[{"page":"341-355.e3","publication":"Neuron","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"orcid":"0000-0001-9242-5601","full_name":"Sweeney, Lora Beatrice Jaeger","last_name":"Sweeney","id":"56BE8254-C4F0-11E9-8E45-0B23E6697425","first_name":"Lora Beatrice Jaeger"},{"full_name":"Bikoff, Jay B.","last_name":"Bikoff","first_name":"Jay B."},{"first_name":"Mariano I.","last_name":"Gabitto","full_name":"Gabitto, Mariano I."},{"full_name":"Brenner-Morton, Susan","last_name":"Brenner-Morton","first_name":"Susan"},{"first_name":"Myungin","full_name":"Baek, Myungin","last_name":"Baek"},{"first_name":"Jerry H.","full_name":"Yang, Jerry H.","last_name":"Yang"},{"first_name":"Esteban G.","full_name":"Tabak, Esteban G.","last_name":"Tabak"},{"first_name":"Jeremy S.","last_name":"Dasen","full_name":"Dasen, Jeremy S."},{"first_name":"Christopher R.","last_name":"Kintner","full_name":"Kintner, Christopher R."},{"first_name":"Thomas M.","full_name":"Jessell, Thomas M.","last_name":"Jessell"}],"publication_identifier":{"issn":["0896-6273"]},"month":"01","day":"04","language":[{"iso":"eng"}],"year":"2018","intvolume":"        97","date_updated":"2024-01-31T10:13:54Z","doi":"10.1016/j.neuron.2017.12.029","date_published":"2018-01-04T00:00:00Z","citation":{"apa":"Sweeney, L. B., Bikoff, J. B., Gabitto, M. I., Brenner-Morton, S., Baek, M., Yang, J. H., … Jessell, T. M. (2018). Origin and segmental diversity of spinal inhibitory interneurons. <i>Neuron</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuron.2017.12.029\">https://doi.org/10.1016/j.neuron.2017.12.029</a>","ama":"Sweeney LB, Bikoff JB, Gabitto MI, et al. Origin and segmental diversity of spinal inhibitory interneurons. <i>Neuron</i>. 2018;97(2):341-355.e3. doi:<a href=\"https://doi.org/10.1016/j.neuron.2017.12.029\">10.1016/j.neuron.2017.12.029</a>","ista":"Sweeney LB, Bikoff JB, Gabitto MI, Brenner-Morton S, Baek M, Yang JH, Tabak EG, Dasen JS, Kintner CR, Jessell TM. 2018. Origin and segmental diversity of spinal inhibitory interneurons. Neuron. 97(2), 341–355.e3.","ieee":"L. B. Sweeney <i>et al.</i>, “Origin and segmental diversity of spinal inhibitory interneurons,” <i>Neuron</i>, vol. 97, no. 2. Elsevier, p. 341–355.e3, 2018.","chicago":"Sweeney, Lora B., Jay B. Bikoff, Mariano I. Gabitto, Susan Brenner-Morton, Myungin Baek, Jerry H. Yang, Esteban G. Tabak, Jeremy S. Dasen, Christopher R. Kintner, and Thomas M. Jessell. “Origin and Segmental Diversity of Spinal Inhibitory Interneurons.” <i>Neuron</i>. Elsevier, 2018. <a href=\"https://doi.org/10.1016/j.neuron.2017.12.029\">https://doi.org/10.1016/j.neuron.2017.12.029</a>.","mla":"Sweeney, Lora B., et al. “Origin and Segmental Diversity of Spinal Inhibitory Interneurons.” <i>Neuron</i>, vol. 97, no. 2, Elsevier, 2018, p. 341–355.e3, doi:<a href=\"https://doi.org/10.1016/j.neuron.2017.12.029\">10.1016/j.neuron.2017.12.029</a>.","short":"L.B. Sweeney, J.B. Bikoff, M.I. Gabitto, S. Brenner-Morton, M. Baek, J.H. Yang, E.G. Tabak, J.S. Dasen, C.R. Kintner, T.M. Jessell, Neuron 97 (2018) 341–355.e3."},"_id":"7698","publisher":"Elsevier","date_created":"2020-04-30T10:35:13Z","quality_controlled":"1","volume":97,"abstract":[{"lang":"eng","text":"Motor output varies along the rostro-caudal axis of the tetrapod spinal cord. At limb levels, ∼60 motor pools control the alternation of flexor and extensor muscles about each joint, whereas at thoracic levels as few as 10 motor pools supply muscle groups that support posture, inspiration, and expiration. Whether such differences in motor neuron identity and muscle number are associated with segmental distinctions in interneuron diversity has not been resolved. We show that select combinations of nineteen transcription factors that specify lumbar V1 inhibitory interneurons generate subpopulations enriched at limb and thoracic levels. Specification of limb and thoracic V1 interneurons involves the Hox gene Hoxc9 independently of motor neurons. Thus, early Hox patterning of the spinal cord determines the identity of V1 interneurons and motor neurons. These studies reveal a developmental program of V1 interneuron diversity, providing insight into the organization of inhibitory interneurons associated with differential motor output."}],"oa_version":"None","type":"journal_article","publication_status":"published","status":"public","article_processing_charge":"No","issue":"2","title":"Origin and segmental diversity of spinal inhibitory interneurons","article_type":"original","extern":"1"},{"acknowledged_ssus":[{"_id":"M-Shop"},{"_id":"NanoFab"}],"has_accepted_license":"1","intvolume":"         9","scopus_import":"1","date_published":"2018-09-25T00:00:00Z","related_material":{"record":[{"relation":"popular_science","id":"7977"},{"status":"public","relation":"dissertation_contains","id":"7996"}]},"publication":"Nature Communications","language":[{"iso":"eng"}],"day":"25","ddc":["530"],"type":"journal_article","oa_version":"Published Version","isi":1,"issue":"3902 ","project":[{"name":"Towards Spin qubits and Majorana fermions in Germanium selfassembled hut-wires","grant_number":"335497","_id":"25517E86-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"},{"call_identifier":"FWF","_id":"2552F888-B435-11E9-9278-68D0E5697425","grant_number":"Y00715","name":"Loch Spin-Qubits und Majorana-Fermionen in Germanium"}],"_id":"77","volume":9,"abstract":[{"text":"Holes confined in quantum dots have gained considerable interest in the past few years due to their potential as spin qubits. Here we demonstrate two-axis control of a spin 3/2 qubit in natural Ge. The qubit is formed in a hut wire double quantum dot device. The Pauli spin blockade principle allowed us to demonstrate electric dipole spin resonance by applying a radio frequency electric field to one of the electrodes defining the double quantum dot. Coherent hole spin oscillations with Rabi frequencies reaching 140 MHz are demonstrated and dephasing times of 130 ns are measured. The reported results emphasize the potential of Ge as a platform for fast and electrically tunable hole spin qubit devices.","lang":"eng"}],"year":"2018","date_updated":"2023-09-08T11:44:02Z","doi":"10.1038/s41467-018-06418-4","external_id":{"isi":["000445560800010"]},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","tmp":{"short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png"},"author":[{"full_name":"Watzinger, Hannes","last_name":"Watzinger","first_name":"Hannes","id":"35DF8E50-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Kukucka, Josip","last_name":"Kukucka","first_name":"Josip","id":"3F5D8856-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Vukusic","full_name":"Vukusic, Lada","orcid":"0000-0003-2424-8636","id":"31E9F056-F248-11E8-B48F-1D18A9856A87","first_name":"Lada"},{"first_name":"Fei","last_name":"Gao","full_name":"Gao, Fei"},{"first_name":"Ting","full_name":"Wang, Ting","last_name":"Wang"},{"first_name":"Friedrich","last_name":"Schäffler","full_name":"Schäffler, Friedrich"},{"last_name":"Zhang","full_name":"Zhang, Jian","first_name":"Jian"},{"id":"38DB5788-F248-11E8-B48F-1D18A9856A87","first_name":"Georgios","full_name":"Katsaros, Georgios","orcid":"0000-0001-8342-202X","last_name":"Katsaros"}],"department":[{"_id":"GeKa"}],"month":"09","ec_funded":1,"publication_status":"published","status":"public","article_processing_charge":"Yes","title":"A germanium hole spin qubit","article_type":"original","citation":{"mla":"Watzinger, Hannes, et al. “A Germanium Hole Spin Qubit.” <i>Nature Communications</i>, vol. 9, no. 3902, Nature Publishing Group, 2018, doi:<a href=\"https://doi.org/10.1038/s41467-018-06418-4\">10.1038/s41467-018-06418-4</a>.","chicago":"Watzinger, Hannes, Josip Kukucka, Lada Vukušić, Fei Gao, Ting Wang, Friedrich Schäffler, Jian Zhang, and Georgios Katsaros. “A Germanium Hole Spin Qubit.” <i>Nature Communications</i>. Nature Publishing Group, 2018. <a href=\"https://doi.org/10.1038/s41467-018-06418-4\">https://doi.org/10.1038/s41467-018-06418-4</a>.","short":"H. Watzinger, J. Kukucka, L. Vukušić, F. Gao, T. Wang, F. Schäffler, J. Zhang, G. Katsaros, Nature Communications 9 (2018).","ama":"Watzinger H, Kukucka J, Vukušić L, et al. A germanium hole spin qubit. <i>Nature Communications</i>. 2018;9(3902). doi:<a href=\"https://doi.org/10.1038/s41467-018-06418-4\">10.1038/s41467-018-06418-4</a>","apa":"Watzinger, H., Kukucka, J., Vukušić, L., Gao, F., Wang, T., Schäffler, F., … Katsaros, G. (2018). A germanium hole spin qubit. <i>Nature Communications</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/s41467-018-06418-4\">https://doi.org/10.1038/s41467-018-06418-4</a>","ieee":"H. Watzinger <i>et al.</i>, “A germanium hole spin qubit,” <i>Nature Communications</i>, vol. 9, no. 3902. Nature Publishing Group, 2018.","ista":"Watzinger H, Kukucka J, Vukušić L, Gao F, Wang T, Schäffler F, Zhang J, Katsaros G. 2018. A germanium hole spin qubit. Nature Communications. 9(3902)."},"oa":1,"publisher":"Nature Publishing Group","file":[{"date_updated":"2020-07-14T12:48:02Z","checksum":"e7148c10a64497e279c4de570b6cc544","content_type":"application/pdf","relation":"main_file","creator":"dernst","date_created":"2018-12-17T10:28:30Z","file_id":"5687","file_name":"2018_NatureComm_Watzinger.pdf","file_size":1063469,"access_level":"open_access"}],"file_date_updated":"2020-07-14T12:48:02Z","date_created":"2018-12-11T11:44:30Z","quality_controlled":"1"},{"publication_identifier":{"issn":["2041-1723"]},"author":[{"first_name":"Chloe X.","last_name":"Yap","full_name":"Yap, Chloe X."},{"full_name":"Sidorenko, Julia","last_name":"Sidorenko","first_name":"Julia"},{"full_name":"Wu, Yang","last_name":"Wu","first_name":"Yang"},{"first_name":"Kathryn E.","full_name":"Kemper, Kathryn E.","last_name":"Kemper"},{"last_name":"Yang","full_name":"Yang, Jian","first_name":"Jian"},{"first_name":"Naomi R.","full_name":"Wray, Naomi R.","last_name":"Wray"},{"last_name":"Robinson","orcid":"0000-0001-8982-8813","full_name":"Robinson, Matthew Richard","first_name":"Matthew Richard","id":"E5D42276-F5DA-11E9-8E24-6303E6697425"},{"first_name":"Peter M.","last_name":"Visscher","full_name":"Visscher, Peter M."}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_number":"5407","publication":"Nature Communications","language":[{"iso":"eng"}],"day":"20","month":"12","year":"2018","date_published":"2018-12-20T00:00:00Z","doi":"10.1038/s41467-018-07862-y","date_updated":"2021-01-12T08:15:02Z","intvolume":"         9","publisher":"Springer Nature","oa":1,"_id":"7712","citation":{"chicago":"Yap, Chloe X., Julia Sidorenko, Yang Wu, Kathryn E. Kemper, Jian Yang, Naomi R. Wray, Matthew Richard Robinson, and Peter M. Visscher. “Dissection of Genetic Variation and Evidence for Pleiotropy in Male Pattern Baldness.” <i>Nature Communications</i>. Springer Nature, 2018. <a href=\"https://doi.org/10.1038/s41467-018-07862-y\">https://doi.org/10.1038/s41467-018-07862-y</a>.","mla":"Yap, Chloe X., et al. “Dissection of Genetic Variation and Evidence for Pleiotropy in Male Pattern Baldness.” <i>Nature Communications</i>, vol. 9, 5407, Springer Nature, 2018, doi:<a href=\"https://doi.org/10.1038/s41467-018-07862-y\">10.1038/s41467-018-07862-y</a>.","short":"C.X. Yap, J. Sidorenko, Y. Wu, K.E. Kemper, J. Yang, N.R. Wray, M.R. Robinson, P.M. Visscher, Nature Communications 9 (2018).","apa":"Yap, C. X., Sidorenko, J., Wu, Y., Kemper, K. E., Yang, J., Wray, N. R., … Visscher, P. M. (2018). Dissection of genetic variation and evidence for pleiotropy in male pattern baldness. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41467-018-07862-y\">https://doi.org/10.1038/s41467-018-07862-y</a>","ama":"Yap CX, Sidorenko J, Wu Y, et al. Dissection of genetic variation and evidence for pleiotropy in male pattern baldness. <i>Nature Communications</i>. 