@article{ChipmanFerrierBrenaetal.2014, author = {Chipman, Ariel D. and Ferrier, David E. K. and Brena, Carlo and Qu, Jiaxin and Hughes, Daniel S. T. and Schroeder, Reinhard and Torres-Oliva, Montserrat and Znassi, Nadia and Jiang, Huaiyang and Almeida, Francisca C. and Alonso, Claudio R. and Apostolou, Zivkos and Aqrawi, Peshtewani and Arthur, Wallace and Barna, Jennifer C. J. and Blankenburg, Kerstin P. and Brites, Daniela and Capella-Gutierrez, Salvador and Coyle, Marcus and Dearden, Peter K. and Du Pasquier, Louis and Duncan, Elizabeth J. and Ebert, Dieter and Eibner, Cornelius and Erikson, Galina and Evans, Peter D. and Extavour, Cassandra G. and Francisco, Liezl and Gabaldon, Toni and Gillis, William J. and Goodwin-Horn, Elizabeth A. and Green, Jack E. and Griffiths-Jones, Sam and Grimmelikhuijzen, Cornelis J. P. and Gubbala, Sai and Guigo, Roderic and Han, Yi and Hauser, Frank and Havlak, Paul and Hayden, Luke and Helbing, Sophie and Holder, Michael and Hui, Jerome H. L. and Hunn, Julia P. and Hunnekuhl, Vera S. and Jackson, LaRonda and Javaid, Mehwish and Jhangiani, Shalini N. and Jiggins, Francis M. and Jones, Tamsin E. and Kaiser, Tobias S. and Kalra, Divya and Kenny, Nathan J. and Korchina, Viktoriya and Kovar, Christie L. and Kraus, F. Bernhard and Lapraz, Francois and Lee, Sandra L. and Lv, Jie and Mandapat, Christigale and Manning, Gerard and Mariotti, Marco and Mata, Robert and Mathew, Tittu and Neumann, Tobias and Newsham, Irene and Ngo, Dinh N. and Ninova, Maria and Okwuonu, Geoffrey and Ongeri, Fiona and Palmer, William J. and Patil, Shobha and Patraquim, Pedro and Pham, Christopher and Pu, Ling-Ling and Putman, Nicholas H. and Rabouille, Catherine and Ramos, Olivia Mendivil and Rhodes, Adelaide C. and Robertson, Helen E. and Robertson, Hugh M. and Ronshaugen, Matthew and Rozas, Julio and Saada, Nehad and Sanchez-Gracia, Alejandro and Scherer, Steven E. and Schurko, Andrew M. and Siggens, Kenneth W. and Simmons, DeNard and Stief, Anna and Stolle, Eckart and Telford, Maximilian J. and Tessmar-Raible, Kristin and Thornton, Rebecca and van der Zee, Maurijn and von Haeseler, Arndt and Williams, James M. and Willis, Judith H. and Wu, Yuanqing and Zou, Xiaoyan and Lawson, Daniel and Muzny, Donna M. and Worley, Kim C. and Gibbs, Richard A. and Akam, Michael and Richards, Stephen}, title = {The first myriapod genome sequence reveals conservative arthropod gene content and genome organisation in the centipede Strigamia maritima}, series = {PLoS biology}, volume = {12}, journal = {PLoS biology}, number = {11}, publisher = {PLoS}, address = {San Fransisco}, issn = {1545-7885}, doi = {10.1371/journal.pbio.1002005}, pages = {24}, year = {2014}, abstract = {Myriapods (e. g., centipedes and millipedes) display a simple homonomous body plan relative to other arthropods. All members of the class are terrestrial, but they attained terrestriality independently of insects. Myriapoda is the only arthropod class not represented by a sequenced genome. We present an analysis of the genome of the centipede Strigamia maritima. It retains a compact genome that has undergone less gene loss and shuffling than previously sequenced arthropods, and many orthologues of genes conserved from the bilaterian ancestor that have been lost in insects. Our analysis locates many genes in conserved macro-synteny contexts, and many small-scale examples of gene clustering. We describe several examples where S. maritima shows different solutions from insects to similar problems. The insect olfactory receptor gene family is absent from S. maritima, and olfaction in air is likely effected by expansion of other receptor gene families. For some genes S. maritima has evolved paralogues to generate coding sequence diversity, where insects use alternate splicing. This is most striking for the Dscam gene, which in Drosophila generates more than 100,000 alternate splice forms, but in S. maritima is encoded by over 100 paralogues. We see an intriguing linkage between the absence of any known photosensory proteins in a blind organism and the additional absence of canonical circadian clock genes. The phylogenetic position of myriapods allows us to identify where in arthropod phylogeny several particular molecular mechanisms and traits emerged. For example, we conclude that juvenile hormone signalling evolved with the emergence of the exoskeleton in the arthropods and that RR-1 containing cuticle proteins evolved in the lineage leading to Mandibulata. We also identify when various gene expansions and losses occurred. The genome of S. maritima offers us a unique glimpse into the ancestral arthropod genome, while also displaying many adaptations to its specific life history.