TY  - GEN
A1  - Gorski, Mathias
A1  - Jung, Bettina
A1  - Li, Yong
A1  - Matias-Garcia, Pamela R.
A1  - Wuttke, Matthias
A1  - Coassin, Stefan
A1  - Thio, Chris H. L.
A1  - Kleber, Marcus E.
A1  - Winkler, Thomas W.
A1  - Wanner, Veronika
A1  - Chai, Jin-Fang
A1  - Chu, Audrey Y.
A1  - Cocca, Massimiliano
A1  - Feitosa, Mary F.
A1  - Ghasemi, Sahar
A1  - Hoppmann, Anselm
A1  - Horn, Katrin
A1  - Li, Man
A1  - Nutile, Teresa
A1  - Scholz, Markus
A1  - Sieber, Karsten B.
A1  - Teumer, Alexander
A1  - Tin, Adrienne
A1  - Wang, Judy
A1  - Tayo, Bamidele O.
A1  - Ahluwalia, Tarunveer S.
A1  - Almgren, Peter
A1  - Bakker, Stephan J. L.
A1  - Banas, Bernhard
A1  - Bansal, Nisha
A1  - Biggs, Mary L.
A1  - Boerwinkle, Eric
A1  - Böttinger, Erwin
A1  - Brenner, Hermann
A1  - Carroll, Robert J.
A1  - Chalmers, John
A1  - Chee, Miao-Li
A1  - Chee, Miao-Ling
A1  - Cheng, Ching-Yu
A1  - Coresh, Josef
A1  - de Borst, Martin H.
A1  - Degenhardt, Frauke
A1  - Eckardt, Kai-Uwe
A1  - Endlich, Karlhans
A1  - Franke, Andre
A1  - Freitag-Wolf, Sandra
A1  - Gampawar, Piyush
A1  - Gansevoort, Ron T.
A1  - Ghanbari, Mohsen
A1  - Gieger, Christian
A1  - Hamet, Pavel
A1  - Ho, Kevin
A1  - Hofer, Edith
A1  - Holleczek, Bernd
A1  - Foo, Valencia Hui Xian
A1  - Hutri-Kahonen, Nina
A1  - Hwang, Shih-Jen
A1  - Ikram, M. Arfan
A1  - Josyula, Navya Shilpa
A1  - Kahonen, Mika
A1  - Khor, Chiea-Chuen
A1  - Koenig, Wolfgang
A1  - Kramer, Holly
A1  - Kraemer, Bernhard K.
A1  - Kuehnel, Brigitte
A1  - Lange, Leslie A.
A1  - Lehtimaki, Terho
A1  - Lieb, Wolfgang
A1  - Loos, Ruth J. F.
A1  - Lukas, Mary Ann
A1  - Lyytikainen, Leo-Pekka
A1  - Meisinger, Christa
A1  - Meitinger, Thomas
A1  - Melander, Olle
A1  - Milaneschi, Yuri
A1  - Mishra, Pashupati P.
A1  - Mononen, Nina
A1  - Mychaleckyj, Josyf C.
A1  - Nadkarni, Girish N.
A1  - Nauck, Matthias
A1  - Nikus, Kjell
A1  - Ning, Boting
A1  - Nolte, Ilja M.
A1  - O'Donoghue, Michelle L.
A1  - Orho-Melander, Marju
A1  - Pendergrass, Sarah A.
A1  - Penninx, Brenda W. J. H.
A1  - Preuss, Michael H.
A1  - Psaty, Bruce M.
A1  - Raffield, Laura M.
A1  - Raitakari, Olli T.
A1  - Rettig, Rainer
A1  - Rheinberger, Myriam
A1  - Rice, Kenneth M.
A1  - Rosenkranz, Alexander R.
A1  - Rossing, Peter
A1  - Rotter, Jerome
A1  - Sabanayagam, Charumathi
A1  - Schmidt, Helena
A1  - Schmidt, Reinhold
A1  - Schoettker, Ben
A1  - Schulz, Christina-Alexandra
A1  - Sedaghat, Sanaz
A1  - Shaffer, Christian M.