2018;9. doi:<a href=\"https://doi.org/10.1038/s41467-018-07862-y\">10.1038/s41467-018-07862-y</a>","ista":"Yap CX, Sidorenko J, Wu Y, Kemper KE, Yang J, Wray NR, Robinson MR, Visscher PM. 2018. Dissection of genetic variation and evidence for pleiotropy in male pattern baldness. Nature Communications. 9, 5407.","ieee":"C. X. Yap <i>et al.</i>, “Dissection of genetic variation and evidence for pleiotropy in male pattern baldness,” <i>Nature Communications</i>, vol. 9. Springer Nature, 2018."},"abstract":[{"lang":"eng","text":"Male pattern baldness (MPB) is a sex-limited, age-related, complex trait. We study MPB genetics in 205,327 European males from the UK Biobank. Here we show that MPB is strongly heritable and polygenic, with pedigree-heritability of 0.62 (SE = 0.03) estimated from close relatives, and SNP-heritability of 0.39 (SE = 0.01) from conventionally-unrelated males. We detect 624 near-independent genome-wide loci, contributing SNP-heritability of 0.25 (SE = 0.01), of which 26 X-chromosome loci explain 11.6%. Autosomal genetic variance is enriched for common variants and regions of lower linkage disequilibrium. We identify plausible genetic correlations between MPB and multiple sex-limited markers of earlier puberty, increased bone mineral density (rg = 0.15) and pancreatic β-cell function (rg = 0.12). Correlations with reproductive traits imply an effect on fitness, consistent with an estimated linear selection gradient of -0.018 per MPB standard deviation. Overall, we provide genetic insights into MPB: a phenotype of interest in its own right, with value as a model sex-limited, complex trait."}],"volume":9,"main_file_link":[{"url":"https://doi.org/10.1038/s41467-018-07862-y","open_access":"1"}],"quality_controlled":"1","date_created":"2020-04-30T10:41:19Z","status":"public","publication_status":"published","oa_version":"Published Version","type":"journal_article","extern":"1","article_type":"original","title":"Dissection of genetic variation and evidence for pleiotropy in male pattern baldness","article_processing_charge":"No"},{"article_processing_charge":"No","title":"Global genetic differentiation of complex traits shaped by natural selection in humans","article_type":"original","extern":"1","type":"journal_article","oa_version":"Published Version","publication_status":"published","status":"public","date_created":"2020-04-30T10:41:36Z","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1038/s41467-018-04191-y"}],"volume":9,"quality_controlled":"1","abstract":[{"lang":"eng","text":"There are mean differences in complex traits among global human populations. We hypothesize that part of the phenotypic differentiation is due to natural selection. To address this hypothesis, we assess the differentiation in allele frequencies of trait-associated SNPs among African, Eastern Asian, and European populations for ten complex traits using data of large sample size (up to ~405,000). We show that SNPs associated with height (P=2.46×10−5), waist-to-hip ratio (P=2.77×10−4), and schizophrenia (P=3.96×10−5) are significantly more differentiated among populations than matched “control” SNPs, suggesting that these trait-associated SNPs have undergone natural selection. We further find that SNPs associated with height (P=2.01×10−6) and schizophrenia (P=5.16×10−18) show significantly higher variance in linkage disequilibrium (LD) scores across populations than control SNPs. Our results support the hypothesis that natural selection has shaped the genetic differentiation of complex traits, such as height and schizophrenia, among worldwide populations."}],"oa":1,"_id":"7713","citation":{"short":"J. Guo, Y. Wu, Z. Zhu, Z. Zheng, M. Trzaskowski, J. Zeng, M.R. Robinson, P.M. Visscher, J. Yang, Nature Communications 9 (2018).","mla":"Guo, Jing, et al. “Global Genetic Differentiation of Complex Traits Shaped by Natural Selection in Humans.” <i>Nature Communications</i>, vol. 9, 1865, Springer Nature, 2018, doi:<a href=\"https://doi.org/10.1038/s41467-018-04191-y\">10.1038/s41467-018-04191-y</a>.","chicago":"Guo, Jing, Yang Wu, Zhihong Zhu, Zhili Zheng, Maciej Trzaskowski, Jian Zeng, Matthew Richard Robinson, Peter M. Visscher, and Jian Yang. “Global Genetic Differentiation of Complex Traits Shaped by Natural Selection in Humans.” <i>Nature Communications</i>. Springer Nature, 2018. <a href=\"https://doi.org/10.1038/s41467-018-04191-y\">https://doi.org/10.1038/s41467-018-04191-y</a>.","ieee":"J. Guo <i>et al.</i>, “Global genetic differentiation of complex traits shaped by natural selection in humans,” <i>Nature Communications</i>, vol. 9. Springer Nature, 2018.","ista":"Guo J, Wu Y, Zhu Z, Zheng Z, Trzaskowski M, Zeng J, Robinson MR, Visscher PM, Yang J. 2018. Global genetic differentiation of complex traits shaped by natural selection in humans. Nature Communications. 9, 1865.","ama":"Guo J, Wu Y, Zhu Z, et al. Global genetic differentiation of complex traits shaped by natural selection in humans. <i>Nature Communications</i>. 2018;9. doi:<a href=\"https://doi.org/10.1038/s41467-018-04191-y\">10.1038/s41467-018-04191-y</a>","apa":"Guo, J., Wu, Y., Zhu, Z., Zheng, Z., Trzaskowski, M., Zeng, J., … Yang, J. (2018). Global genetic differentiation of complex traits shaped by natural selection in humans. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41467-018-04191-y\">https://doi.org/10.1038/s41467-018-04191-y</a>"},"publisher":"Springer Nature","intvolume":"         9","date_updated":"2021-01-12T08:15:02Z","doi":"10.1038/s41467-018-04191-y","date_published":"2018-05-14T00:00:00Z","year":"2018","month":"05","language":[{"iso":"eng"}],"day":"14","article_number":"1865","publication":"Nature Communications","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"last_name":"Guo","full_name":"Guo, Jing","first_name":"Jing"},{"first_name":"Yang","last_name":"Wu","full_name":"Wu, Yang"},{"full_name":"Zhu, Zhihong","last_name":"Zhu","first_name":"Zhihong"},{"first_name":"Zhili","last_name":"Zheng","full_name":"Zheng, Zhili"},{"first_name":"Maciej","last_name":"Trzaskowski","full_name":"Trzaskowski, Maciej"},{"last_name":"Zeng","full_name":"Zeng, Jian","first_name":"Jian"},{"first_name":"Matthew Richard","id":"E5D42276-F5DA-11E9-8E24-6303E6697425","full_name":"Robinson, Matthew Richard","orcid":"0000-0001-8982-8813","last_name":"Robinson"},{"last_name":"Visscher","full_name":"Visscher, Peter M.","first_name":"Peter M."},{"last_name":"Yang","full_name":"Yang, Jian","first_name":"Jian"}],"publication_identifier":{"issn":["2041-1723"]}},{"status":"public","publication_status":"published","type":"journal_article","oa_version":"Published Version","extern":"1","article_type":"original","title":"Causal associations between risk factors and common diseases inferred from GWAS summary data","article_processing_charge":"No","publisher":"Springer Nature","_id":"7714","oa":1,"citation":{"ieee":"Z. Zhu <i>et al.</i>, “Causal associations between risk factors and common diseases inferred from GWAS summary data,” <i>Nature Communications</i>, vol. 9. Springer Nature, 2018.","ista":"Zhu Z, Zheng Z, Zhang F, Wu Y, Trzaskowski M, Maier R, Robinson MR, McGrath JJ, Visscher PM, Wray NR, Yang J. 2018. Causal associations between risk factors and common diseases inferred from GWAS summary data. Nature Communications. 9, 224.","ama":"Zhu Z, Zheng Z, Zhang F, et al. Causal associations between risk factors and common diseases inferred from GWAS summary data. <i>Nature Communications</i>. 2018;9. doi:<a href=\"https://doi.org/10.1038/s41467-017-02317-2\">10.1038/s41467-017-02317-2</a>","apa":"Zhu, Z., Zheng, Z., Zhang, F., Wu, Y., Trzaskowski, M., Maier, R., … Yang, J. (2018). Causal associations between risk factors and common diseases inferred from GWAS summary data. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41467-017-02317-2\">https://doi.org/10.1038/s41467-017-02317-2</a>","short":"Z. Zhu, Z. Zheng, F. Zhang, Y. Wu, M. Trzaskowski, R. Maier, M.R. Robinson, J.J. McGrath, P.M. Visscher, N.R. Wray, J. Yang, Nature Communications 9 (2018).","mla":"Zhu, Zhihong, et al. “Causal Associations between Risk Factors and Common Diseases Inferred from GWAS Summary Data.” <i>Nature Communications</i>, vol. 9, 224, Springer Nature, 2018, doi:<a href=\"https://doi.org/10.1038/s41467-017-02317-2\">10.1038/s41467-017-02317-2</a>.","chicago":"Zhu, Zhihong, Zhili Zheng, Futao Zhang, Yang Wu, Maciej Trzaskowski, Robert Maier, Matthew Richard Robinson, et al. “Causal Associations between Risk Factors and Common Diseases Inferred from GWAS Summary Data.” <i>Nature Communications</i>. Springer Nature, 2018. <a href=\"https://doi.org/10.1038/s41467-017-02317-2\">https://doi.org/10.1038/s41467-017-02317-2</a>."},"abstract":[{"text":"Health risk factors such as body mass index (BMI) and serum cholesterol are associated with many common diseases. It often remains unclear whether the risk factors are cause or consequence of disease, or whether the associations are the result of confounding. We develop and apply a method (called GSMR) that performs a multi-SNP Mendelian randomization analysis using summary-level data from genome-wide association studies to test the causal associations of BMI, waist-to-hip ratio, serum cholesterols, blood pressures, height, and years of schooling (EduYears) with common diseases (sample sizes of up to 405,072). We identify a number of causal associations including a protective effect of LDL-cholesterol against type-2 diabetes (T2D) that might explain the side effects of statins on T2D, a protective effect of EduYears against Alzheimer’s disease, and bidirectional associations with opposite effects (e.g., higher BMI increases the risk of T2D but the effect of T2D on BMI is negative).","lang":"eng"}],"main_file_link":[{"url":"https://doi.org/10.1038/s41467-017-02317-2","open_access":"1"}],"volume":9,"quality_controlled":"1","date_created":"2020-04-30T10:41:55Z","year":"2018","date_published":"2018-01-15T00:00:00Z","doi":"10.1038/s41467-017-02317-2","date_updated":"2021-01-12T08:15:03Z","intvolume":"         9","publication_identifier":{"issn":["2041-1723"]},"author":[{"full_name":"Zhu, Zhihong","last_name":"Zhu","first_name":"Zhihong"},{"full_name":"Zheng, Zhili","last_name":"Zheng","first_name":"Zhili"},{"full_name":"Zhang, Futao","last_name":"Zhang","first_name":"Futao"},{"first_name":"Yang","full_name":"Wu, Yang","last_name":"Wu"},{"full_name":"Trzaskowski, Maciej","last_name":"Trzaskowski","first_name":"Maciej"},{"first_name":"Robert","full_name":"Maier, Robert","last_name":"Maier"},{"last_name":"Robinson","orcid":"0000-0001-8982-8813","full_name":"Robinson, Matthew Richard","id":"E5D42276-F5DA-11E9-8E24-6303E6697425","first_name":"Matthew Richard"},{"last_name":"McGrath","full_name":"McGrath, John J.","first_name":"John J."},{"first_name":"Peter M.","last_name":"Visscher","full_name":"Visscher, Peter M."},{"first_name":"Naomi R.","last_name":"Wray","full_name":"Wray, Naomi R."},{"full_name":"Yang, Jian","last_name":"Yang","first_name":"Jian"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_number":"224","publication":"Nature Communications","day":"15","language":[{"iso":"eng"}],"month":"01"},{"month":"11","day":"26","language":[{"iso":"eng"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication":"Nature Human Behaviour","page":"948-954","publication_identifier":{"issn":["2397-3374"]},"author":[{"last_name":"Yengo","full_name":"Yengo, Loic","first_name":"Loic"},{"first_name":"Matthew Richard","id":"E5D42276-F5DA-11E9-8E24-6303E6697425","full_name":"Robinson, Matthew Richard","orcid":"0000-0001-8982-8813","last_name":"Robinson"},{"first_name":"Matthew C.","full_name":"Keller, Matthew C.","last_name":"Keller"},{"full_name":"Kemper, Kathryn E.","last_name":"Kemper","first_name":"Kathryn E."