}, language = {en} } @article{ParagasHumphreysMinetal.2017, author = {Paragas, Erickson M. and Humphreys, Sara C. and Min, Joshua and Joswig-Jones, Carolyn A. and Leimk{\"u}hler, Silke and Jones, Jeffrey P.}, title = {ecoAO}, series = {ACS OMEGA}, volume = {2}, journal = {ACS OMEGA}, publisher = {American Chemical Society}, address = {Washington}, issn = {2470-1343}, doi = {10.1021/acsomega.7b01054}, pages = {4820 -- 4827}, year = {2017}, abstract = {Although aldehyde oxidase (AO) is an important hepatic drug-metabolizing enzyme, it remains understudied and is consequently often overlooked in preclinical studies, an oversight that has resulted in the failure of multiple clinical trials. AO's preclusion to investigation stems from the following: (1) difficulties synthesizing metabolic standards due to the chemospecificity and regiospecificity of the enzyme and (2) significant inherent variability across existing in vitro systems including liver cytosol, S9 fractions, and primary hepatocytes, which lack specificity and generate discordant expression and activity profiles. Here, we describe a practical bacterial biotransformation system, ecoAO, addressing both issues simultaneously. ecoAO is a cell paste of MoCo-producing Escherichia coli strain TP1017 expressing human AO. It exhibits specific activity toward known substrates, zoniporide, 4-trans-(N,N-dimethylamino)cinnamaldehyde, O6-benzylguanine, and zaleplon; it also has utility as a biocatalyst, yielding milligram quantities of synthetically challenging metabolite standards such as 2-oxo-zoniporide. Moreover, ecoAO enables routine determination of kcat and V/K, which are essential parameters for accurate in vivo clearance predictions. Furthermore, ecoAO has potential as a preclinical in vitro screening tool for AO activity, as demonstrated by its metabolism of 3-aminoquinoline, a previously uncharacterized substrate. ecoAO promises to provide easy access to metabolites with the potential to improve pharmacokinetic clearance predictions and guide drug development.}, language = {en} } @article{WarringtonBeaumontHorikoshietal.2019, author = {Warrington, Nicole and Beaumont, Robin and Horikoshi, Momoko and Day, Felix R. and Helgeland, {\O}yvind and Laurin, Charles and Bacelis, Jonas and Peng, Shouneng and Hao, Ke and Feenstra, Bjarke and Wood, Andrew R. and Mahajan, Anubha and Tyrrell, Jessica and Robertson, Neil R. and Rayner, N. William and Qiao, Zhen and Moen, Gunn-Helen and Vaudel, Marc and Marsit, Carmen and Chen, Jia and Nodzenski, Michael and Schnurr, Theresia M. and Zafarmand, Mohammad Hadi and Bradfield, Jonathan P. and Grarup, Niels and Kooijman, Marjolein N. and Li-Gao, Ruifang and Geller, Frank and Ahluwalia, Tarunveer Singh and Paternoster, Lavinia and Rueedi, Rico and Huikari, Ville and Hottenga, Jouke-Jan and Lyytik{\"a}inen, Leo-Pekka and Cavadino, Alana and Metrustry, Sarah and Cousminer, Diana L. and Wu, Ying and Thiering, Elisabeth Paula and Wang, Carol A. and Have, Christian Theil and Vilor-Tejedor, Natalia and Joshi, Peter K. and Painter, Jodie N. and Ntalla, Ioanna and Myhre, Ronny and Pitk{\"a}nen, Niina and van Leeuwen, Elisabeth M. and Joro, Raimo and Lagou, Vasiliki and Richmond, Rebecca C. and Espinosa, Ana and Barton, Sheila J. and Inskip, Hazel M. and Holloway, John W. and Santa-Marina, Loreto and Estivill, Xavier and Ang, Wei and Marsh, Julie A. and Reichetzeder, Christoph and Marullo, Letizia and Hocher, Berthold and Lunetta, Kathryn L. and Murabito, Joanne M. and Relton, Caroline L. and Kogevinas, Manolis and Chatzi, Leda and Allard, Catherine and Bouchard, Luigi and Hivert, Marie-France and Zhang, Ge and Muglia, Louis J. and Heikkinen, Jani and Morgen, Camilla S. and van Kampen, Antoine H. C. and van Schaik, Barbera D. C. and Mentch, Frank D. and Langenberg, Claudia and Scott, Robert A. and Zhao, Jing Hua and Hemani, Gibran and Ring, Susan M. and Bennett, Amanda J. and Gaulton, Kyle J. and Fernandez-Tajes, Juan and van Zuydam, Natalie R. and