A1  - Strauch, Konstantin
A1  - Szymczak, Silke
A1  - Taylor, Kent D.
A1  - Tremblay, Johanne
A1  - Chaker, Layal
A1  - van der Harst, Pim
A1  - van der Most, Peter J.
A1  - Verweij, Niek
A1  - Voelker, Uwe
A1  - Waldenberger, Melanie
A1  - Wallentin, Lars
A1  - Waterworth, Dawn M.
A1  - White, Harvey D.
A1  - Wilson, James G.
A1  - Wong, Tien-Yin
A1  - Woodward, Mark
A1  - Yang, Qiong
A1  - Yasuda, Masayuki
A1  - Yerges-Armstrong, Laura M.
A1  - Zhang, Yan
A1  - Snieder, Harold
A1  - Wanner, Christoph
A1  - Boger, Carsten A.
A1  - Kottgen, Anna
A1  - Kronenberg, Florian
A1  - Pattaro, Cristian
A1  - Heid, Iris M.
T1  - Meta-analysis uncovers genome-wide significant variants for rapid kidney function decline
T2  - Zweitveröffentlichungen der Universität Potsdam : Reihe der Digital Engineering Fakultät
N2  - Rapid decline of glomerular filtration rate estimated from creatinine (eGFRcrea) is associated with severe clinical endpoints. In contrast to cross-sectionally assessed eGFRcrea, the genetic basis for rapid eGFRcrea decline is largely unknown. To help define this, we meta-analyzed 42 genome-wide association studies from the Chronic Kidney Diseases Genetics Consortium and United Kingdom Biobank to identify genetic loci for rapid eGFRcrea decline. Two definitions of eGFRcrea decline were used: 3 mL/min/1.73m(2)/year or more ("Rapid3"; encompassing 34,874 cases, 107,090 controls) and eGFRcrea decline 25% or more and eGFRcrea under 60 mL/min/1.73m(2) at follow-up among those with eGFRcrea 60 mL/min/1.73m(2) or more at baseline ("CKDi25"; encompassing 19,901 cases, 175,244 controls). Seven independent variants were identified across six loci for Rapid3 and/or CKDi25: consisting of five variants at four loci with genome-wide significance (near UMOD-PDILT (2), PRKAG2, WDR72, OR2S2) and two variants among 265 known eGFRcrea variants (near GATM, LARP4B). All these loci were novel for Rapid3 and/or CKDi25 and our bioinformatic follow-up prioritized variants and genes underneath these loci. The OR2S2 locus is novel for any eGFRcrea trait including interesting candidates. For the five genome-wide significant lead variants, we found supporting effects for annual change in blood urea nitrogen or cystatin-based eGFR, but not for GATM or (LARP4B). Individuals at high compared to those at low genetic risk (8-14 vs. 0-5 adverse alleles) had a 1.20-fold increased risk of acute kidney injury (95% confidence interval 1.08-1.33). Thus, our identified loci for rapid kidney function decline may help prioritize therapeutic targets and identify mechanisms and individuals at risk for sustained deterioration of kidney function.
T3  - Zweitveröffentlichungen der Universität Potsdam : Reihe der Digital Engineering Fakultät - 19 
KW  - acute kidney injury
KW  - end-stage kidney disease
KW  - genome-wide association
KW  - study
KW  - rapid eGFRcrea decline
Y1  - 2020
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-565379
IS  - 19
ER  - 
TY  - GEN
A1  - Kaminski, Jakob A.
A1  - Schlagenhauf, Florian
A1  - Rapp, Michael Armin
A1  - Awasthi, Swapnil
A1  - Ruggeri, Barbara
A1  - Deserno, Lorenz
A1  - Banaschewski, Tobias
A1  - Bokde, Arun L. W.