},{"last_name":"Yang","full_name":"Yang, Yuanhao","first_name":"Yuanhao"},{"first_name":"Maciej","full_name":"Trzaskowski, Maciej","last_name":"Trzaskowski"},{"first_name":"Jacob","full_name":"Gratten, Jacob","last_name":"Gratten"},{"full_name":"Turley, Patrick","last_name":"Turley","first_name":"Patrick"},{"first_name":"David","full_name":"Cesarini, David","last_name":"Cesarini"},{"last_name":"Benjamin","full_name":"Benjamin, Daniel J.","first_name":"Daniel J."},{"first_name":"Naomi R.","full_name":"Wray, Naomi R.","last_name":"Wray"},{"last_name":"Goddard","full_name":"Goddard, Michael E.","first_name":"Michael E."},{"last_name":"Yang","full_name":"Yang, Jian","first_name":"Jian"},{"first_name":"Peter M.","full_name":"Visscher, Peter M.","last_name":"Visscher"}],"date_updated":"2021-01-12T08:15:03Z","intvolume":"         2","doi":"10.1038/s41562-018-0476-3","date_published":"2018-11-26T00:00:00Z","year":"2018","volume":2,"quality_controlled":"1","date_created":"2020-04-30T10:42:12Z","abstract":[{"lang":"eng","text":"Preference for mates with similar phenotypes; that is, assortative mating, is widely observed in humans1,2,3,4,5 and has evolutionary consequences6,7,8. Under Fisher's classical theory6, assortative mating is predicted to induce a signature in the genome at trait-associated loci that can be detected and quantified. Here, we develop and apply a method to quantify assortative mating on a specific trait by estimating the correlation (θ) between genetic predictors of the trait from single nucleotide polymorphisms on odd- versus even-numbered chromosomes. We show by theory and simulation that the effect of assortative mating can be quantified in the presence of population stratification. We applied this approach to 32 complex traits and diseases using single nucleotide polymorphism data from ~400,000 unrelated individuals of European ancestry. We found significant evidence of assortative mating for height (θ = 3.2%) and educational attainment (θ = 2.7%), both of which were consistent with theoretical predictions. Overall, our results imply that assortative mating involves multiple traits and affects the genomic architecture of loci that are associated with these traits, and that the consequence of mate choice can be detected from a random sample of genomes."}],"publisher":"Springer Nature","citation":{"ista":"Yengo L, Robinson MR, Keller MC, Kemper KE, Yang Y, Trzaskowski M, Gratten J, Turley P, Cesarini D, Benjamin DJ, Wray NR, Goddard ME, Yang J, Visscher PM. 2018. Imprint of assortative mating on the human genome. Nature Human Behaviour. 2(12), 948–954.","ieee":"L. Yengo <i>et al.</i>, “Imprint of assortative mating on the human genome,” <i>Nature Human Behaviour</i>, vol. 2, no. 12. Springer Nature, pp. 948–954, 2018.","apa":"Yengo, L., Robinson, M. R., Keller, M. C., Kemper, K. E., Yang, Y., Trzaskowski, M., … Visscher, P. M. (2018). Imprint of assortative mating on the human genome. <i>Nature Human Behaviour</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41562-018-0476-3\">https://doi.org/10.1038/s41562-018-0476-3</a>","ama":"Yengo L, Robinson MR, Keller MC, et al. Imprint of assortative mating on the human genome. <i>Nature Human Behaviour</i>. 2018;2(12):948-954. doi:<a href=\"https://doi.org/10.1038/s41562-018-0476-3\">10.1038/s41562-018-0476-3</a>","short":"L. Yengo, M.R. Robinson, M.C. Keller, K.E. Kemper, Y. Yang, M. Trzaskowski, J. Gratten, P. Turley, D. Cesarini, D.J. Benjamin, N.R. Wray, M.E. Goddard, J. Yang, P.M. Visscher, Nature Human Behaviour 2 (2018) 948–954.","mla":"Yengo, Loic, et al. “Imprint of Assortative Mating on the Human Genome.” <i>Nature Human Behaviour</i>, vol. 2, no. 12, Springer Nature, 2018, pp. 948–54, doi:<a href=\"https://doi.org/10.1038/s41562-018-0476-3\">10.1038/s41562-018-0476-3</a>.","chicago":"Yengo, Loic, Matthew Richard Robinson, Matthew C. Keller, Kathryn E. Kemper, Yuanhao Yang, Maciej Trzaskowski, Jacob Gratten, et al. “Imprint of Assortative Mating on the Human Genome.” <i>Nature Human Behaviour</i>. Springer Nature, 2018. <a href=\"https://doi.org/10.1038/s41562-018-0476-3\">https://doi.org/10.1038/s41562-018-0476-3</a>."},"_id":"7715","title":"Imprint of assortative mating on the human genome","article_processing_charge":"No","issue":"12","extern":"1","article_type":"original","oa_version":"None","type":"journal_article","status":"public","publication_status":"published"},{"abstract":[{"text":"Genomic prediction has the potential to contribute to precision medicine. However, to date, the utility of such predictors is limited due to low accuracy for most traits. Here theory and simulation study are used to demonstrate that widespread pleiotropy among phenotypes can be utilised to improve genomic risk prediction. We show how a genetic predictor can be created as a weighted index that combines published genome-wide association study (GWAS) summary statistics across many different traits. We apply this framework to predict risk of schizophrenia and bipolar disorder in the Psychiatric Genomics consortium data, finding substantial heterogeneity in prediction accuracy increases across cohorts. For six additional phenotypes in the UK Biobank data, we find increases in prediction accuracy ranging from 0.7% for height to 47% for type 2 diabetes, when using a multi-trait predictor that combines published summary statistics from multiple traits, as compared to a predictor based only on one trait.","lang":"eng"}],"quality_controlled":"1","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1038/s41467-017-02769-6"}],"volume":9,"date_created":"2020-04-30T10:42:29Z","publisher":"Springer Nature","_id":"7716","citation":{"short":"R.M. Maier, Z. Zhu, S.H. Lee, M. Trzaskowski, D.M. Ruderfer, E.A. Stahl, S. Ripke, N.R. Wray, J. Yang, P.M. Visscher, M.R. Robinson, Nature Communications 9 (2018).","chicago":"Maier, Robert M., Zhihong Zhu, Sang Hong Lee, Maciej Trzaskowski, Douglas M. Ruderfer, Eli A. Stahl, Stephan Ripke, et al. “Improving Genetic Prediction by Leveraging Genetic Correlations among Human Diseases and Traits.” <i>Nature Communications</i>. Springer Nature, 2018. <a href=\"https://doi.org/10.1038/s41467-017-02769-6\">https://doi.org/10.1038/s41467-017-02769-6</a>.","mla":"Maier, Robert M., et al. “Improving Genetic Prediction by Leveraging Genetic Correlations among Human Diseases and Traits.” <i>Nature Communications</i>, vol. 9, 989, Springer Nature, 2018, doi:<a href=\"https://doi.org/10.1038/s41467-017-02769-6\">10.1038/s41467-017-02769-6</a>.","ista":"Maier RM, Zhu Z, Lee SH, Trzaskowski M, Ruderfer DM, Stahl EA, Ripke S, Wray NR, Yang J, Visscher PM, Robinson MR. 2018. Improving genetic prediction by leveraging genetic correlations among human diseases and traits. Nature Communications. 9, 989.","ieee":"R. M. Maier <i>et al.</i>, “Improving genetic prediction by leveraging genetic correlations among human diseases and traits,” <i>Nature Communications</i>, vol. 9. Springer Nature, 2018.","apa":"Maier, R. M., Zhu, Z., Lee, S. H., Trzaskowski, M., Ruderfer, D. M., Stahl, E. A., … Robinson, M. R. (2018). Improving genetic prediction by leveraging genetic correlations among human diseases and traits. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41467-017-02769-6\">https://doi.org/10.1038/s41467-017-02769-6</a>","ama":"Maier RM, Zhu Z, Lee SH, et al. Improving genetic prediction by leveraging genetic correlations among human diseases and traits. <i>Nature Communications</i>. 2018;9. doi:<a href=\"https://doi.org/10.1038/s41467-017-02769-6\">10.1038/s41467-017-02769-6</a>"},"oa":1,"extern":"1","article_type":"original","title":"Improving genetic prediction by leveraging genetic correlations among human diseases and traits","article_processing_charge":"No","publication_status":"published","status":"public","type":"journal_article","oa_version":"Published Version","language":[{"iso":"eng"}],"day":"07","month":"03","publication_identifier":{"issn":["2041-1723"]},"author":[{"full_name":"Maier, Robert M.","last_name":"Maier","first_name":"Robert M."},{"last_name":"Zhu","full_name":"Zhu, Zhihong","first_name":"Zhihong"},{"last_name":"Lee","full_name":"Lee, Sang Hong","first_name":"Sang Hong"},{"first_name":"Maciej","last_name":"Trzaskowski","full_name":"Trzaskowski, Maciej"},{"first_name":"Douglas M.","full_name":"Ruderfer, Douglas M.","last_name":"Ruderfer"},{"first_name":"Eli A.","last_name":"Stahl","full_name":"Stahl, Eli A."},{"last_name":"Ripke","full_name":"Ripke, Stephan","first_name":"Stephan"},{"first_name":"Naomi R.","full_name":"Wray, Naomi R.","last_name":"Wray"},{"full_name":"Yang, Jian","last_name":"Yang","first_name":"Jian"},{"first_name":"Peter M.","full_name":"Visscher, Peter M.","last_name":"Visscher"},{"orcid":"0000-0001-8982-8813","full_name":"Robinson, Matthew Richard","last_name":"Robinson","first_name":"Matthew Richard","id":"E5D42276-F5DA-11E9-8E24-6303E6697425"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_number":"989","publication":"Nature Communications","date_published":"2018-03-07T00:00:00Z","doi":"10.1038/s41467-017-02769-6","date_updated":"2021-01-12T08:15:03Z","intvolume":"         9","year":"2018"},{"abstract":[{"lang":"eng","text":"Background: DNA methylation levels change along with age, but few studies have examined the variation in the rate of such changes between individuals.\r\nMethods: We performed a longitudinal analysis to quantify the variation in the rate of change of DNA methylation between individuals using whole blood DNA methylation array profiles collected at 2–4 time points (N = 2894) in 954 individuals (67–90 years).\r\nResults: After stringent quality control, we identified 1507 DNA methylation CpG sites (rsCpGs) with statistically significant variation in the rate of change (random slope) of DNA methylation among individuals in a mixed linear model analysis. Genes in the vicinity of these rsCpGs were found to be enriched in Homeobox transcription factors and the Wnt signalling pathway, both of which are related to ageing processes. Furthermore, we investigated the SNP effect on the random slope. We found that 4 out of 1507 rsCpGs had one significant (P < 5 × 10−8/1507) SNP effect and 343 rsCpGs had at least one SNP effect (436 SNP-probe pairs) reaching genome-wide significance (P < 5 × 10−8). Ninety-five percent of the significant (P < 5 × 10−8) SNPs are on different chromosomes from their corresponding probes.\r\nConclusions: We identified CpG sites that have variability in the rate of change of DNA methylation between individuals, and our results suggest a genetic basis of this variation. Genes around these CpG sites have been reported to be involved in the ageing process."}],"volume":10,"_id":"7717","issue":"1","type":"journal_article","oa_version":"Published Version","language":[{"iso":"eng"}],"day":"22","publication_identifier":{"issn":["1756-994X"]},"publication":"Genome Medicine","date_published":"2018-10-22T00:00:00Z","intvolume":"        10","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1186/s13073-018-0585-7"}],"quality_controlled":"1","date_created":"2020-04-30T10:42:50Z","publisher":"Springer Nature","citation":{"apa":"Zhang, Q., Marioni, R. E., Robinson, M. R., Higham, J., Sproul, D., Wray, N. R., … Visscher, P. M. (2018). Genotype effects contribute to variation in longitudinal methylome patterns in older people. <i>Genome Medicine</i>. Springer Nature. <a href=\"https://doi.org/10.1186/s13073-018-0585-7\">https://doi.org/10.1186/s13073-018-0585-7</a>","ama":"Zhang Q, Marioni RE, Robinson MR, et al. Genotype effects contribute to variation in longitudinal methylome patterns in older people. <i>Genome Medicine</i>. 