Medina-Gomez, Carolina and de Haan, Hugoline G. and Rosendaal, Frits R. and Kutalik, Zolt{\´a}n and Marques-Vidal, Pedro and Das, Shikta and Willemsen, Gonneke and Mbarek, Hamdi and M{\"u}ller-Nurasyid, Martina and Standl, Marie and Appel, Emil V. R. and Fonvig, Cilius Esmann and Trier, Caecilie and van Beijsterveldt, Catharina E. M. and Murcia, Mario and Bustamante, Mariona and Bon{\`a}s-Guarch, S{\´i}lvia and Hougaard, David M. and Mercader, Josep M. and Linneberg, Allan and Schraut, Katharina E. and Lind, Penelope A. and Medland, Sarah Elizabeth and Shields, Beverley M. and Knight, Bridget A. and Chai, Jin-Fang and Panoutsopoulou, Kalliope and Bartels, Meike and S{\´a}nchez, Friman and Stokholm, Jakob and Torrents, David and Vinding, Rebecca K. and Willems, Sara M. and Atalay, Mustafa and Chawes, Bo L. and Kovacs, Peter and Prokopenko, Inga and Tuke, Marcus A. and Yaghootkar, Hanieh and Ruth, Katherine S. and Jones, Samuel E. and Loh, Po-Ru and Murray, Anna and Weedon, Michael N. and T{\"o}njes, Anke and Stumvoll, Michael and Michaelsen, Kim Fleischer and Eloranta, Aino-Maija and Lakka, Timo A. and van Duijn, Cornelia M. and Kiess, Wieland and Koerner, Antje and Niinikoski, Harri and Pahkala, Katja and Raitakari, Olli T. and Jacobsson, Bo and Zeggini, Eleftheria and Dedoussis, George V. and Teo, Yik-Ying and Saw, Seang-Mei and Montgomery, Grant W. and Campbell, Harry and Wilson, James F. and Vrijkotte, Tanja G. M. and Vrijheid, Martine and de Geus, Eco J. C. N. and Hayes, M. Geoffrey and Kadarmideen, Haja N. and Holm, Jens-Christian and Beilin, Lawrence J. and Pennell, Craig E. and Heinrich, Joachim and Adair, Linda S. and Borja, Judith B. and Mohlke, Karen L. and Eriksson, Johan G. and Widen, Elisabeth E. and Hattersley, Andrew T. and Spector, Tim D. and Kaehoenen, Mika and Viikari, Jorma S. and Lehtimaeki, Terho and Boomsma, Dorret I. and Sebert, Sylvain and Vollenweider, Peter and Sorensen, Thorkild I. A. and Bisgaard, Hans and Bonnelykke, Klaus and Murray, Jeffrey C. and Melbye, Mads and Nohr, Ellen A. and Mook-Kanamori, Dennis O. and Rivadeneira, Fernando and Hofman, Albert and Felix, Janine F. and Jaddoe, Vincent W. V. and Hansen, Torben and Pisinger, Charlotta and Vaag, Allan A. and Pedersen, Oluf and Uitterlinden, Andre G. and Jarvelin, Marjo-Riitta and Power, Christine and Hypponen, Elina and Scholtens, Denise M. and Lowe, William L. and Smith, George Davey and Timpson, Nicholas J. and Morris, Andrew P. and Wareham, Nicholas J. and Hakonarson, Hakon and Grant, Struan F. A. and Frayling, Timothy M. and Lawlor, Debbie A. and Njolstad, Pal R. and Johansson, Stefan and Ong, Ken K. and McCarthy, Mark I. and Perry, John R. B. and Evans, David M. and Freathy, Rachel M.}, title = {Maternal and fetal genetic effects on birth weight and their relevance to cardio-metabolic risk factors}, series = {Nature genetics}, volume = {51}, journal = {Nature genetics}, number = {5}, publisher = {Nature Publ. Group}, address = {New York}, organization = {EGG Consortium}, issn = {1061-4036}, pages = {804 -- +}, year = {2019}, abstract = {Birth weight variation is influenced by fetal and maternal genetic and non-genetic factors, and has been reproducibly associated with future cardio-metabolic health outcomes. In expanded genome-wide association analyses of own birth weight (n = 321,223) and offspring birth weight (n = 230,069 mothers), we identified 190 independent association signals (129 of which are novel). We used structural equation modeling to decompose the contributions of direct fetal and indirect maternal genetic effects, then applied Mendelian randomization to illuminate causal pathways. For example, both indirect maternal and direct fetal genetic effects drive the observational relationship between lower birth weight and higher later blood pressure: maternal blood pressure-raising alleles reduce offspring birth weight, but only direct fetal effects of these alleles, once inherited, increase later offspring blood pressure. Using maternal birth weight-lowering genotypes to proxy for an adverse intrauterine environment provided no evidence that it causally raises offspring blood pressure, indicating that the inverse birth weight-blood pressure association is attributable to genetic effects, and not to intrauterine programming.