studies show that there are differences in drug efficiencies at different GABA(B) receptors, so it is expected that GABA(B)-receptor (GABA(B)R) subtypes exist. Two GABA(B)-receptor splice variants have been cloned (GABA(B)R1a and GABA(B)R1b), but native GABA(B) receptors and recombinant receptors showed unexplained differences in agonist-binding potencies. Moreover, the activation of presumed effector ion channels in heterologous cells expressing the recombinant receptors proved difficult. Here we describe a new GABA(B) receptor subtype, GABA(B)R2, which does not bind available GABA(B) antagonists with measurable potency. GABA(B)R1a, GABA(B)R1b and GABA(B)R2 alone do not activate Kir3-type potassium channels efficiently, but co- expression of these receptors yields a robust coupling to activation of Kir3 channels. We provide evidence for the assembly of heteromeric GABA(B) receptors in vivo and show that GABA(B)R2 and GABA(B)R1a/b proteins immunoprecipitate and localize together at dendritic spines. The heteromeric receptor complexes exhibit a significant increase in agonist- and partial- agonist-binding potencies as compared with individual receptors and probably represent the predominant native GABA(B) receptor. Heteromeric assembly among G-protein-coupled receptors has not, to our knowledge, been described before.\r\n","lang":"eng"}],"author":[{"first_name":"Klemens","last_name":"Kaupmann","full_name":"Kaupmann, Klemens"},{"last_name":"Malitschek","full_name":"Malitschek, Barbara","first_name":"Barbara"},{"first_name":"Valérie","full_name":"Schuler, Valérie","last_name":"Schuler"},{"full_name":"Heid, Jacob","last_name":"Heid","first_name":"Jacob"},{"first_name":"Wolfgang","last_name":"Froestl","full_name":"Froestl, Wolfgang"},{"last_name":"Beck","full_name":"Beck, Pascal","first_name":"Pascal"},{"first_name":"Johannes","last_name":"Mosbacher","full_name":"Mosbacher, Johannes"},{"first_name":"Serge","full_name":"Bischoff, Serge","last_name":"Bischoff"},{"last_name":"Kulik","full_name":"Kulik, Ákos","first_name":"Ákos"},{"first_name":"Ryuichi","orcid":"0000-0001-8761-9444","full_name":"Shigemoto, Ryuichi","last_name":"Shigemoto","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Andreas","last_name":"Karschin","full_name":"Karschin, Andreas"},{"full_name":"Bettler, Bernhard","last_name":"Bettler","first_name":"Bernhard"}],"publication_status":"published","citation":{"mla":"Kaupmann, Klemens, et al. “ GABA(B)-Receptor Subtypes Assemble into Functional Heteromeric Complexes.” <i>Nature</i>, vol. 396, no. 6712, Nature Publishing Group, 1998, pp. 683–87, doi:<a href=\"https://doi.org/10.1038/25360\">10.1038/25360</a>.","ama":"Kaupmann K, Malitschek B, Schuler V, et al.  GABA(B)-receptor subtypes assemble into functional heteromeric complexes. <i>Nature</i>. 1998;396(6712):683-687. doi:<a href=\"https://doi.org/10.1038/25360\">10.1038/25360</a>","short":"K. Kaupmann, B. Malitschek, V. Schuler, J. Heid, W. Froestl, P. Beck, J. Mosbacher, S. Bischoff, Á. Kulik, R. Shigemoto, A. Karschin, B. Bettler, Nature 396 (1998) 683–687.","ista":"Kaupmann K, Malitschek B, Schuler V, Heid J, Froestl W, Beck P, Mosbacher J, Bischoff S, Kulik Á, Shigemoto R, Karschin A, Bettler B. 1998.  GABA(B)-receptor subtypes assemble into functional heteromeric complexes. Nature. 396(6712), 683–687.","apa":"Kaupmann, K., Malitschek, B., Schuler, V., Heid, J., Froestl, W., Beck, P., … Bettler, B. (1998).  GABA(B)-receptor subtypes assemble into functional heteromeric complexes. <i>Nature</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/25360\">https://doi.org/10.1038/25360</a>","ieee":"K. Kaupmann <i>et al.</i>, “ GABA(B)-receptor subtypes assemble into functional heteromeric complexes,” <i>Nature</i>, vol. 396, no. 6712. Nature Publishing Group, pp. 683–687, 1998.","chicago":"Kaupmann, Klemens, Barbara Malitschek, Valérie Schuler, Jacob Heid, Wolfgang Froestl, Pascal Beck, Johannes Mosbacher, et al. “ GABA(B)-Receptor Subtypes Assemble into Functional Heteromeric Complexes.” <i>Nature</i>. Nature Publishing Group, 1998. <a href=\"https://doi.org/10.1038/25360\">https://doi.org/10.1038/25360</a>."},"_id":"2588","pmid":1,"extern":"1","publication_identifier":{"issn":["0028-0836"]},"user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","acknowledgement":"We thank D. Ristig, A. Begrich, I. Meigel and S. Leonhard for technical assistance.","oa_version":"None","quality_controlled":"1","date_updated":"2022-08-31T12:43:05Z","volume":396,"publist_id":"4309","article_processing_charge":"No","external_id":{"pmid":["9872317"]},"title":" GABA(B)-receptor subtypes assemble into functional heteromeric complexes","doi":"10.1038/25360","year":"1998"}]