@misc{RiedelsbergerDreyerGonzalez2015,
  author    = {Riedelsberger, Janin and Dreyer, Ingo and Gonzalez, Wendy},
  title     = {Outward rectification of voltage-gated K+ channels evolved at least twice in life history},
  series = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  journal   = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  number    = {521},
  issn      = {1866-8372},
  doi       = {10.25932/publishup-40959},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-409594},
  pages     = {17},
  year      = {2015},
  abstract  = {Voltage-gated potassium (K+) channels are present in all living systems. Despite high structural similarities in the transmembrane domains (TMD), this K+ channel type segregates into at least two main functional categories-hyperpolarization-activated, inward-rectifying (Kin) and depolarization-activated, outward-rectifying (Kout) channels. Voltage-gated K+ channels sense the membrane voltage via a voltage-sensing domain that is connected to the conduction pathway of the channel. It has been shown that the voltage-sensing mechanism is the same in Kin and Kout channels, but its performance results in opposite pore conformations. It is not known how the different coupling of voltage-sensor and pore is implemented. Here, we studied sequence and structural data of voltage-gated K+ channels from animals and plants with emphasis on the property of opposite rectification. We identified structural hotspots that alone allow already the distinction between Kin and Kout channels. Among them is a loop between TMD S5 and the pore that is very short in animal Kout, longer in plant and animal Kin and the longest in plant Kout channels. In combination with further structural and phylogenetic analyses this finding suggests that outward-rectification evolved twice and independently in the animal and plant kingdom.},
  language  = {en}
}
@misc{OmidbakhshfardNeerakkalGuptaetal.2020,
  author    = {Omidbakhshfard, Mohammad Amin and Neerakkal, Sujeeth and Gupta, Saurabh and Omranian, Nooshin and Guinan, Kieran J. and Brotman, Yariv and Nikoloski, Zoran and Fernie, Alisdair R. and Mueller-Roeber, Bernd and Gechev, Tsanko S.},
  title     = {A Biostimulant Obtained from the Seaweed Ascophyllum nodosum Protects Arabidopsis thaliana from Severe Oxidative Stress},
  series = {Postprints der Universit{\"a}t Potsdam : Mathematisch Naturwissenschaftliche Reihe},
  journal   = {Postprints der Universit{\"a}t Potsdam : Mathematisch Naturwissenschaftliche Reihe},
  number    = {823},
  issn      = {1866-8372},
  doi       = {10.25932/publishup-44509},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-445093},
  pages     = {26},
  year      = {2020},
  abstract  = {Abiotic stresses cause oxidative damage in plants. Here, we demonstrate that foliar application of an extract from the seaweed Ascophyllum nodosum, SuperFifty (SF), largely prevents paraquat (PQ)-induced oxidative stress in Arabidopsis thaliana. While PQ-stressed plants develop necrotic lesions, plants pre-treated with SF (i.e., primed plants) were unaffected by PQ. Transcriptome analysis revealed induction of reactive oxygen species (ROS) marker genes, genes involved in ROS-induced programmed cell death, and autophagy-related genes after PQ treatment. These changes did not occur in PQ-stressed plants primed with SF. In contrast, upregulation of several carbohydrate metabolism genes, growth, and hormone signaling as well as antioxidant-related genes were specific to SF-primed plants. Metabolomic analyses revealed accumulation of the stress-protective metabolite maltose and the tricarboxylic acid cycle intermediates fumarate and malate in SF-primed plants. Lipidome analysis indicated that those lipids associated with oxidative stress-induced cell death and chloroplast degradation, such as triacylglycerols (TAGs), declined upon SF priming. Our study demonstrated that SF confers tolerance to PQ-induced oxidative stress in A. thaliana, an effect achieved by modulating a range of processes at the transcriptomic, metabolic, and lipid levels.},
  language  = {en}
}
@misc{BrzezinkaAltmannBaeurle2018,
  author    = {Brzezinka, Krzysztof and Altmann, Simone and B{\"a}urle, Isabel},
  title     = {BRUSHY1/TONSOKU/MGOUN3 is required for heat stress memory},
  series = {Postprints der Universit{\"a}t Potsdam Mathematisch-Naturwissenschaftliche Reihe},
  journal   = {Postprints der Universit{\"a}t Potsdam Mathematisch-Naturwissenschaftliche Reihe},
  number    = {788},
  issn      = {1866-8372},
  doi       = {10.25932/publishup-43621},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-436219},
  pages     = {11},
  year      = {2018},
  abstract  = {Plants encounter biotic and abiotic stresses many times during their life cycle and this limits their productivity. Moderate heat stress (HS) primes a plant to survive higher temperatures that are lethal in the naive state. Once temperature stress subsides, the memory of the priming event is actively retained for several days preparing the plant to better cope with recurring HS. Recently, chromatin regulation at different levels has been implicated in HS memory. Here, we report that the chromatin protein BRUSHY1 (BRU1)/TONSOKU/MGOUN3 plays a role in the HS memory in Arabidopsis thaliana. BRU1 is also involved in transcriptional gene silencing and DNA damage repair. This corresponds with the functions of its mammalian orthologue TONSOKU-LIKE/NF Kappa BIL2. During HS memory, BRU1 is required to maintain sustained induction of HS memory-associated genes, whereas it is dispensable for the acquisition of thermotolerance. In summary, we report that BRU1 is required for HS memory in A. thaliana, and propose a model where BRU1 mediates the epigenetic inheritance of chromatin states across DNA replication and cell division.},
  language  = {en}
}