}, language = {en} } @article{BeaumontWarringtonCavadinoetal.2018, author = {Beaumont, Robin N. and Warrington, Nicole M. and Cavadino, Alana and Tyrrell, Jessica and Nodzenski, Michael and Horikoshi, Momoko and Geller, Frank and Myhre, Ronny and Richmond, Rebecca C. and Paternoster, Lavinia and Bradfield, Jonathan P. and Kreiner-Moller, Eskil and Huikari, Ville and Metrustry, Sarah and Lunetta, Kathryn L. and Painter, Jodie N. and Hottenga, Jouke-Jan and Allard, Catherine and Barton, Sheila J. and Espinosa, Ana and Marsh, Julie A. and Potter, Catherine and Zhang, Ge and Ang, Wei and Berry, Diane J. and Bouchard, Luigi and Das, Shikta and Hakonarson, Hakon and Heikkinen, Jani and Helgeland, Oyvind and Hocher, Berthold and Hofman, Albert and Inskip, Hazel M. and Jones, Samuel E. and Kogevinas, Manolis and Lind, Penelope A. and Marullo, Letizia and Medland, Sarah E. and Murray, Anna and Murray, Jeffrey C. and Njolstad, Pal R. and Nohr, Ellen A. and Reichetzeder, Christoph and Ring, Susan M. and Ruth, Katherine S. and Santa-Marina, Loreto and Scholtens, Denise M. and Sebert, Sylvain and Sengpiel, Verena and Tuke, Marcus A. and Vaudel, Marc and Weedon, Michael N. and Willemsen, Gonneke and Wood, Andrew R. and Yaghootkar, Hanieh and Muglia, Louis J. and Bartels, Meike and Relton, Caroline L. and Pennell, Craig E. and Chatzi, Leda and Estivill, Xavier and Holloway, John W. and Boomsma, Dorret I. and Montgomery, Grant W. and Murabito, Joanne M. and Spector, Tim D. and Power, Christine and Jarvelin, Marjo-Ritta and Bisgaard, Hans and Grant, Struan F. A. and Sorensen, Thorkild I. A. and Jaddoe, Vincent W. and Jacobsson, Bo and Melbye, Mads and McCarthy, Mark I. and Hattersley, Andrew T. and Hayes, M. Geoffrey and Frayling, Timothy M. and Hivert, Marie-France and Felix, Janine F. and Hypponen, Elina and Lowe, William L. and Evans, David M. and Lawlor, Debbie A. and Feenstra, Bjarke and Freathy, Rachel M.}, title = {Genome-wide association study of offspring birth weight in 86 577 women identifies five novel loci and highlights maternal genetic effects that are independent of fetal genetics}, series = {Human molecular genetics}, volume = {27}, journal = {Human molecular genetics}, number = {4}, publisher = {Oxford Univ. Press}, address = {Oxford}, organization = {Early Growth Genetics EGG}, issn = {0964-6906}, doi = {10.1093/hmg/ddx429}, pages = {742 -- 756}, year = {2018}, abstract = {Genome-wide association studies of birth weight have focused on fetal genetics, whereas relatively little is known about the role of maternal genetic variation. We aimed to identify maternal genetic variants associated with birth weight that could highlight potentially relevant maternal determinants of fetal growth. We meta-analysed data on up to 8.7 million SNPs in up to 86 577 women of European descent from the Early Growth Genetics (EGG) Consortium and the UK Biobank. We used structural equation modelling (SEM) and analyses of mother-child pairs to quantify the separate maternal and fetal genetic effects. Maternal SNPs at 10 loci (MTNR1B, HMGA2, SH2B3, KCNAB1, L3MBTL3, GCK, EBF1, TCF7L2, ACTL9, CYP3A7) were associated with offspring birth weight at P< 5 x 10(-8). In SEM analyses, at least 7 of the 10 associations were consistent with effects of the maternal genotype acting via the intrauterine environment, rather than via effects of shared alleles with the fetus. Variants, or correlated proxies, at many of the loci had been previously associated with adult traits, including fasting glucose (MTNR1B, GCK and TCF7L2) and sex hormone levels (CYP3A7), and one (EBF1) with gestational duration. The identified associations indicate that genetic effects on maternal glucose, cytochrome P450 activity and gestational duration, and potentially on maternal blood pressure and immune function, are relevant for fetal growth. Further characterization of these associations in mechanistic and causal analyses will enhance understanding of the potentially modifiable maternal determinants of fetal growth, with the goal of reducing the morbidity and mortality associated with low and high birth weights.