2018;10(1). doi:<a href=\"https://doi.org/10.1186/s13073-018-0585-7\">10.1186/s13073-018-0585-7</a>","ista":"Zhang Q, Marioni RE, Robinson MR, Higham J, Sproul D, Wray NR, Deary IJ, McRae AF, Visscher PM. 2018. Genotype effects contribute to variation in longitudinal methylome patterns in older people. Genome Medicine. 10(1), 75.","ieee":"Q. Zhang <i>et al.</i>, “Genotype effects contribute to variation in longitudinal methylome patterns in older people,” <i>Genome Medicine</i>, vol. 10, no. 1. Springer Nature, 2018.","chicago":"Zhang, Qian, Riccardo E Marioni, Matthew Richard Robinson, Jon Higham, Duncan Sproul, Naomi R Wray, Ian J Deary, Allan F McRae, and Peter M Visscher. “Genotype Effects Contribute to Variation in Longitudinal Methylome Patterns in Older People.” <i>Genome Medicine</i>. Springer Nature, 2018. <a href=\"https://doi.org/10.1186/s13073-018-0585-7\">https://doi.org/10.1186/s13073-018-0585-7</a>.","mla":"Zhang, Qian, et al. “Genotype Effects Contribute to Variation in Longitudinal Methylome Patterns in Older People.” <i>Genome Medicine</i>, vol. 10, no. 1, 75, Springer Nature, 2018, doi:<a href=\"https://doi.org/10.1186/s13073-018-0585-7\">10.1186/s13073-018-0585-7</a>.","short":"Q. Zhang, R.E. Marioni, M.R. Robinson, J. Higham, D. Sproul, N.R. Wray, I.J. Deary, A.F. McRae, P.M. Visscher, Genome Medicine 10 (2018)."},"oa":1,"extern":"1","article_type":"original","title":"Genotype effects contribute to variation in longitudinal methylome patterns in older people","article_processing_charge":"No","publication_status":"published","status":"public","month":"10","author":[{"first_name":"Qian","full_name":"Zhang, Qian","last_name":"Zhang"},{"first_name":"Riccardo E","full_name":"Marioni, Riccardo E","last_name":"Marioni"},{"orcid":"0000-0001-8982-8813","full_name":"Robinson, Matthew Richard","last_name":"Robinson","first_name":"Matthew Richard","id":"E5D42276-F5DA-11E9-8E24-6303E6697425"},{"full_name":"Higham, Jon","last_name":"Higham","first_name":"Jon"},{"first_name":"Duncan","last_name":"Sproul","full_name":"Sproul, Duncan"},{"full_name":"Wray, Naomi R","last_name":"Wray","first_name":"Naomi R"},{"full_name":"Deary, Ian J","last_name":"Deary","first_name":"Ian J"},{"first_name":"Allan F","last_name":"McRae","full_name":"McRae, Allan F"},{"first_name":"Peter M","full_name":"Visscher, Peter M","last_name":"Visscher"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_number":"75","doi":"10.1186/s13073-018-0585-7","date_updated":"2021-01-12T08:15:04Z","year":"2018"},{"year":"2018","doi":"10.1126/science.aar8486","date_updated":"2021-01-12T08:15:04Z","pmid":1,"author":[{"first_name":"Serena","full_name":"Tucci, Serena","last_name":"Tucci"},{"first_name":"Samuel H.","full_name":"Vohr, Samuel H.","last_name":"Vohr"},{"first_name":"Rajiv C.","last_name":"McCoy","full_name":"McCoy, Rajiv C."},{"last_name":"Vernot","full_name":"Vernot, Benjamin","first_name":"Benjamin"},{"full_name":"Robinson, Matthew Richard","orcid":"0000-0001-8982-8813","last_name":"Robinson","first_name":"Matthew Richard","id":"E5D42276-F5DA-11E9-8E24-6303E6697425"},{"full_name":"Barbieri, Chiara","last_name":"Barbieri","first_name":"Chiara"},{"first_name":"Brad J.","full_name":"Nelson, Brad J.","last_name":"Nelson"},{"first_name":"Wenqing","last_name":"Fu","full_name":"Fu, Wenqing"},{"last_name":"Purnomo","full_name":"Purnomo, Gludhug A.","first_name":"Gludhug A."},{"first_name":"Herawati","last_name":"Sudoyo","full_name":"Sudoyo, Herawati"},{"first_name":"Evan E.","last_name":"Eichler","full_name":"Eichler, Evan E."},{"full_name":"Barbujani, Guido","last_name":"Barbujani","first_name":"Guido"},{"first_name":"Peter M.","full_name":"Visscher, Peter M.","last_name":"Visscher"},{"first_name":"Joshua M.","last_name":"Akey","full_name":"Akey, Joshua M."},{"first_name":"Richard E.","full_name":"Green, Richard E.","last_name":"Green"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","page":"511-516","external_id":{"pmid":["30072539"]},"month":"08","status":"public","publication_status":"published","extern":"1","article_type":"original","title":"Evolutionary history and adaptation of a human pygmy population of Flores Island, Indonesia","article_processing_charge":"No","publisher":"American Association for the Advancement of Science","citation":{"mla":"Tucci, Serena, et al. “Evolutionary History and Adaptation of a Human Pygmy Population of Flores Island, Indonesia.” <i>Science</i>, vol. 361, no. 6401, American Association for the Advancement of Science, 2018, pp. 511–16, doi:<a href=\"https://doi.org/10.1126/science.aar8486\">10.1126/science.aar8486</a>.","chicago":"Tucci, Serena, Samuel H. Vohr, Rajiv C. McCoy, Benjamin Vernot, Matthew Richard Robinson, Chiara Barbieri, Brad J. Nelson, et al. “Evolutionary History and Adaptation of a Human Pygmy Population of Flores Island, Indonesia.” <i>Science</i>. American Association for the Advancement of Science, 2018. <a href=\"https://doi.org/10.1126/science.aar8486\">https://doi.org/10.1126/science.aar8486</a>.","short":"S. Tucci, S.H. Vohr, R.C. McCoy, B. Vernot, M.R. Robinson, C. Barbieri, B.J. Nelson, W. Fu, G.A. Purnomo, H. Sudoyo, E.E. Eichler, G. Barbujani, P.M. Visscher, J.M. Akey, R.E. Green, Science 361 (2018) 511–516.","apa":"Tucci, S., Vohr, S. H., McCoy, R. C., Vernot, B., Robinson, M. R., Barbieri, C., … Green, R. E. (2018). Evolutionary history and adaptation of a human pygmy population of Flores Island, Indonesia. <i>Science</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/science.aar8486\">https://doi.org/10.1126/science.aar8486</a>","ama":"Tucci S, Vohr SH, McCoy RC, et al. Evolutionary history and adaptation of a human pygmy population of Flores Island, Indonesia. <i>Science</i>. 2018;361(6401):511-516. doi:<a href=\"https://doi.org/10.1126/science.aar8486\">10.1126/science.aar8486</a>","ista":"Tucci S, Vohr SH, McCoy RC, Vernot B, Robinson MR, Barbieri C, Nelson BJ, Fu W, Purnomo GA, Sudoyo H, Eichler EE, Barbujani G, Visscher PM, Akey JM, Green RE. 2018. Evolutionary history and adaptation of a human pygmy population of Flores Island, Indonesia. Science. 361(6401), 511–516.","ieee":"S. Tucci <i>et al.</i>, “Evolutionary history and adaptation of a human pygmy population of Flores Island, Indonesia,” <i>Science</i>, vol. 361, no. 6401. American Association for the Advancement of Science, pp. 511–516, 2018."},"quality_controlled":"1","date_created":"2020-04-30T10:43:24Z","date_published":"2018-08-03T00:00:00Z","intvolume":"       361","publication_identifier":{"issn":["0036-8075","1095-9203"]},"publication":"Science","language":[{"iso":"eng"}],"day":"03","oa_version":"None","type":"journal_article","issue":"6401","_id":"7718","abstract":[{"text":"Flores Island, Indonesia, was inhabited by the small-bodied hominin species Homo floresiensis, which has an unknown evolutionary relationship to modern humans. This island is also home to an extant human pygmy population. Here we describe genome-scale single-nucleotide polymorphism data and whole-genome sequences from a contemporary human pygmy population living on Flores near the cave where H. floresiensis was found. The genomes of Flores pygmies reveal a complex history of admixture with Denisovans and Neanderthals but no evidence for gene flow with other archaic hominins. Modern individuals bear the signatures of recent positive selection encompassing the FADS (fatty acid desaturase) gene cluster, likely related to diet, and polygenic selection acting on standing variation that contributed to their short-stature phenotype. Thus, multiple independent instances of hominin insular dwarfism occurred on Flores.","lang":"eng"}],"volume":361},{"publication_status":"published","status":"public","article_type":"original","extern":"1","article_processing_charge":"No","title":"Embracing polygenicity: A review of methods and tools for psychiatric genetics research","oa":1,"citation":{"short":"R.M. Maier, P.M. Visscher, M.R. Robinson, N.R. Wray, Psychological Medicine 48 (2018) 1055–1067.","chicago":"Maier, R. M., P. M. Visscher, Matthew Richard Robinson, and N. R. Wray. “Embracing Polygenicity: A Review of Methods and Tools for Psychiatric Genetics Research.” <i>Psychological Medicine</i>. Cambridge University Press, 2018. <a href=\"https://doi.org/10.1017/s0033291717002318\">https://doi.org/10.1017/s0033291717002318</a>.","mla":"Maier, R. M., et al. “Embracing Polygenicity: A Review of Methods and Tools for Psychiatric Genetics Research.” <i>Psychological Medicine</i>, vol. 48, no. 7, Cambridge University Press, 2018, pp. 1055–67, doi:<a href=\"https://doi.org/10.1017/s0033291717002318\">10.1017/s0033291717002318</a>.","ieee":"R. M. Maier, P. M. Visscher, M. R. Robinson, and N. R. Wray, “Embracing polygenicity: A review of methods and tools for psychiatric genetics research,” <i>Psychological Medicine</i>, vol. 48, no. 7. Cambridge University Press, pp. 1055–1067, 2018.","ista":"Maier RM, Visscher PM, Robinson MR, Wray NR. 2018. Embracing polygenicity: A review of methods and tools for psychiatric genetics research. Psychological Medicine. 48(7), 1055–1067.","ama":"Maier RM, Visscher PM, Robinson MR, Wray NR. Embracing polygenicity: A review of methods and tools for psychiatric genetics research. <i>Psychological Medicine</i>. 2018;48(7):1055-1067. doi:<a href=\"https://doi.org/10.1017/s0033291717002318\">10.1017/s0033291717002318</a>","apa":"Maier, R. M., Visscher, P. M., Robinson, M. R., &#38; Wray, N. R. (2018). Embracing polygenicity: A review of methods and tools for psychiatric genetics research. <i>Psychological Medicine</i>. Cambridge University Press. <a href=\"https://doi.org/10.1017/s0033291717002318\">https://doi.org/10.1017/s0033291717002318</a>"},"publisher":"Cambridge University Press","date_created":"2020-04-30T10:44:35Z","main_file_link":[{"url":"https://doi.org/10.1017/s0033291717002318","open_access":"1"}],"quality_controlled":"1","year":"2018","doi":"10.1017/s0033291717002318","date_updated":"2021-01-12T08:15:05Z","author":[{"first_name":"R. M.","last_name":"Maier","full_name":"Maier, R. M."},{"full_name":"Visscher, P. M.","last_name":"Visscher","first_name":"P. M."},{"last_name":"Robinson","orcid":"0000-0001-8982-8813","full_name":"Robinson, Matthew Richard","first_name":"Matthew Richard","id":"E5D42276-F5DA-11E9-8E24-6303E6697425"},{"full_name":"Wray, N. R.","last_name":"Wray","first_name":"N. R."