@article{AartsAndersonAndersonetal.2015, author = {Aarts, Alexander A. and Anderson, Joanna E. and Anderson, Christopher J. and Attridge, Peter R. and Attwood, Angela and Axt, Jordan and Babel, Molly and Bahnik, Stepan and Baranski, Erica and Barnett-Cowan, Michael and Bartmess, Elizabeth and Beer, Jennifer and Bell, Raoul and Bentley, Heather and Beyan, Leah and Binion, Grace and Borsboom, Denny and Bosch, Annick and Bosco, Frank A. and Bowman, Sara D. and Brandt, Mark J. and Braswell, Erin and Brohmer, Hilmar and Brown, Benjamin T. and Brown, Kristina and Bruening, Jovita and Calhoun-Sauls, Ann and Callahan, Shannon P. and Chagnon, Elizabeth and Chandler, Jesse and Chartier, Christopher R. and Cheung, Felix and Christopherson, Cody D. and Cillessen, Linda and Clay, Russ and Cleary, Hayley and Cloud, Mark D. and Cohn, Michael and Cohoon, Johanna and Columbus, Simon and Cordes, Andreas and Costantini, Giulio and Alvarez, Leslie D. Cramblet and Cremata, Ed and Crusius, Jan and DeCoster, Jamie and DeGaetano, Michelle A. and Della Penna, Nicolas and den Bezemer, Bobby and Deserno, Marie K. and Devitt, Olivia and Dewitte, Laura and Dobolyi, David G. and Dodson, Geneva T. and Donnellan, M. Brent and Donohue, Ryan and Dore, Rebecca A. and Dorrough, Angela and Dreber, Anna and Dugas, Michelle and Dunn, Elizabeth W. and Easey, Kayleigh and Eboigbe, Sylvia and Eggleston, Casey and Embley, Jo and Epskamp, Sacha and Errington, Timothy M. and Estel, Vivien and Farach, Frank J. and Feather, Jenelle and Fedor, Anna and Fernandez-Castilla, Belen and Fiedler, Susann and Field, James G. and Fitneva, Stanka A. and Flagan, Taru and Forest, Amanda L. and Forsell, Eskil and Foster, Joshua D. and Frank, Michael C. and Frazier, Rebecca S. and Fuchs, Heather and Gable, Philip and Galak, Jeff and Galliani, Elisa Maria and Gampa, Anup and Garcia, Sara and Gazarian, Douglas and Gilbert, Elizabeth and Giner-Sorolla, Roger and Gl{\"o}ckner, Andreas and G{\"o}llner, Lars and Goh, Jin X. and Goldberg, Rebecca and Goodbourn, Patrick T. and Gordon-McKeon, Shauna and Gorges, Bryan and Gorges, Jessie and Goss, Justin and Graham, Jesse and Grange, James A. and Gray, Jeremy and Hartgerink, Chris and Hartshorne, Joshua and Hasselman, Fred and Hayes, Timothy and Heikensten, Emma and Henninger, Felix and Hodsoll, John and Holubar, Taylor and Hoogendoorn, Gea and Humphries, Denise J. and Hung, Cathy O. -Y. and Immelman, Nathali and Irsik, Vanessa C. and Jahn, Georg and Jaekel, Frank and Jekel, Marc and Johannesson, Magnus and Johnson, Larissa G. and Johnson, David J. and Johnson, Kate M. and Johnston, William J. and Jonas, Kai and Joy-Gaba, Jennifer A. and Kappes, Heather Barry and Kelso, Kim and Kidwell, Mallory C. and Kim, Seung Kyung and Kirkhart, Matthew and Kleinberg, Bennett and Knezevic, Goran and Kolorz, Franziska Maria and Kossakowski, Jolanda J. and Krause, Robert Wilhelm and Krijnen, Job and Kuhlmann, Tim and Kunkels, Yoram K. and Kyc, Megan M. and Lai, Calvin K. and Laique, Aamir and Lakens, Daniel and Lane, Kristin A. and Lassetter, Bethany and Lazarevic, Ljiljana B. and LeBel, Etienne P. and Lee, Key Jung and Lee, Minha and Lemm, Kristi and Levitan, Carmel A. and Lewis, Melissa and Lin, Lin and Lin, Stephanie and Lippold, Matthias and Loureiro, Darren and Luteijn, Ilse and Mackinnon, Sean and Mainard, Heather N. and Marigold, Denise C. and Martin, Daniel P. and Martinez, Tylar and Masicampo, E. J. and Matacotta, Josh and Mathur, Maya and May, Michael and Mechin, Nicole and Mehta, Pranjal and Meixner, Johannes and Melinger, Alissa and Miller, Jeremy K. and Miller, Mallorie and Moore, Katherine and M{\"o}schl, Marcus and Motyl, Matt and M{\"u}ller, Stephanie M. and Munafo, Marcus and Neijenhuijs, Koen I. and Nervi, Taylor and Nicolas, Gandalf and Nilsonne, Gustav and Nosek, Brian A. and Nuijten, Michele B. and Olsson, Catherine and Osborne, Colleen and Ostkamp, Lutz and Pavel, Misha and Penton-Voak, Ian S. and Perna, Olivia and Pernet, Cyril and Perugini, Marco and Pipitone, R. Nathan and Pitts, Michael and Plessow, Franziska and Prenoveau, Jason M. and Rahal, Rima-Maria and Ratliff, Kate A. and Reinhard, David and Renkewitz, Frank and Ricker, Ashley A. and Rigney, Anastasia and Rivers, Andrew M. and Roebke, Mark and Rutchick, Abraham M. and Ryan, Robert S. and Sahin, Onur and Saide, Anondah and