}, language = {en} } @misc{BeaumontWarringtonCavadinoetal.2017, author = {Beaumont, Robin N. and Warrington, Nicole M. and Cavadino, Alana and Tyrrell, Jessica and Nodzenski, Michael and Horikoshi, Momoko and Geller, Frank and Myhre, Ronny and Richmond, Rebecca C. and Paternoster, Lavinia and Bradfield, Jonathan P. and Kreiner-M{\o}ller, Eskil and Huikari, Ville and Metrustry, Sarah and Lunetta, Kathryn L. and Painter, Jodie N. and Hottenga, Jouke-Jan and Allard, Catherine and Barton, Sheila J. and Espinosa, Ana and Marsh, Julie A. and Potter, Catherine and Zhang, Ge and Ang, Wei and Berry, Diane J. and Bouchard, Luigi and Das, Shikta and Hakonarson, Hakon and Heikkinen, Jani and Helgeland, {\O}yvind and Hocher, Berthold and Hofman, Albert and Inskip, Hazel M. and Jones, Samuel E. and Kogevinas, Manolis and Lind, Penelope A. and Marullo, Letizia and Medland, Sarah E. and Murray, Anna and Murray, Jeffrey C. and Nj{\o}lstad, Pa ̊l R. and Nohr, Ellen A. and Reichetzeder, Christoph and Ring, Susan M. and Ruth, Katherine S. and Santa-Marina, Loreto and Scholtens, Denise M. and Sebert, Sylvain and Sengpiel, Verena and Tuke, Marcus A. and Vaudel, Marc and Weedon, Michael N. and Willemsen, Gonneke and Wood, Andrew R. and Yaghootkar, Hanieh and Muglia, Louis J. and Bartels, Meike and Relton, Caroline L. and Pennell, Craig E. and Chatzi, Leda and Estivill, Xavier and Holloway, John W. and Boomsma, Dorret I. and Montgomery, Grant W. and Murabito, Joanne M. and Spector, Tim D. and Power, Christine and Ja ̈rvelin, Marjo-Ritta and Bisgaard, Hans and Grant, Struan F.A. and S{\o}rensen, Thorkild I.A. and Jaddoe, Vincent W. and Jacobsson, Bo and Melbye, Mads and McCarthy, Mark I. and Hattersley, Andrew T. and Hayes, M. Geoffrey and Frayling, Timothy M. and Hivert, Marie-France and Felix, Janine F. and Hyppo ̈nen, Elina and Lowe, William L. , Jr and Evans, David M. and Lawlor, Debbie A. and Feenstra, Bjarke and Freathy, Rachel M.}, title = {Genome-wide association study of offspring birth weight in 86 577 women identifies five novel loci and highlights maternal genetic effects that are independent of fetal genetics}, series = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe}, journal = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe}, number = {628}, issn = {1866-8372}, doi = {10.25932/publishup-42310}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-423100}, pages = {15}, year = {2017}, abstract = {Genome-wide association studies of birth weight have focused on fetal genetics, whereas relatively little is known about the role of maternal genetic variation. We aimed to identify maternal genetic variants associated with birth weight that could highlight potentially relevant maternal determinants of fetal growth. We meta-analysed data on up to 8.7 million SNPs in up to 86 577 women of European descent from the Early Growth Genetics (EGG) Consortium and the UK Biobank. We used structural equation modelling (SEM) and analyses of mother-child pairs to quantify the separate maternal and fetal genetic effects. Maternal SNPs at 10 loci (MTNR1B, HMGA2, SH2B3, KCNAB1, L3MBTL3, GCK, EBF1, TCF7L2, ACTL9, CYP3A7) were associated with offspring birth weight at P < 5 {\^A} 10 {\`A}8 . In SEM analyses, at least 7 of the 10 associations were consistent with effects of the maternal genotype acting via the intrauterine environment, rather than via effects of shared alleles with the fetus. Variants, or correlated proxies, at many of the loci had been previously associated with adult traits, including fasting glucose (MTNR1B, GCK and TCF7L2) and sex hormone levels (CYP3A7), and one (EBF1) with gestational duration. The identified associations indicate that genetic effects on maternal glucose, cytochrome P450 activity and gestational duration, and potentially on maternal blood pressure and immune function, are relevant for fetal growth. Further characterization of these associations in mechanistic and causal analyses will enhance understanding of the potentially modifiable maternal determinants of fetal growth, with the goal of reducing the morbidity and mortality associated with low and high birth weights.