}],"page":"1055-1067","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","month":"05","oa_version":"Published Version","type":"journal_article","issue":"7","_id":"7721","abstract":[{"text":"The availability of genome-wide genetic data on hundreds of thousands of people has led to an equally rapid growth in methodologies available to analyse these data. While the motivation for undertaking genome-wide association studies (GWAS) is identification of genetic markers associated with complex traits, once generated these data can be used for many other analyses. GWAS have demonstrated that complex traits exhibit a highly polygenic genetic architecture, often with shared genetic risk factors across traits. New methods to analyse data from GWAS are increasingly being used to address a diverse set of questions about the aetiology of complex traits and diseases, including psychiatric disorders. Here, we give an overview of some of these methods and present examples of how they have contributed to our understanding of psychiatric disorders. We consider: (i) estimation of the extent of genetic influence on traits, (ii) uncovering of shared genetic control between traits, (iii) predictions of genetic risk for individuals, (iv) uncovering of causal relationships between traits, (v) identifying causal single-nucleotide polymorphisms and genes or (vi) the detection of genetic heterogeneity. This classification helps organise the large number of recently developed methods, although some could be placed in more than one category. While some methods require GWAS data on individual people, others simply use GWAS summary statistics data, allowing novel well-powered analyses to be conducted at a low computational burden.","lang":"eng"}],"volume":48,"date_published":"2018-05-01T00:00:00Z","intvolume":"        48","publication_identifier":{"issn":["0033-2917","1469-8978"]},"publication":"Psychological Medicine","day":"01","language":[{"iso":"eng"}]},{"year":"2018","doi":"10.1038/s41588-018-0101-4","date_published":"2018-04-16T00:00:00Z","date_updated":"2021-01-12T08:15:06Z","intvolume":"        50","publication_identifier":{"issn":["1061-4036","1546-1718"]},"author":[{"first_name":"Jian","last_name":"Zeng","full_name":"Zeng, Jian"},{"full_name":"de Vlaming, Ronald","last_name":"de Vlaming","first_name":"Ronald"},{"first_name":"Yang","last_name":"Wu","full_name":"Wu, Yang"},{"id":"E5D42276-F5DA-11E9-8E24-6303E6697425","first_name":"Matthew Richard","last_name":"Robinson","orcid":"0000-0001-8982-8813","full_name":"Robinson, Matthew Richard"},{"first_name":"Luke R.","full_name":"Lloyd-Jones, Luke R.","last_name":"Lloyd-Jones"},{"last_name":"Yengo","full_name":"Yengo, Loic","first_name":"Loic"},{"last_name":"Yap","full_name":"Yap, Chloe X.","first_name":"Chloe X."},{"full_name":"Xue, Angli","last_name":"Xue","first_name":"Angli"},{"last_name":"Sidorenko","full_name":"Sidorenko, Julia","first_name":"Julia"},{"full_name":"McRae, Allan F.","last_name":"McRae","first_name":"Allan F."},{"first_name":"Joseph E.","full_name":"Powell, Joseph E.","last_name":"Powell"},{"last_name":"Montgomery","full_name":"Montgomery, Grant W.","first_name":"Grant W."},{"first_name":"Andres","last_name":"Metspalu","full_name":"Metspalu, Andres"},{"last_name":"Esko","full_name":"Esko, Tonu","first_name":"Tonu"},{"first_name":"Greg","full_name":"Gibson, Greg","last_name":"Gibson"},{"first_name":"Naomi R.","full_name":"Wray, Naomi R.","last_name":"Wray"},{"full_name":"Visscher, Peter M.","last_name":"Visscher","first_name":"Peter M."},{"first_name":"Jian","last_name":"Yang","full_name":"Yang, Jian"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication":"Nature Genetics","page":"746-753","day":"16","language":[{"iso":"eng"}],"month":"04","publication_status":"published","status":"public","oa_version":"None","type":"journal_article","extern":"1","article_type":"original","title":"Signatures of negative selection in the genetic architecture of human complex traits","issue":"5","article_processing_charge":"No","publisher":"Springer Nature","citation":{"ista":"Zeng J, de Vlaming R, Wu Y, Robinson MR, Lloyd-Jones LR, Yengo L, Yap CX, Xue A, Sidorenko J, McRae AF, Powell JE, Montgomery GW, Metspalu A, Esko T, Gibson G, Wray NR, Visscher PM, Yang J. 2018. Signatures of negative selection in the genetic architecture of human complex traits. Nature Genetics. 50(5), 746–753.","ieee":"J. Zeng <i>et al.</i>, “Signatures of negative selection in the genetic architecture of human complex traits,” <i>Nature Genetics</i>, vol. 50, no. 5. Springer Nature, pp. 746–753, 2018.","apa":"Zeng, J., de Vlaming, R., Wu, Y., Robinson, M. R., Lloyd-Jones, L. R., Yengo, L., … Yang, J. (2018). Signatures of negative selection in the genetic architecture of human complex traits. <i>Nature Genetics</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41588-018-0101-4\">https://doi.org/10.1038/s41588-018-0101-4</a>","ama":"Zeng J, de Vlaming R, Wu Y, et al. Signatures of negative selection in the genetic architecture of human complex traits. <i>Nature Genetics</i>. 2018;50(5):746-753. doi:<a href=\"https://doi.org/10.1038/s41588-018-0101-4\">10.1038/s41588-018-0101-4</a>","short":"J. Zeng, R. de Vlaming, Y. Wu, M.R. Robinson, L.R. Lloyd-Jones, L. Yengo, C.X. Yap, A. Xue, J. Sidorenko, A.F. McRae, J.E. Powell, G.W. Montgomery, A. Metspalu, T. Esko, G. Gibson, N.R. Wray, P.M. Visscher, J. Yang, Nature Genetics 50 (2018) 746–753.","chicago":"Zeng, Jian, Ronald de Vlaming, Yang Wu, Matthew Richard Robinson, Luke R. Lloyd-Jones, Loic Yengo, Chloe X. Yap, et al. “Signatures of Negative Selection in the Genetic Architecture of Human Complex Traits.” <i>Nature Genetics</i>. Springer Nature, 2018. <a href=\"https://doi.org/10.1038/s41588-018-0101-4\">https://doi.org/10.1038/s41588-018-0101-4</a>.","mla":"Zeng, Jian, et al. “Signatures of Negative Selection in the Genetic Architecture of Human Complex Traits.” <i>Nature Genetics</i>, vol. 50, no. 5, Springer Nature, 2018, pp. 746–53, doi:<a href=\"https://doi.org/10.1038/s41588-018-0101-4\">10.1038/s41588-018-0101-4</a>."},"_id":"7722","abstract":[{"lang":"eng","text":"We develop a Bayesian mixed linear model that simultaneously estimates single-nucleotide polymorphism (SNP)-based heritability, polygenicity (proportion of SNPs with nonzero effects), and the relationship between SNP effect size and minor allele frequency for complex traits in conventionally unrelated individuals using genome-wide SNP data. We apply the method to 28 complex traits in the UK Biobank data (N = 126,752) and show that on average, 6% of SNPs have nonzero effects, which in total explain 22% of phenotypic variance. We detect significant (P < 0.05/28) signatures of natural selection in the genetic architecture of 23 traits, including reproductive, cardiovascular, and anthropometric traits, as well as educational attainment. The significant estimates of the relationship between effect size and minor allele frequency in complex traits are consistent with a model of negative (or purifying) selection, as confirmed by forward simulation. We conclude that negative selection acts pervasively on the genetic variants associated with human complex traits."}],"quality_controlled":"1","volume":50,"date_created":"2020-04-30T10:44:57Z"},{"date_published":"2018-04-01T00:00:00Z","doi":"10.1534/genetics.117.300360","intvolume":"       208","date_updated":"2021-01-12T08:15:06Z","year":"2018","day":"01","language":[{"iso":"eng"}],"month":"04","author":[{"first_name":"Luke R.","full_name":"Lloyd-Jones, Luke R.","last_name":"Lloyd-Jones"},{"id":"E5D42276-F5DA-11E9-8E24-6303E6697425","first_name":"Matthew Richard","orcid":"0000-0001-8982-8813","full_name":"Robinson, Matthew Richard","last_name":"Robinson"},{"full_name":"Yang, Jian","last_name":"Yang","first_name":"Jian"},{"first_name":"Peter M.","full_name":"Visscher, Peter M.","last_name":"Visscher"}],"publication_identifier":{"issn":["0016-6731","1943-2631"]},"page":"1397-1408","publication":"Genetics","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_type":"original","extern":"1","article_processing_charge":"No","issue":"4","title":"Transformation of summary statistics from linear mixed model association on all-or-none traits to odds ratio","status":"public","publication_status":"published","oa_version":"None","type":"journal_article","abstract":[{"lang":"eng","text":"Genome-wide association studies (GWAS) have identified thousands of loci that are robustly associated with complex diseases. The use of linear mixed model (LMM) methodology for GWAS is becoming more prevalent due to its ability to control for population structure and cryptic relatedness and to increase power. The odds ratio (OR) is a common measure of the association of a disease with an exposure (e.g., a genetic variant) and is readably available from logistic regression. However, when the LMM is applied to all-or-none traits it provides estimates of genetic effects on the observed 0–1 scale, a different scale to that in logistic regression. This limits the comparability of results across studies, for example in a meta-analysis, and makes the interpretation of the magnitude of an effect from an LMM GWAS difficult. In this study, we derived transformations from the genetic effects estimated under the LMM to the OR that only rely on summary statistics. To test the proposed transformations, we used real genotypes from two large, publicly available data sets to simulate all-or-none phenotypes for a set of scenarios that differ in underlying model, disease prevalence, and heritability. Furthermore, we applied these transformations to GWAS summary statistics for type 2 diabetes generated from 108,042 individuals in the UK Biobank. In both simulation and real-data application, we observed very high concordance between the transformed OR from the LMM and either the simulated truth or estimates from logistic regression. The transformations derived and validated in this study improve the comparability of results from prospective and already performed LMM GWAS on complex diseases by providing a reliable transformation to a common comparative scale for the genetic effects."}],"date_created":"2020-04-30T10:45:19Z","volume":208,"quality_controlled":"1","citation":{"ista":"Lloyd-Jones LR, Robinson MR, Yang J, Visscher PM. 2018. Transformation of summary statistics from linear mixed model association on all-or-none traits to odds ratio. Genetics. 208(4), 1397–1408.","ieee":"L. R. Lloyd-Jones, M. R. Robinson, J. Yang, and P. M. Visscher, “Transformation of summary statistics from linear mixed model association on all-or-none traits to odds ratio,” <i>Genetics</i>, vol. 208, no. 4. Genetics Society of America, pp. 1397–1408, 2018.","apa":"Lloyd-Jones, L. R., Robinson, M. R., Yang, J., &#38; Visscher, P. M. (2018). Transformation of summary statistics from linear mixed model association on all-or-none traits to odds ratio. <i>Genetics</i>. Genetics Society of America. <a href=\"https://doi.org/10.1534/genetics.117.300360\">https://doi.org/10.1534/genetics.117.300360</a>","ama":"Lloyd-Jones LR, Robinson MR, Yang J, Visscher PM. Transformation of summary statistics from linear mixed model association on all-or-none traits to odds ratio. <i>Genetics</i>. 2018;208(4):1397-1408. doi:<a href=\"https://doi.org/10.1534/genetics.117.300360\">10.1534/genetics.117.300360</a>","short":"L.R. Lloyd-Jones, M.R. Robinson, J. Yang, P.M. Visscher, Genetics 208 (2018) 1397–1408.","mla":"Lloyd-Jones, Luke R., et al. “Transformation of Summary Statistics from Linear Mixed Model Association on All-or-None Traits to Odds Ratio.” <i>Genetics</i>, vol. 208, no. 4, Genetics Society of America, 2018, pp. 1397–408, doi:<a href=\"https://doi.org/10.1534/genetics.117.300360\">10.1534/genetics.117.300360</a>.","chicago":"Lloyd-Jones, Luke R., Matthew Richard Robinson, Jian Yang, and Peter M. Visscher. “Transformation of Summary Statistics from Linear Mixed Model Association on All-or-None Traits to Odds Ratio.” <i>Genetics</i>. Genetics Society of America, 2018. <a href=\"https://doi.org/10.1534/genetics.117.300360\">https://doi.org/10.1534/genetics.117.300360</a>."},"_id":"7723","publisher":"Genetics Society of America"},{"publication_status":"published","status":"public","type":"journal_article","oa_version":"None","extern":"1","article_type":"original","title":"Evidence of directional and stabilizing selection in contemporary humans","article_processing_charge":"No","issue":"1","publisher":"Proceedings of the National Academy of Sciences","citation":{"ista":"Sanjak JS, Sidorenko J, Robinson MR, Thornton KR, Visscher PM. 2018. Evidence of directional and stabilizing selection in contemporary humans. Proceedings of the National Academy of Sciences. 