Sandstrom, Gillian M. and Santos, David and Saxe, Rebecca and Schlegelmilch, Rene and Schmidt, Kathleen and Scholz, Sabine and Seibel, Larissa and Selterman, Dylan Faulkner and Shaki, Samuel and Simpson, William B. and Sinclair, H. Colleen and Skorinko, Jeanine L. M. and Slowik, Agnieszka and Snyder, Joel S. and Soderberg, Courtney and Sonnleitner, Carina and Spencer, Nick and Spies, Jeffrey R. and Steegen, Sara and Stieger, Stefan and Strohminger, Nina and Sullivan, Gavin B. and Talhelm, Thomas and Tapia, Megan and te Dorsthorst, Anniek and Thomae, Manuela and Thomas, Sarah L. and Tio, Pia and Traets, Frits and Tsang, Steve and Tuerlinckx, Francis and Turchan, Paul and Valasek, Milan and Van Aert, Robbie and van Assen, Marcel and van Bork, Riet and van de Ven, Mathijs and van den Bergh, Don and van der Hulst, Marije and van Dooren, Roel and van Doorn, Johnny and van Renswoude, Daan R. and van Rijn, Hedderik and Vanpaemel, Wolf and Echeverria, Alejandro Vasquez and Vazquez, Melissa and Velez, Natalia and Vermue, Marieke and Verschoor, Mark and Vianello, Michelangelo and Voracek, Martin and Vuu, Gina and Wagenmakers, Eric-Jan and Weerdmeester, Joanneke and Welsh, Ashlee and Westgate, Erin C. and Wissink, Joeri and Wood, Michael and Woods, Andy and Wright, Emily and Wu, Sining and Zeelenberg, Marcel and Zuni, Kellylynn}, title = {Estimating the reproducibility of psychological science}, series = {Science}, volume = {349}, journal = {Science}, number = {6251}, publisher = {American Assoc. for the Advancement of Science}, address = {Washington}, organization = {Open Sci Collaboration}, issn = {1095-9203}, doi = {10.1126/science.aac4716}, pages = {8}, year = {2015}, abstract = {Reproducibility is a defining feature of science, but the extent to which it characterizes current research is unknown. We conducted replications of 100 experimental and correlational studies published in three psychology journals using high-powered designs and original materials when available. Replication effects were half the magnitude of original effects, representing a substantial decline. Ninety-seven percent of original studies had statistically significant results. Thirty-six percent of replications had statistically significant results; 47\% of original effect sizes were in the 95\% confidence interval of the replication effect size; 39\% of effects were subjectively rated to have replicated the original result; and if no bias in original results is assumed, combining original and replication results left 68\% with statistically significant effects. Correlational tests suggest that replication success was better predicted by the strength of original evidence than by characteristics of the original and replication teams.}, language = {en} } @article{MeyerRaberEbertetal.2015, author = {Meyer, S. and Raber, G. and Ebert, Franziska and Leffers, L. and M{\"u}ller, Sandra Marie and Taleshi, M. S. and Francesconi, Kevin A. and Schwerdtle, Tanja}, title = {In vitro toxicological characterisation of arsenic-containing fatty acids and three of their metabolites}, series = {Toxicology research}, volume = {5}, journal = {Toxicology research}, number = {4}, publisher = {Royal Society of Chemistry}, address = {Cambridge}, issn = {2045-4538}, doi = {10.1039/c5tx00122f}, pages = {1289 -- 1296}, year = {2015}, abstract = {Arsenic-containing fatty acids are a group of fat-soluble arsenic species (arsenolipids) which are present in marine fish and other seafood. Recently, it has been shown that arsenic-containing hydrocarbons, another group of arsenolipids, exert toxicity in similar concentrations comparable to arsenite although the toxic modes of action differ. Hence, a risk assessment of arsenolipids is urgently needed. In this study the cellular toxicity of a saturated (AsFA 362) and an unsaturated (AsFA 388) arsenic-containing fatty acid and three of their proposed metabolites (DMAV, DMAPr and thio-DMAPr) were investigated in human liver cells (HepG2). Even though both arsenic-containing fatty acids were less toxic as compared to arsenic-containing hydrocarbons and arsenite, significant effects were observable at μM concentrations. DMAV causes effects in a similar concentration range and it could be seen that it is metabolised to its highly toxic thio analogue thio-DMAV in HepG2 cells. Nevertheless, DMAPr and thio-DMAPr did not exert any cytotoxicity. In summary, our data indicate that risks to human health related to the presence of arsenic-containing fatty acids in marine food cannot be excluded. This stresses the need for a full in vitro and in vivo toxicological characterisation of these arsenolipids.