}, language = {en} } @article{SramaKruegerYamaguchietal.2012, author = {Srama, Ralf and Krueger, H. and Yamaguchi, T. and Stephan, T. and Burchell, M. and Kearsley, A. T. and Sterken, V. and Postberg, F. and Kempf, S. and Gr{\"u}n, Eberhard and Altobelli, Nicolas and Ehrenfreund, P. and Dikarev, V. and Horanyi, M. and Sternovsky, Zoltan and Carpenter, J. D. and Westphal, A. and Gainsforth, Z. and Krabbe, A. and Agarwal, Jessica and Yano, H. and Blum, J. and Henkel, H. and Hillier, J. and Hoppe, P. and Trieloff, M. and Hsu, S. and Mocker, A. and Fiege, K. and Green, S. F. and Bischoff, A. and Esposito, F. and Laufer, R. and Hyde, T. W. and Herdrich, G. and Fasoulas, S. and Jaeckel, A. and Jones, G. and Jenniskens, P. and Khalisi, E. and Moragas-Klostermeyer, Georg and Spahn, Frank and Keller, H. U. and Frisch, P. and Levasseur-Regourd, A. C. and Pailer, N. and Altwegg, K. and Engrand, C. and Auer, S. and Silen, J. and Sasaki, S. and Kobayashi, M. and Schmidt, J. and Kissel, J. and Marty, B. and Michel, P. and Palumbo, P. and Vaisberg, O. and Baggaley, J. and Rotundi, A. and Roeser, H. P.}, title = {SARIM PLUS-sample return of comet 67P/CG and of interstellar matter}, series = {EXPERIMENTAL ASTRONOMY}, volume = {33}, journal = {EXPERIMENTAL ASTRONOMY}, number = {2-3}, publisher = {SPRINGER}, address = {DORDRECHT}, issn = {0922-6435}, doi = {10.1007/s10686-011-9285-7}, pages = {723 -- 751}, year = {2012}, abstract = {The Stardust mission returned cometary, interplanetary and (probably) interstellar dust in 2006 to Earth that have been analysed in Earth laboratories worldwide. Results of this mission have changed our view and knowledge on the early solar nebula. The Rosetta mission is on its way to land on comet 67P/Churyumov-Gerasimenko and will investigate for the first time in great detail the comet nucleus and its environment starting in 2014. Additional astronomy and planetary space missions will further contribute to our understanding of dust generation, evolution and destruction in interstellar and interplanetary space and provide constraints on solar system formation and processes that led to the origin of life on Earth. One of these missions, SARIM-PLUS, will provide a unique perspective by measuring interplanetary and interstellar dust with high accuracy and sensitivity in our inner solar system between 1 and 2 AU. SARIM-PLUS employs latest in-situ techniques for a full characterisation of individual micrometeoroids (flux, mass, charge, trajectory, composition()) and collects and returns these samples to Earth for a detailed analysis. The opportunity to visit again the target comet of the Rosetta mission 67P/Churyumov-Gerasimeenternko, and to investigate its dusty environment six years after Rosetta with complementary methods is unique and strongly enhances and supports the scientific exploration of this target and the entire Rosetta mission. Launch opportunities are in 2020 with a backup window starting early 2026. The comet encounter occurs in September 2021 and the reentry takes place in early 2024. An encounter speed of 6 km/s ensures comparable results to the Stardust mission.}, language = {en} } @article{ReadKegelKluteetal.2013, author = {Read, Betsy A. and Kegel, Jessica and Klute, Mary J. and Kuo, Alan and Lefebvre, Stephane C. and Maumus, Florian and Mayer, Christoph and Miller, John and Monier, Adam and Salamov, Asaf and Young, Jeremy and Aguilar, Maria and Claverie, Jean-Michel and Frickenhaus, Stephan and Gonzalez, Karina and Herman, Emily K. and Lin, Yao-Cheng and Napier, Johnathan and Ogata, Hiroyuki and Sarno, Analissa F. and Shmutz, Jeremy and Schroeder, Declan and de Vargas, Colomban and Verret, Frederic and von Dassow, Peter and Valentin, Klaus and Van de Peer, Yves and Wheeler, Glen and Dacks, Joel B. and Delwiche, Charles F. and Dyhrman, Sonya T. and Gl{\"o}ckner, Gernot and John, Uwe and Richards, Thomas and Worden, Alexandra Z. and Zhang, Xiaoyu and Grigoriev, Igor V. and Allen, Andrew E. and Bidle, Kay and Borodovsky, M. and Bowler, C. and Brownlee, Colin and Cock, J. Mark and Elias, Marek and Gladyshev, Vadim N. and Groth, Marco and Guda, Chittibabu and Hadaegh, Ahmad and Iglesias-Rodriguez, Maria Debora and Jenkins, J. and Jones, Bethan M. and Lawson, Tracy and Leese, Florian and Lindquist, Erika and Lobanov, Alexei and Lomsadze, Alexandre and Malik, Shehre-Banoo and Marsh, Mary E. and Mackinder, Luke and Mock, Thomas and M{\"u}ller-R{\"o}ber, Bernd and Pagarete, Antonio and Parker, Micaela and Probert, Ian and Quesneville, Hadi and Raines, Christine and Rensing, Stefan A. and Riano-Pachon, Diego Mauricio and Richier, Sophie and Rokitta, Sebastian and Shiraiwa, Yoshihiro and Soanes, Darren M. and van der Giezen, Mark and Wahlund, Thomas M. and Williams, Bryony and Wilson, Willie and Wolfe, Gordon and Wurch, Louie L.