115(1), 151–156.","ieee":"J. S. Sanjak, J. Sidorenko, M. R. Robinson, K. R. Thornton, and P. M. Visscher, “Evidence of directional and stabilizing selection in contemporary humans,” <i>Proceedings of the National Academy of Sciences</i>, vol. 115, no. 1. Proceedings of the National Academy of Sciences, pp. 151–156, 2018.","apa":"Sanjak, J. S., Sidorenko, J., Robinson, M. R., Thornton, K. R., &#38; Visscher, P. M. (2018). Evidence of directional and stabilizing selection in contemporary humans. <i>Proceedings of the National Academy of Sciences</i>. Proceedings of the National Academy of Sciences. <a href=\"https://doi.org/10.1073/pnas.1707227114\">https://doi.org/10.1073/pnas.1707227114</a>","ama":"Sanjak JS, Sidorenko J, Robinson MR, Thornton KR, Visscher PM. Evidence of directional and stabilizing selection in contemporary humans. <i>Proceedings of the National Academy of Sciences</i>. 2018;115(1):151-156. doi:<a href=\"https://doi.org/10.1073/pnas.1707227114\">10.1073/pnas.1707227114</a>","short":"J.S. Sanjak, J. Sidorenko, M.R. Robinson, K.R. Thornton, P.M. Visscher, Proceedings of the National Academy of Sciences 115 (2018) 151–156.","mla":"Sanjak, Jaleal S., et al. “Evidence of Directional and Stabilizing Selection in Contemporary Humans.” <i>Proceedings of the National Academy of Sciences</i>, vol. 115, no. 1, Proceedings of the National Academy of Sciences, 2018, pp. 151–56, doi:<a href=\"https://doi.org/10.1073/pnas.1707227114\">10.1073/pnas.1707227114</a>.","chicago":"Sanjak, Jaleal S., Julia Sidorenko, Matthew Richard Robinson, Kevin R. Thornton, and Peter M. Visscher. “Evidence of Directional and Stabilizing Selection in Contemporary Humans.” <i>Proceedings of the National Academy of Sciences</i>. Proceedings of the National Academy of Sciences, 2018. <a href=\"https://doi.org/10.1073/pnas.1707227114\">https://doi.org/10.1073/pnas.1707227114</a>."},"_id":"7724","abstract":[{"text":"Modern molecular genetic datasets, primarily collected to study the biology of human health and disease, can be used to directly measure the action of natural selection and reveal important features of contemporary human evolution. Here we leverage the UK Biobank data to test for the presence of linear and nonlinear natural selection in a contemporary population of the United Kingdom. We obtain phenotypic and genetic evidence consistent with the action of linear/directional selection. Phenotypic evidence suggests that stabilizing selection, which acts to reduce variance in the population without necessarily modifying the population mean, is widespread and relatively weak in comparison with estimates from other species.","lang":"eng"}],"quality_controlled":"1","volume":115,"date_created":"2020-04-30T10:45:43Z","year":"2018","date_published":"2018-01-02T00:00:00Z","related_material":{"link":[{"relation":"erratum","url":"https://doi.org/10.1073/pnas.1806837115"}]},"doi":"10.1073/pnas.1707227114","date_updated":"2021-01-12T08:15:07Z","intvolume":"       115","publication_identifier":{"issn":["0027-8424","1091-6490"]},"author":[{"last_name":"Sanjak","full_name":"Sanjak, Jaleal S.","first_name":"Jaleal S."},{"first_name":"Julia","full_name":"Sidorenko, Julia","last_name":"Sidorenko"},{"first_name":"Matthew Richard","id":"E5D42276-F5DA-11E9-8E24-6303E6697425","last_name":"Robinson","orcid":"0000-0001-8982-8813","full_name":"Robinson, Matthew Richard"},{"first_name":"Kevin R.","last_name":"Thornton","full_name":"Thornton, Kevin R."},{"first_name":"Peter M.","last_name":"Visscher","full_name":"Visscher, Peter M."}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","page":"151-156","publication":"Proceedings of the National Academy of Sciences","language":[{"iso":"eng"}],"day":"02","month":"01"},{"date_updated":"2021-01-12T08:15:18Z","intvolume":"         9","date_published":"2018-10-19T00:00:00Z","doi":"10.1038/s41467-018-06851-5","year":"2018","month":"10","language":[{"iso":"eng"}],"day":"19","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_number":"4348","publication":"Nature Communications","publication_identifier":{"issn":["2041-1723"]},"author":[{"last_name":"Goodrich","orcid":"0000-0002-1307-5074","full_name":"Goodrich, Carl Peter","first_name":"Carl Peter","id":"EB352CD2-F68A-11E9-89C5-A432E6697425"},{"first_name":"Michael P.","full_name":"Brenner, Michael P.","last_name":"Brenner"},{"last_name":"Ribbeck","full_name":"Ribbeck, Katharina","first_name":"Katharina"}],"title":"Enhanced diffusion by binding to the crosslinks of a polymer gel","article_processing_charge":"No","extern":"1","article_type":"original","type":"journal_article","oa_version":"Published Version","publication_status":"published","status":"public","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1038/s41467-018-06851-5"}],"volume":9,"quality_controlled":"1","date_created":"2020-04-30T11:38:01Z","abstract":[{"lang":"eng","text":"Creating a selective gel that filters particles based on their interactions is a major goal of nanotechnology, with far-reaching implications from drug delivery to controlling assembly pathways. However, this is particularly difficult when the particles are larger than the gel’s characteristic mesh size because such particles cannot passively pass through the gel. Thus, filtering requires the interacting particles to transiently reorganize the gel’s internal structure. While significant advances, e.g., in DNA engineering, have enabled the design of nano-materials with programmable interactions, it is not clear what physical principles such a designer gel could exploit to achieve selective permeability. We present an equilibrium mechanism where crosslink binding dynamics are affected by interacting particles such that particle diffusion is enhanced. In addition to revealing specific design rules for manufacturing selective gels, our results have the potential to explain the origin of selective permeability in certain biological materials, including the nuclear pore complex."}],"publisher":"Springer Nature","citation":{"short":"C.P. Goodrich, M.P. Brenner, K. Ribbeck, Nature Communications 9 (2018).","mla":"Goodrich, Carl Peter, et al. “Enhanced Diffusion by Binding to the Crosslinks of a Polymer Gel.” <i>Nature Communications</i>, vol. 9, 4348, Springer Nature, 2018, doi:<a href=\"https://doi.org/10.1038/s41467-018-06851-5\">10.1038/s41467-018-06851-5</a>.","chicago":"Goodrich, Carl Peter, Michael P. Brenner, and Katharina Ribbeck. “Enhanced Diffusion by Binding to the Crosslinks of a Polymer Gel.” <i>Nature Communications</i>. Springer Nature, 2018. <a href=\"https://doi.org/10.1038/s41467-018-06851-5\">https://doi.org/10.1038/s41467-018-06851-5</a>.","ieee":"C. P. Goodrich, M. P. Brenner, and K. Ribbeck, “Enhanced diffusion by binding to the crosslinks of a polymer gel,” <i>Nature Communications</i>, vol. 9. Springer Nature, 2018.","ista":"Goodrich CP, Brenner MP, Ribbeck K. 2018. Enhanced diffusion by binding to the crosslinks of a polymer gel. Nature Communications. 9, 4348.","ama":"Goodrich CP, Brenner MP, Ribbeck K. Enhanced diffusion by binding to the crosslinks of a polymer gel. <i>Nature Communications</i>. 2018;9. doi:<a href=\"https://doi.org/10.1038/s41467-018-06851-5\">10.1038/s41467-018-06851-5</a>","apa":"Goodrich, C. P., Brenner, M. P., &#38; Ribbeck, K. (2018). Enhanced diffusion by binding to the crosslinks of a polymer gel. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41467-018-06851-5\">https://doi.org/10.1038/s41467-018-06851-5</a>"},"_id":"7754","oa":1},{"department":[{"_id":"GaNo"}],"author":[{"id":"3E57A680-F248-11E8-B48F-1D18A9856A87","first_name":"Gaia","last_name":"Novarino","orcid":"0000-0002-7673-7178","full_name":"Novarino, Gaia"}],"publist_id":"7365","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","article_number":"eaar7514","publication":"Science Translational Medicine","language":[{"iso":"eng"}],"day":"10","month":"01","year":"2018","date_published":"2018-01-10T00:00:00Z","doi":"10.1126/scitranslmed.aar7514","date_updated":"2021-01-12T07:59:42Z","scopus_import":1,"intvolume":"        10","publisher":"American Association for the Advancement of Science","_id":"456","citation":{"ista":"Novarino G. 2018. Zika-associated microcephaly: Reduce the stress and race for the treatment. Science Translational Medicine. 10(423), eaar7514.","ieee":"G. Novarino, “Zika-associated microcephaly: Reduce the stress and race for the treatment,” <i>Science Translational Medicine</i>, vol. 10, no. 423. American Association for the Advancement of Science, 2018.","apa":"Novarino, G. (2018). Zika-associated microcephaly: Reduce the stress and race for the treatment. <i>Science Translational Medicine</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/scitranslmed.aar7514\">https://doi.org/10.1126/scitranslmed.aar7514</a>","ama":"Novarino G. Zika-associated microcephaly: Reduce the stress and race for the treatment. <i>Science Translational Medicine</i>. 2018;10(423). doi:<a href=\"https://doi.org/10.1126/scitranslmed.aar7514\">10.1126/scitranslmed.aar7514</a>","short":"G. Novarino, Science Translational Medicine 10 (2018).","mla":"Novarino, Gaia. “Zika-Associated Microcephaly: Reduce the Stress and Race for the Treatment.” <i>Science Translational Medicine</i>, vol. 10, no. 423, eaar7514, American Association for the Advancement of Science, 2018, doi:<a href=\"https://doi.org/10.1126/scitranslmed.aar7514\">10.1126/scitranslmed.aar7514</a>.","chicago":"Novarino, Gaia. “Zika-Associated Microcephaly: Reduce the Stress and Race for the Treatment.” <i>Science Translational Medicine</i>. American Association for the Advancement of Science, 2018. <a href=\"https://doi.org/10.1126/scitranslmed.aar7514\">https://doi.org/10.1126/scitranslmed.aar7514</a>."},"abstract":[{"lang":"eng","text":"Inhibition of the endoplasmic reticulum stress pathway may hold the key to Zika virus-associated microcephaly treatment. "}],"volume":10,"quality_controlled":"1","date_created":"2018-12-11T11:46:34Z","status":"public","publication_status":"published","oa_version":"None","type":"journal_article","title":"Zika-associated microcephaly: Reduce the stress and race for the treatment","issue":"423"},{"date_created":"2018-12-11T11:46:35Z","quality_controlled":"1","citation":{"ieee":"M. Pleska, M. Lang, D. Refardt, B. Levin, and C. C. Guet, “Phage-host population dynamics promotes prophage acquisition in bacteria with innate immunity,” <i>Nature Ecology and Evolution</i>, vol. 2, no. 2. Springer Nature, pp. 359–366, 2018.","ista":"Pleska M, Lang M, Refardt D, Levin B, Guet CC. 2018. Phage-host population dynamics promotes prophage acquisition in bacteria with innate immunity. Nature Ecology and Evolution. 2(2), 359–366.","ama":"Pleska M, Lang M, Refardt D, Levin B, Guet CC. Phage-host population dynamics promotes prophage acquisition in bacteria with innate immunity. <i>Nature Ecology and Evolution</i>. 2018;2(2):359-366. doi:<a href=\"https://doi.org/10.1038/s41559-017-0424-z\">10.1038/s41559-017-0424-z</a>","apa":"Pleska, M., Lang, M., Refardt, D., Levin, B., &#38; Guet, C. C. (2018). Phage-host population dynamics promotes prophage acquisition in bacteria with innate immunity. <i>Nature Ecology and Evolution</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41559-017-0424-z\">https://doi.org/10.1038/s41559-017-0424-z</a>","short":"M. Pleska, M. Lang, D. Refardt, B. Levin, C.C. Guet, Nature Ecology and Evolution 2 (2018) 359–366.","mla":"Pleska, Maros, et al. “Phage-Host Population Dynamics Promotes Prophage Acquisition in Bacteria with Innate Immunity.” <i>Nature Ecology and Evolution</i>, vol. 2, no. 2, Springer Nature, 2018, pp. 359–66, doi:<a href=\"https://doi.org/10.1038/s41559-017-0424-z\">10.1038/s41559-017-0424-z</a>.","chicago":"Pleska, Maros, Moritz Lang, Dominik Refardt, Bruce Levin, and Calin C Guet. “Phage-Host Population Dynamics Promotes Prophage Acquisition in Bacteria with Innate Immunity.” <i>Nature Ecology and Evolution</i>. Springer Nature, 2018. <a href=\"https://doi.org/10.1038/s41559-017-0424-z\">https://doi.org/10.1038/s41559-017-0424-z</a>."