}, language = {en} } @misc{MeyerRaberEbertetal.2015, author = {Meyer, S. and Raber, G. and Ebert, Franziska and Leffers, L. and M{\"u}ller, Sandra Marie and Taleshi, M. S. and Francesconi, Kevin A. and Schwerdtle, Tanja}, title = {In vitro toxicological characterisation of arsenic-containing fatty acids and three of their metabolites}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-82008}, year = {2015}, abstract = {Arsenic-containing fatty acids are a group of fat-soluble arsenic species (arsenolipids) which are present in marine fish and other seafood. Recently, it has been shown that arsenic-containing hydrocarbons, another group of arsenolipids, exert toxicity in similar concentrations comparable to arsenite although the toxic modes of action differ. Hence, a risk assessment of arsenolipids is urgently needed. In this study the cellular toxicity of a saturated (AsFA 362) and an unsaturated (AsFA 388) arsenic-containing fatty acid and three of their proposed metabolites (DMAV, DMAPr and thio-DMAPr) were investigated in human liver cells (HepG2). Even though both arsenic-containing fatty acids were less toxic as compared to arsenic-containing hydrocarbons and arsenite, significant effects were observable at μM concentrations. DMAV causes effects in a similar concentration range and it could be seen that it is metabolised to its highly toxic thio analogue thio-DMAV in HepG2 cells. Nevertheless, DMAPr and thio-DMAPr did not exert any cytotoxicity. In summary, our data indicate that risks to human health related to the presence of arsenic-containing fatty acids in marine food cannot be excluded. This stresses the need for a full in vitro and in vivo toxicological characterisation of these arsenolipids.}, language = {en} } @misc{PetrovHilleMuellerRoeberetal.2015, author = {Petrov, Veselin and Hille, Jacques and M{\"u}ller-R{\"o}ber, Bernd and Gechev, Tsanko S.}, title = {ROS-mediated abiotic stress-induced programmed cell death in plants}, series = {Frontiers in plant science}, volume = {6}, journal = {Frontiers in plant science}, publisher = {Frontiers Research Foundation}, address = {Lausanne}, issn = {1664-462X}, doi = {10.3389/fpls.2015.00069}, pages = {16}, year = {2015}, abstract = {During the course of their ontogenesis plants are continuously exposed to a large variety of abiotic stress factors which can damage tissues and jeopardize the survival of the organism unless properly countered. While animals can simply escape and thus evade stressors, plants as sessile organisms have developed complex strategies to withstand them. When the intensity of a detrimental factor is high, one of the defense programs employed by plants is the induction of programmed cell death (PCD). This is an active, genetically controlled process which is initiated to isolate and remove damaged tissues thereby ensuring the survival of the organism. The mechanism of PCD induction usually includes an increase in the levels of reactive oxygen species (ROS) which are utilized as mediators of the stress signal. Abiotic stress-induced PCD is not only a process of fundamental biological importance, but also of considerable interest to agricultural practice as it has the potential to significantly influence crop yield. Therefore, numerous scientific enterprises have focused on elucidating the mechanisms leading to and controlling PCD in response to adverse conditions in plants. This knowledge may help develop novel strategies to obtain more resilient crop varieties with improved tolerance and enhanced productivity. The aim of the present review is to summarize the recent advances in research on ROS-induced PCD related to abiotic stress and the role of the organelles in the process.}, language = {en} } @misc{BeninaRibeiroGechevetal.2015, author = {Benina, Maria and Ribeiro, Dimas Mendes and Gechev, Tsanko S. and M{\"u}ller-R{\"o}ber, Bernd and Schippers, Jos H. M.