}, title = {Pan genome of the phytoplankton Emiliania underpins its global distribution}, series = {Nature : the international weekly journal of science}, volume = {499}, journal = {Nature : the international weekly journal of science}, number = {7457}, publisher = {Nature Publ. Group}, address = {London}, organization = {Emiliania Huxleyi Annotation}, issn = {0028-0836}, doi = {10.1038/nature12221}, pages = {209 -- 213}, year = {2013}, abstract = {Coccolithophores have influenced the global climate for over 200 million years(1). These marine phytoplankton can account for 20 per cent of total carbon fixation in some systems(2). They form blooms that can occupy hundreds of thousands of square kilometres and are distinguished by their elegantly sculpted calcium carbonate exoskeletons (coccoliths), rendering them visible from space(3). Although coccolithophores export carbon in the form of organic matter and calcite to the sea floor, they also release CO2 in the calcification process. Hence, they have a complex influence on the carbon cycle, driving either CO2 production or uptake, sequestration and export to the deep ocean(4). Here we report the first haptophyte reference genome, from the coccolithophore Emiliania huxleyi strain CCMP1516, and sequences from 13 additional isolates. Our analyses reveal a pan genome (core genes plus genes distributed variably between strains) probably supported by an atypical complement of repetitive sequence in the genome. Comparisons across strains demonstrate that E. huxleyi, which has long been considered a single species, harbours extensive genome variability reflected in different metabolic repertoires. Genome variability within this species complex seems to underpin its capacity both to thrive in habitats ranging from the equator to the subarctic and to form large-scale episodic blooms under a wide variety of environmental conditions.}, language = {en} } @article{JonesArpGrosseetal.2020, author = {Jones, Benjamin M. and Arp, Christopher D. and Grosse, Guido and Nitze, Ingmar and Lara, Mark J. and Whitman, Matthew S. and Farquharson, Louise M. and Kanevskiy, Mikhail and Parsekian, Andrew D. and Breen, Amy L. and Ohara, Nori and Rangel, Rodrigo Correa and Hinkel, Kenneth M.}, title = {Identifying historical and future potential lake drainage events on the western Arctic coastal plain of Alaska}, series = {Permafrost and Periglacial Processes}, volume = {31}, journal = {Permafrost and Periglacial Processes}, number = {1}, publisher = {Wiley}, address = {New York}, doi = {10.1002/ppp.2038}, pages = {110 -- 127}, year = {2020}, abstract = {Arctic lakes located in permafrost regions are susceptible to catastrophic drainage. In this study, we reconstructed historical lake drainage events on the western Arctic Coastal Plain of Alaska between 1955 and 2017 using USGS topographic maps, historical aerial photography (1955), and Landsat Imagery (ca. 1975, ca. 2000, and annually since 2000). We identified 98 lakes larger than 10 ha that partially (>25\% of area) or completely drained during the 62-year period. Decadal-scale lake drainage rates progressively declined from 2.0 lakes/yr (1955-1975), to 1.6 lakes/yr (1975-2000), and to 1.2 lakes/yr (2000-2017) in the ~30,000-km(2) study area. Detailed Landsat trend analysis between 2000 and 2017 identified two years, 2004 and 2006, with a cluster (five or more) of lake drainages probably associated with bank overtopping or headward erosion. To identify future potential lake drainages, we combined the historical lake drainage observations with a geospatial dataset describing lake elevation, hydrologic connectivity, and adjacent lake margin topographic gradients developed with a 5-m-resolution digital surface model. We identified ~1900 lakes likely to be prone to drainage in the future. Of the 20 lakes that drained in the most recent study period, 85\% were identified in this future lake drainage potential dataset. Our assessment of historical lake drainage magnitude, mechanisms and pathways, and identification of potential future lake drainages provides insights into how arctic lowland landscapes may change and evolve in the coming decades to centuries.}, language = {en} } @misc{JonesArpGrosseetal.2020, author = {Jones, Benjamin M. and Arp, Christopher D. and Grosse, Guido and Nitze, Ingmar and Lara, Mark J. and Whitman, Matthew S. and Farquharson, Louise M. and Kanevskiy, Mikhail and Parsekian, Andrew D. and Breen, Amy L. and Ohara, Nori and Rangel, Rodrigo Correa and Hinkel, Kenneth M.