},"publisher":"Springer Nature","article_processing_charge":"No","title":"Phage-host population dynamics promotes prophage acquisition in bacteria with innate immunity","ec_funded":1,"publication_status":"published","status":"public","month":"02","page":"359 - 366","external_id":{"isi":["000426516400027"]},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","author":[{"first_name":"Maros","id":"4569785E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-7460-7479","full_name":"Pleska, Maros","last_name":"Pleska"},{"id":"29E0800A-F248-11E8-B48F-1D18A9856A87","first_name":"Moritz","full_name":"Lang, Moritz","last_name":"Lang"},{"full_name":"Refardt, Dominik","last_name":"Refardt","first_name":"Dominik"},{"first_name":"Bruce","last_name":"Levin","full_name":"Levin, Bruce"},{"first_name":"Calin C","id":"47F8433E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6220-2052","full_name":"Guet, Calin C","last_name":"Guet"}],"department":[{"_id":"CaGu"},{"_id":"GaTk"}],"date_updated":"2023-09-15T12:04:57Z","doi":"10.1038/s41559-017-0424-z","year":"2018","volume":2,"abstract":[{"lang":"eng","text":"Temperate bacteriophages integrate in bacterial genomes as prophages and represent an important source of genetic variation for bacterial evolution, frequently transmitting fitness-augmenting genes such as toxins responsible for virulence of major pathogens. However, only a fraction of bacteriophage infections are lysogenic and lead to prophage acquisition, whereas the majority are lytic and kill the infected bacteria. Unless able to discriminate lytic from lysogenic infections, mechanisms of immunity to bacteriophages are expected to act as a double-edged sword and increase the odds of survival at the cost of depriving bacteria of potentially beneficial prophages. We show that although restriction-modification systems as mechanisms of innate immunity prevent both lytic and lysogenic infections indiscriminately in individual bacteria, they increase the number of prophage-acquiring individuals at the population level. We find that this counterintuitive result is a consequence of phage-host population dynamics, in which restriction-modification systems delay infection onset until bacteria reach densities at which the probability of lysogeny increases. These results underscore the importance of population-level dynamics as a key factor modulating costs and benefits of immunity to temperate bacteriophages"}],"project":[{"_id":"25681D80-B435-11E9-9278-68D0E5697425","name":"International IST Postdoc Fellowship Programme","grant_number":"291734","call_identifier":"FP7"},{"_id":"251BCBEC-B435-11E9-9278-68D0E5697425","grant_number":"RGY0079/2011","name":"Multi-Level Conflicts in Evolutionary Dynamics of Restriction-Modification Systems (HFSP Young investigators' grant)"},{"_id":"251D65D8-B435-11E9-9278-68D0E5697425","name":"Effects of Stochasticity on the Function of Restriction-Modi cation Systems at the Single-Cell Level (DOC Fellowship)","grant_number":"24210"}],"_id":"457","isi":1,"issue":"2","type":"journal_article","oa_version":"None","day":"01","language":[{"iso":"eng"}],"publication":"Nature Ecology and Evolution","publist_id":"7364","intvolume":"         2","scopus_import":"1","related_material":{"record":[{"id":"202","status":"public","relation":"dissertation_contains"}]},"date_published":"2018-02-01T00:00:00Z"},{"oa_version":"Preprint","type":"journal_article","isi":1,"issue":"4","project":[{"call_identifier":"FP7","_id":"25681D80-B435-11E9-9278-68D0E5697425","grant_number":"291734","name":"International IST Postdoc Fellowship Programme"}],"_id":"458","volume":370,"abstract":[{"text":"We consider congruences of straight lines in a plane with the combinatorics of the square grid, with all elementary quadrilaterals possessing an incircle. It is shown that all the vertices of such nets (we call them incircular or IC-nets) lie on confocal conics. Our main new results are on checkerboard IC-nets in the plane. These are congruences of straight lines in the plane with the combinatorics of the square grid, combinatorially colored as a checkerboard, such that all black coordinate quadrilaterals possess inscribed circles. We show how this larger class of IC-nets appears quite naturally in Laguerre geometry of oriented planes and spheres and leads to new remarkable incidence theorems. Most of our results are valid in hyperbolic and spherical geometries as well. We present also generalizations in spaces of higher dimension, called checkerboard IS-nets. The construction of these nets is based on a new 9 inspheres incidence theorem.","lang":"eng"}],"scopus_import":"1","intvolume":"       370","date_published":"2018-04-01T00:00:00Z","publication":"Transactions of the American Mathematical Society","publist_id":"7363","language":[{"iso":"eng"}],"day":"01","ec_funded":1,"status":"public","publication_status":"published","article_processing_charge":"No","title":"Incircular nets and confocal conics","citation":{"mla":"Akopyan, Arseniy, and Alexander Bobenko. “Incircular Nets and Confocal Conics.” <i>Transactions of the American Mathematical Society</i>, vol. 370, no. 4, American Mathematical Society, 2018, pp. 2825–54, doi:<a href=\"https://doi.org/10.1090/tran/7292\">10.1090/tran/7292</a>.","chicago":"Akopyan, Arseniy, and Alexander Bobenko. “Incircular Nets and Confocal Conics.” <i>Transactions of the American Mathematical Society</i>. American Mathematical Society, 2018. <a href=\"https://doi.org/10.1090/tran/7292\">https://doi.org/10.1090/tran/7292</a>.","short":"A. Akopyan, A. Bobenko, Transactions of the American Mathematical Society 370 (2018) 2825–2854.","apa":"Akopyan, A., &#38; Bobenko, A. (2018). Incircular nets and confocal conics. <i>Transactions of the American Mathematical Society</i>. American Mathematical Society. <a href=\"https://doi.org/10.1090/tran/7292\">https://doi.org/10.1090/tran/7292</a>","ama":"Akopyan A, Bobenko A. Incircular nets and confocal conics. <i>Transactions of the American Mathematical Society</i>. 2018;370(4):2825-2854. doi:<a href=\"https://doi.org/10.1090/tran/7292\">10.1090/tran/7292</a>","ista":"Akopyan A, Bobenko A. 2018. Incircular nets and confocal conics. Transactions of the American Mathematical Society. 370(4), 2825–2854.","ieee":"A. Akopyan and A. Bobenko, “Incircular nets and confocal conics,” <i>Transactions of the American Mathematical Society</i>, vol. 370, no. 4. American Mathematical Society, pp. 2825–2854, 2018."},"oa":1,"publisher":"American Mathematical Society","date_created":"2018-12-11T11:46:35Z","quality_controlled":"1","main_file_link":[{"url":"https://arxiv.org/abs/1602.04637","open_access":"1"}],"acknowledgement":"DFG Collaborative Research Center TRR 109 “Discretization in Geometry and Dynamics”; People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007-2013) REA grant agreement n◦[291734]","year":"2018","date_updated":"2023-09-11T14:19:12Z","doi":"10.1090/tran/7292","external_id":{"isi":["000423197800019"]},"page":"2825 - 2854","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","author":[{"first_name":"Arseniy","id":"430D2C90-F248-11E8-B48F-1D18A9856A87","last_name":"Akopyan","full_name":"Akopyan, Arseniy","orcid":"0000-0002-2548-617X"},{"last_name":"Bobenko","full_name":"Bobenko, Alexander","first_name":"Alexander"}],"department":[{"_id":"HeEd"}],"month":"04"},{"doi":"10.1103/PhysRevB.98.161122","date_updated":"2023-09-11T12:55:03Z","year":"2018","month":"10","author":[{"full_name":"Hetterich, Daniel","last_name":"Hetterich","first_name":"Daniel"},{"full_name":"Yao, Norman","last_name":"Yao","first_name":"Norman"},{"id":"47809E7E-F248-11E8-B48F-1D18A9856A87","first_name":"Maksym","last_name":"Serbyn","orcid":"0000-0002-2399-5827","full_name":"Serbyn, Maksym"},{"first_name":"Frank","full_name":"Pollmann, Frank","last_name":"Pollmann"},{"full_name":"Trauzettel, Björn","last_name":"Trauzettel","first_name":"Björn"}],"department":[{"_id":"MaSe"}],"article_number":"161122","external_id":{"isi":["000448596500002"],"arxiv":["1806.08316"]},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","article_type":"original","article_processing_charge":"No","title":"Detection and characterization of many-body localization in central spin models","publication_status":"published","status":"public","acknowledgement":"F.P. acknowledges the sup- port of the DFG Research Unit FOR 1807 through Grants No. PO 1370/2-1 and No. TRR80, the Nanosystems Initiative Munich (NIM) by the German Excellence Initiative, and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (Grant Agreement No. 771537). N.Y.Y. acknowledges support from the NSF (PHY-1654740), the ARO STIR program, and a Google research award.","date_created":"2018-12-11T11:44:20Z","quality_controlled":"1","main_file_link":[{"open_access":"1","url":"https://arxiv.org/abs/1806.08316"}],"citation":{"short":"D. Hetterich, N. Yao, M. Serbyn, F. Pollmann, B. Trauzettel, Physical Review B 98 (2018).","mla":"Hetterich, Daniel, et al. “Detection and Characterization of Many-Body Localization in Central Spin Models.” <i>Physical Review B</i>, vol. 98, no. 16, 161122, American Physical Society, 2018, doi:<a href=\"https://doi.org/10.1103/PhysRevB.98.161122\">10.1103/PhysRevB.98.161122</a>.","chicago":"Hetterich, Daniel, Norman Yao, Maksym Serbyn, Frank Pollmann, and Björn Trauzettel. “Detection and Characterization of Many-Body Localization in Central Spin Models.” <i>Physical Review B</i>. American Physical Society, 2018. <a href=\"https://doi.org/10.1103/PhysRevB.98.161122\">https://doi.org/10.1103/PhysRevB.98.161122</a>.","ieee":"D. Hetterich, N. Yao, M. Serbyn, F. Pollmann, and B. Trauzettel, “Detection and characterization of many-body localization in central spin models,” <i>Physical Review B</i>, vol. 98, no. 16. American Physical Society, 2018.","ista":"Hetterich D, Yao N, Serbyn M, Pollmann F, Trauzettel B. 2018. Detection and characterization of many-body localization in central spin models. Physical Review B. 98(16), 161122.","ama":"Hetterich D, Yao N, Serbyn M, Pollmann F, Trauzettel B. Detection and characterization of many-body localization in central spin models. <i>Physical Review B</i>. 