A1  - Bromberg, Uli
A1  - Büchel, Christian
A1  - Quinlan, Erin Burke
A1  - Desrivières, Sylvane
A1  - Flor, Herta
A1  - Frouin, Vincent
A1  - Garavan, Hugh
A1  - Gowland, Penny
A1  - Ittermann, Bernd
A1  - Martinot, Jean-Luc
A1  - Paillère Martinot, Marie-Laure
A1  - Nees, Frauke
A1  - Papadopoulos Orfanos, Dimitri
A1  - Paus, Tomáš
A1  - Poustka, Luise
A1  - Smolka, Michael N.
A1  - Fröhner, Juliane H.
A1  - Walter, Henrik
A1  - Whelan, Robert
A1  - Ripke, Stephan
A1  - Schumann, Gunter
A1  - Heinz, Andreas
T1  - Epigenetic variance in dopamine D2 receptor
BT  - a marker of IQ malleability?
T2  - Postprints der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe
N2  - Genetic and environmental factors both contribute to cognitive test performance. A substantial increase in average intelligence test results in the second half of the previous century within one generation is unlikely to be explained by genetic changes. One possible explanation for the strong malleability of cognitive performance measure is that environmental factors modify gene expression via epigenetic mechanisms. Epigenetic factors may help to understand the recent observations of an association between dopamine-dependent encoding of reward prediction errors and cognitive capacity, which was modulated by adverse life events. The possible manifestation of malleable biomarkers contributing to variance in cognitive test performance, and thus possibly contributing to the "missing heritability" between estimates from twin studies and variance explained by genetic markers, is still unclear. Here we show in 1475 healthy adolescents from the IMaging and GENetics (IMAGEN) sample that general IQ (gIQ) is associated with (1) polygenic scores for intelligence, (2) epigenetic modification of DRD2 gene, (3) gray matter density in striatum, and (4) functional striatal activation elicited by temporarily surprising reward-predicting cues. Comparing the relative importance for the prediction of gIQ in an overlapping subsample, our results demonstrate neurobiological correlates of the malleability of gIQ and point to equal importance of genetic variance, epigenetic modification of DRD2 receptor gene, as well as functional striatal activation, known to influence dopamine neurotransmission. Peripheral epigenetic markers are in need of confirmation in the central nervous system and should be tested in longitudinal settings specifically assessing individual and environmental factors that modify epigenetic structure.
T3  - Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe - 950 
KW  - genome-wide association
KW  - reward anticipation
KW  - human intelligence
KW  - human brain
KW  - stress
KW  - metaanalysis
KW  - striatum
KW  - psychopathology
KW  - prediction
KW  - volume
KW  - epigenetics and behaviour
KW  - human behaviour
KW  - learning and memory
Y1  - 2020
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-425687
SN  - 1866-8372
IS  - 950
ER  - 
TY  - GEN
A1  - Powell, Anahid E.
A1  - Lenhard, Michael
T1  - Control of organ size in plants
T2  - Postprints der Universität Potsdam : Mathematisch Naturwissenschaftliche Reihe
N2  - The size of plant organs, such as leaves and flowers, is determined by an interaction of genotype and environmental influences. Organ growth occurs through the two successive processes of cell proliferation followed by cell expansion. A number of genes influencing either or both of these processes and thus contributing to the control of final organ size have been identified in the last decade. Although the overall picture of the genetic regulation of organ size remains fragmentary, two transcription factor/microRNA-based genetic pathways are emerging in the control of cell proliferation. However, despite this progress, fundamental questions remain unanswered, such as the problem of how the size of a growing organ could be monitored to determine the appropriate time for terminating growth. While genetic analysis will undoubtedly continue to advance our knowledge about size control in plants, a deeper understanding of this and other basic questions will require including advanced live-imaging and mathematical modeling, as impressively demonstrated by some recent examples. This should ultimately allow the comparison of the mechanisms underlying size control in plants and in animals to extract common principles and lineage-specific solutions.
T3  - Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe - 898 
KW  - BHLH transcription factor
KW  - genome-wide association
KW  - arabidopsis-thaliana
KW  - cell-proliferation
KW  - leaf development
KW  - developing leaves
KW  - petal growth
KW  - gene family
KW  - tor kinase
KW  - auxin
Y1  - 2020
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-438029
SN  - 1866-8372
IS  - 898
ER  -