}, title = {A cell type-specific view on the translation of mRNAs from ROS-responsive genes upon paraquat treatment of Arabidopsis thaliana leaves}, series = {Plant, cell \& environment : cell physiology, whole-plant physiology, community physiology}, volume = {38}, journal = {Plant, cell \& environment : cell physiology, whole-plant physiology, community physiology}, number = {2}, publisher = {Wiley-Blackwell}, address = {Hoboken}, issn = {0140-7791}, doi = {10.1111/pce.12355}, pages = {349 -- 363}, year = {2015}, abstract = {Oxidative stress causes dramatic changes in the expression levels of many genes. The formation of a functional protein through successful mRNA translation is central to a coordinated cellular response. To what extent the response towards reactive oxygen species (ROS) is regulated at the translational level is poorly understood. Here we analysed leaf- and tissue-specific translatomes using a set of transgenic Arabidopsis thaliana lines expressing a FLAG-tagged ribosomal protein to immunopurify polysome-bound mRNAs before and after oxidative stress. We determined transcript levels of 171 ROS-responsive genes upon paraquat treatment, which causes formation of superoxide radicals, at the whole-organ level. Furthermore, the translation of mRNAs was determined for five cell types: mesophyll, bundle sheath, phloem companion, epidermal and guard cells. Mesophyll and bundle sheath cells showed the strongest response to paraquat treatment. Interestingly, several ROS-responsive transcription factors displayed cell type-specific translation patterns, while others were translated in all cell types. In part, cell type-specific translation could be explained by the length of the 5-untranslated region (5-UTR) and the presence of upstream open reading frames (uORFs). Our analysis reveals insights into the translational regulation of ROS-responsive genes, which is important to understanding cell-specific responses and functions during oxidative stress. The study illustrates the response of different Arabidopsis thaliana leaf cells and tissues to oxidative stress at the translational level, an aspect of reactive oxygen species (ROS) biology that has been little studied in the past. Our data reveal insights into how translational regulation of ROS-responsive genes is fine-tuned at the cellular level, a phenomenon contributing to the integrated physiological response of leaves to stresses involving changes in ROS levels.}, language = {en} } @misc{PetrovHilleMuellerRoeberetal.2015, author = {Petrov, Veselin and Hille, Jacques and M{\"u}ller-R{\"o}ber, Bernd and Gechev, Tsanko S.}, title = {ROS-mediated abiotic stress-induced programmed cell death in plants}, series = {Postprints der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe}, journal = {Postprints der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe}, number = {425}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-406481}, pages = {16}, year = {2015}, abstract = {During the course of their ontogenesis plants are continuously exposed to a large variety of abiotic stress factors which can damage tissues and jeopardize the survival of the organism unless properly countered. While animals can simply escape and thus evade stressors, plants as sessile organisms have developed complex strategies to withstand them. When the intensity of a detrimental factor is high, one of the defense programs employed by plants is the induction of programmed cell death (PCD). This is an active, genetically controlled process which is initiated to isolate and remove damaged tissues thereby ensuring the survival of the organism. The mechanism of PCD induction usually includes an increase in the levels of reactive oxygen species (ROS) which are utilized as mediators of the stress signal. Abiotic stress-induced PCD is not only a process of fundamental biological importance, but also of considerable interest to agricultural practice as it has the potential to significantly influence crop yield. Therefore, numerous scientific enterprises have focused on elucidating the mechanisms leading to and controlling PCD in response to adverse conditions in plants. This knowledge may help develop novel strategies to obtain more resilient crop varieties with improved tolerance and enhanced productivity. The aim of the present review is to summarize the recent advances in research on ROS-induced PCD related to abiotic stress and the role of the organelles in the process.}, language = {en} }