2018;98(16). doi:<a href=\"https://doi.org/10.1103/PhysRevB.98.161122\">10.1103/PhysRevB.98.161122</a>","apa":"Hetterich, D., Yao, N., Serbyn, M., Pollmann, F., &#38; Trauzettel, B. (2018). Detection and characterization of many-body localization in central spin models. <i>Physical Review B</i>. American Physical Society. <a href=\"https://doi.org/10.1103/PhysRevB.98.161122\">https://doi.org/10.1103/PhysRevB.98.161122</a>"},"oa":1,"publisher":"American Physical Society","date_published":"2018-10-15T00:00:00Z","intvolume":"        98","scopus_import":"1","language":[{"iso":"eng"}],"day":"15","arxiv":1,"publication":"Physical Review B","publist_id":"8008","isi":1,"issue":"16","oa_version":"Preprint","type":"journal_article","abstract":[{"text":"We analyze a disordered central spin model, where a central spin interacts equally with each spin in a periodic one-dimensional (1D) random-field Heisenberg chain. If the Heisenberg chain is initially in the many-body localized (MBL) phase, we find that the coupling to the central spin suffices to delocalize the chain for a substantial range of coupling strengths. We calculate the phase diagram of the model and identify the phase boundary between the MBL and ergodic phase. Within the localized phase, the central spin significantly enhances the rate of the logarithmic entanglement growth and its saturation value. We attribute the increase in entanglement entropy to a nonextensive enhancement of magnetization fluctuations induced by the central spin. Finally, we demonstrate that correlation functions of the central spin can be utilized to distinguish between MBL and ergodic phases of the 1D chain. Hence, we propose the use of a central spin as a possible experimental probe to identify the MBL phase.","lang":"eng"}],"volume":98,"_id":"46"},{"related_material":{"record":[{"id":"12726","status":"public","relation":"dissertation_contains"},{"status":"public","relation":"dissertation_contains","id":"14530"},{"relation":"dissertation_contains","status":"public","id":"7258"}]},"date_published":"2018-01-08T00:00:00Z","scopus_import":"1","intvolume":"        14","publication":"Nature Physics","publist_id":"7360","language":[{"iso":"eng"}],"day":"08","type":"journal_article","oa_version":"Preprint","isi":1,"_id":"461","project":[{"call_identifier":"FP7","name":"Decoding the complexity of turbulence at its origin","grant_number":"306589","_id":"25152F3A-B435-11E9-9278-68D0E5697425"},{"grant_number":"737549","name":"Eliminating turbulence in oil pipelines","_id":"25104D44-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"}],"abstract":[{"text":"Turbulence is the major cause of friction losses in transport processes and it is responsible for a drastic drag increase in flows over bounding surfaces. While much effort is invested into developing ways to control and reduce turbulence intensities, so far no methods exist to altogether eliminate turbulence if velocities are sufficiently large. We demonstrate for pipe flow that appropriate distortions to the velocity profile lead to a complete collapse of turbulence and subsequently friction losses are reduced by as much as 90%. Counterintuitively, the return to laminar motion is accomplished by initially increasing turbulence intensities or by transiently amplifying wall shear. Since neither the Reynolds number nor the shear stresses decrease (the latter often increase), these measures are not indicative of turbulence collapse. Instead, an amplification mechanism                      measuring the interaction between eddies and the mean shear is found to set a threshold below which turbulence is suppressed beyond recovery.","lang":"eng"}],"volume":14,"year":"2018","doi":"10.1038/s41567-017-0018-3","date_updated":"2024-03-25T23:30:20Z","author":[{"last_name":"Kühnen","orcid":"0000-0003-4312-0179","full_name":"Kühnen, Jakob","id":"3A47AE32-F248-11E8-B48F-1D18A9856A87","first_name":"Jakob"},{"first_name":"Baofang","full_name":"Song, Baofang","last_name":"Song"},{"full_name":"Scarselli, Davide","orcid":"0000-0001-5227-4271","last_name":"Scarselli","first_name":"Davide","id":"40315C30-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Budanur, Nazmi B","orcid":"0000-0003-0423-5010","last_name":"Budanur","id":"3EA1010E-F248-11E8-B48F-1D18A9856A87","first_name":"Nazmi B"},{"orcid":"0000-0003-4844-6311","full_name":"Riedl, Michael","last_name":"Riedl","first_name":"Michael","id":"3BE60946-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Ashley","full_name":"Willis, Ashley","last_name":"Willis"},{"full_name":"Avila, Marc","last_name":"Avila","first_name":"Marc"},{"full_name":"Hof, Björn","orcid":"0000-0003-2057-2754","last_name":"Hof","id":"3A374330-F248-11E8-B48F-1D18A9856A87","first_name":"Björn"}],"department":[{"_id":"BjHo"}],"external_id":{"isi":["000429434100020"]},"page":"386-390","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","month":"01","publication_status":"published","status":"public","ec_funded":1,"article_processing_charge":"No","title":"Destabilizing turbulence in pipe flow","oa":1,"citation":{"chicago":"Kühnen, Jakob, Baofang Song, Davide Scarselli, Nazmi B Budanur, Michael Riedl, Ashley Willis, Marc Avila, and Björn Hof. “Destabilizing Turbulence in Pipe Flow.” <i>Nature Physics</i>. Nature Publishing Group, 2018. <a href=\"https://doi.org/10.1038/s41567-017-0018-3\">https://doi.org/10.1038/s41567-017-0018-3</a>.","mla":"Kühnen, Jakob, et al. “Destabilizing Turbulence in Pipe Flow.” <i>Nature Physics</i>, vol. 14, Nature Publishing Group, 2018, pp. 386–90, doi:<a href=\"https://doi.org/10.1038/s41567-017-0018-3\">10.1038/s41567-017-0018-3</a>.","short":"J. Kühnen, B. Song, D. Scarselli, N.B. Budanur, M. Riedl, A. Willis, M. Avila, B. Hof, Nature Physics 14 (2018) 386–390.","apa":"Kühnen, J., Song, B., Scarselli, D., Budanur, N. B., Riedl, M., Willis, A., … Hof, B. (2018). Destabilizing turbulence in pipe flow. <i>Nature Physics</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/s41567-017-0018-3\">https://doi.org/10.1038/s41567-017-0018-3</a>","ama":"Kühnen J, Song B, Scarselli D, et al. Destabilizing turbulence in pipe flow. <i>Nature Physics</i>. 2018;14:386-390. doi:<a href=\"https://doi.org/10.1038/s41567-017-0018-3\">10.1038/s41567-017-0018-3</a>","ista":"Kühnen J, Song B, Scarselli D, Budanur NB, Riedl M, Willis A, Avila M, Hof B. 2018. Destabilizing turbulence in pipe flow. Nature Physics. 14, 386–390.","ieee":"J. Kühnen <i>et al.</i>, “Destabilizing turbulence in pipe flow,” <i>Nature Physics</i>, vol. 14. Nature Publishing Group, pp. 386–390, 2018."},"publisher":"Nature Publishing Group","acknowledgement":"We acknowledge the European Research Council under the European Union’s Seventh Framework Programme (FP/2007-2013)/ERC Grant Agreement 306589, the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement no. 737549) and the Deutsche Forschungsgemeinschaft (Project No. FOR 1182) for financial support. We thank our technician P. Maier for providing highly valuable ideas and greatly supporting us in all technical aspects. We thank M. Schaner for technical drawings, construction and design. We thank M. Schwegel for a Matlab code to post-process experimental data.","date_created":"2018-12-11T11:46:36Z","quality_controlled":"1","main_file_link":[{"open_access":"1","url":"https://arxiv.org/abs/1711.06543"}]},{"author":[{"last_name":"Fan","full_name":"Fan, Ligang","first_name":"Ligang"},{"first_name":"Lei","full_name":"Zhao, Lei","last_name":"Zhao"},{"first_name":"Wei","full_name":"Hu, Wei","last_name":"Hu"},{"first_name":"Weina","full_name":"Li, Weina","last_name":"Li"},{"last_name":"Novák","full_name":"Novák, Ondřej","first_name":"Ondřej"},{"first_name":"Miroslav","full_name":"Strnad, Miroslav","last_name":"Strnad"},{"id":"4542EF9A-F248-11E8-B48F-1D18A9856A87","first_name":"Sibu","last_name":"Simon","full_name":"Simon, Sibu","orcid":"0000-0002-1998-6741"},{"first_name":"Jirí","id":"4159519E-F248-11E8-B48F-1D18A9856A87","last_name":"Friml","orcid":"0000-0002-8302-7596","full_name":"Friml, Jirí"},{"last_name":"Shen","full_name":"Shen, Jinbo","first_name":"Jinbo"},{"full_name":"Jiang, Liwen","last_name":"Jiang","first_name":"Liwen"},{"full_name":"Qiu, Quan","last_name":"Qiu","first_name":"Quan"}],"tmp":{"image":"/images/cc_by_nc.png","name":"Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc/4.0/legalcode","short":"CC BY-NC (4.0)"},"pmid":1,"department":[{"_id":"JiFr"}],"external_id":{"isi":["000426870500012"],"pmid":["29360148"]},"page":"850 - 864","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","month":"05","year":"2018","doi":"10.1111/pce.13153","date_updated":"2023-09-13T09:03:18Z","oa":1,"citation":{"mla":"Fan, Ligang, et al. “NHX Antiporters Regulate the PH of Endoplasmic Reticulum and Auxin-Mediated Development.” <i>Plant, Cell and Environment</i>, vol. 41, Wiley-Blackwell, 2018, pp. 850–64, doi:<a href=\"https://doi.org/10.1111/pce.13153\">10.1111/pce.13153</a>.","chicago":"Fan, Ligang, Lei Zhao, Wei Hu, Weina Li, Ondřej Novák, Miroslav Strnad, Sibu Simon, et al. “NHX Antiporters Regulate the PH of Endoplasmic Reticulum and Auxin-Mediated Development.” <i>Plant, Cell and Environment</i>. Wiley-Blackwell, 2018. <a href=\"https://doi.org/10.1111/pce.13153\">https://doi.org/10.1111/pce.13153</a>.","short":"L. Fan, L. Zhao, W. Hu, W. Li, O. Novák, M. Strnad, S. Simon, J. Friml, J. Shen, L. Jiang, Q. Qiu, Plant, Cell and Environment 41 (2018) 850–864.","apa":"Fan, L., Zhao, L., Hu, W., Li, W., Novák, O., Strnad, M., … Qiu, Q. (2018). NHX antiporters regulate the pH of endoplasmic reticulum and auxin-mediated development. <i>Plant, Cell and Environment</i>. Wiley-Blackwell. <a href=\"https://doi.org/10.1111/pce.13153\">https://doi.org/10.1111/pce.13153</a>","ama":"Fan L, Zhao L, Hu W, et al. NHX antiporters regulate the pH of endoplasmic reticulum and auxin-mediated development. <i>Plant, Cell and Environment</i>. 2018;41:850-864. doi:<a href=\"https://doi.org/10.1111/pce.13153\">10.1111/pce.13153</a>","ista":"Fan L, Zhao L, Hu W, Li W, Novák O, Strnad M, Simon S, Friml J, Shen J, Jiang L, Qiu Q. 2018. NHX antiporters regulate the pH of endoplasmic reticulum and auxin-mediated development. Plant, Cell and Environment. 41, 850–864.","ieee":"L. Fan <i>et al.</i>, “NHX antiporters regulate the pH of endoplasmic reticulum and auxin-mediated development,” <i>Plant, Cell and Environment</i>, vol. 41. Wiley-Blackwell, pp. 850–864, 2018."},"publisher":"Wiley-Blackwell","file":[{"date_updated":"2020-07-14T12:46:32Z","relation":"main_file","content_type":"application/pdf","checksum":"6a20f843565f962cb20281cdf5e40914","date_created":"2019-11-18T16:22:22Z","creator":"dernst","file_name":"2018_PlantCellEnv_Fan.pdf","file_id":"7042","file_size":1937976,"access_level":"open_access"}],"acknowledgement":"This work was supported by the National Natural Science Foundation of China (31571464, 31371438 and 31070222 to Q.S.Q.), the National Basic Research Program of China (973 project, 2013CB429904 to Q.S.Q.), the Research Fund for the Doctoral Program of Higher Education of China (20130211110001 to Q.S.Q.), the Ministry of Education, Youth and Sports of the Czech Republic (the National Program for Sustainability I, LO1204), and The Czech Science Foundation GAČR (GA13–40637S) to JF. We thank Dr. Tom J. Guilfoyle for DR5::GUS line and Dr. Jia Li for pBIB‐RFP vector and DR5::GFP line. We thank Liping Guan and Yang Zhao for their help with the confocal microscope assay. ","file_date_updated":"2020-07-14T12:46:32Z","date_created":"2018-12-11T11:46:36Z","quality_controlled":"1","publication_status":"published","status":"public","article_type":"original","article_processing_charge":"No","title":"NHX antiporters regulate the pH of endoplasmic reticulum and auxin-mediated development","publication":"Plant, Cell and Environment","publist_id":"7359","day":"01","language":[{"iso":"eng"}],"ddc":["580"],"has_accepted_license":"1","date_published":"2018-05-01T00:00:00Z","scopus_import":"1","intvolume":"        41","_id":"462","license":"https://creativecommons.org/licenses/by-nc/4.0/","abstract":[{"lang":"eng","text":"AtNHX5 and AtNHX6 are endosomal Na+,K+/H+ antiporters that are critical for growth and development in Arabidopsis, but the mechanism behind their action remains unknown. Here, we report that AtNHX5 and AtNHX6, functioning as H+ leak, control auxin homeostasis and auxin-mediated development. We found that nhx5 nhx6 exhibited growth variations of auxin-related defects. We further showed that nhx5 nhx6 was affected in auxin homeostasis. Genetic analysis showed that AtNHX5 and AtNHX6 were required for the function of the ER-localized auxin transporter PIN5. Although AtNHX5 and AtNHX6 were co-localized with PIN5 at ER, they did not interact directly. Instead, the conserved acidic residues in AtNHX5 and AtNHX6, which are essential for exchange activity, were required for PIN5 function. AtNHX5 and AtNHX6 regulated the pH in ER. Overall, AtNHX5 and AtNHX6 may regulate auxin transport across the ER via the pH gradient created by their transport activity. H+-leak pathway provides a fine-tuning mechanism that controls cellular auxin fluxes. "}],"volume":41,"oa_version":"Submitted Version","type":"journal_article","isi":1}]