}, title = {Identifying historical and future potential lake drainage events on the western Arctic coastal plain of Alaska}, series = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe}, journal = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe}, number = {1}, issn = {1866-8372}, doi = {10.25932/publishup-61043}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-610435}, pages = {20}, year = {2020}, abstract = {Arctic lakes located in permafrost regions are susceptible to catastrophic drainage. In this study, we reconstructed historical lake drainage events on the western Arctic Coastal Plain of Alaska between 1955 and 2017 using USGS topographic maps, historical aerial photography (1955), and Landsat Imagery (ca. 1975, ca. 2000, and annually since 2000). We identified 98 lakes larger than 10 ha that partially (>25\% of area) or completely drained during the 62-year period. Decadal-scale lake drainage rates progressively declined from 2.0 lakes/yr (1955-1975), to 1.6 lakes/yr (1975-2000), and to 1.2 lakes/yr (2000-2017) in the ~30,000-km(2) study area. Detailed Landsat trend analysis between 2000 and 2017 identified two years, 2004 and 2006, with a cluster (five or more) of lake drainages probably associated with bank overtopping or headward erosion. To identify future potential lake drainages, we combined the historical lake drainage observations with a geospatial dataset describing lake elevation, hydrologic connectivity, and adjacent lake margin topographic gradients developed with a 5-m-resolution digital surface model. We identified ~1900 lakes likely to be prone to drainage in the future. Of the 20 lakes that drained in the most recent study period, 85\% were identified in this future lake drainage potential dataset. Our assessment of historical lake drainage magnitude, mechanisms and pathways, and identification of potential future lake drainages provides insights into how arctic lowland landscapes may change and evolve in the coming decades to centuries.}, language = {en} } @article{JonesGrosseFarquharsonetal.2022, author = {Jones, Benjamin M. and Grosse, Guido and Farquharson, Louise M. and Roy-L{\´e}veill{\´e}e, Pascale and Veremeeva, Alexandra and Kanevskiy, Mikhail Z. and Gaglioti, Benjamin and Breen, Amy L. and Parsekian, Andrew D. and Ulrich, Mathias and Hinkel, Kenneth M.}, title = {Lake and drained lake basin systems in lowland permafrost regions}, series = {Nature reviews earth and environment}, volume = {3}, journal = {Nature reviews earth and environment}, number = {1}, publisher = {Springer Nature}, address = {London}, issn = {2662-138X}, doi = {10.1038/s43017-021-00238-9}, pages = {85 -- 98}, year = {2022}, abstract = {The formation, growth and drainage of lakes in Arctic and boreal lowland permafrost regions influence landscape and ecosystem processes. These lake and drained lake basin (L-DLB) systems occupy >20\% of the circumpolar Northern Hemisphere permafrost region and similar to 50\% of the area below 300 m above sea level. Climate change is causing drastic impacts to L-DLB systems, with implications for permafrost dynamics, ecosystem functioning, biogeochemical processes and human livelihoods in lowland permafrost regions. In this Review, we discuss how an increase in the number of lakes as a result of permafrost thaw and an intensifying hydrologic regime are not currently offsetting the land area gained through lake drainage, enhancing the dominance of drained lake basins (DLBs).The contemporary transition from lakes to DLBs decreases hydrologic storage, leads to permafrost aggradation, increases carbon sequestration and diversifies the shifting habitat mosaic in Arctic and boreal regions. However, further warming could inhibit permafrost aggradation in DLBs, disrupting the trajectory of important microtopographic controls on carbon fluxes and ecosystem processes in permafrost-region L-DLB systems. Further research is needed to understand the future dynamics of L-DLB systems to improve Earth system models, permafrost carbon feedback assessments, permafrost hydrology linkages, infrastructure development in permafrost regions and the well-being of northern socio-ecological systems.}, language = {en} }