@article{BaeurleBrzezinkaAltmann2018, author = {B{\"a}urle, Isabel and Brzezinka, Krzysztof and Altmann, Simone}, title = {BRUSHY1/TONSOKU/MGOUN3 is required for heat stress memory}, series = {Plant Cell \& Environment}, volume = {42}, journal = {Plant Cell \& Environment}, doi = {10.1111/pce.13365}, pages = {771 -- 781}, 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 na{\"i}ve 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/NFΚBIL2. 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} } @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} } @article{SedaghatmehrThirumalaikumarKamranfaretal.2019, author = {Sedaghatmehr, Mastoureh and Thirumalaikumar, Venkatesh P. and Kamranfar, Iman and Marmagne, Anne and Masclaux-Daubresse, Celine and Balazadeh, Salma}, title = {A regulatory role of autophagy for resetting the memory of heat stress in plants}, series = {Plant, cell \& environment : cell physiology, whole-plant physiology, community physiology}, volume = {42}, journal = {Plant, cell \& environment : cell physiology, whole-plant physiology, community physiology}, number = {3}, publisher = {Wiley}, address = {Hoboken}, issn = {0140-7791}, doi = {10.1111/pce.13426}, pages = {1054 -- 1064}, year = {2019}, abstract = {As sessile life forms, plants are repeatedly confronted with adverse environmental conditions, which can impair development, growth, and reproduction. During evolution, plants have established mechanisms to orchestrate the delicate balance between growth and stress tolerance, to reset cellular biochemistry once stress vanishes, or to keep a molecular memory, which enables survival of a harsher stress that may arise later. Although there are several examples of memory in diverse plants species, the molecular machinery underlying the formation, duration, and resetting of stress memories is largely unknown so far. We report here that autophagy, a central self-degradative process, assists in resetting cellular memory of heat stress (HS) in Arabidopsis thaliana. Autophagy is induced by thermopriming (moderate HS) and, intriguingly, remains high long after stress termination. We demonstrate that autophagy mediates the specific degradation of heat shock proteins at later stages of the thermorecovery phase leading to the accumulation of protein aggregates after the second HS and a compromised heat tolerance. Autophagy mutants retain heat shock proteins longer than wild type and concomitantly display improved thermomemory. Our findings reveal a novel regulatory mechanism for HS memory in plants.}, language = {en} } @article{LaemkeBrzezinkaAltmannetal.2016, author = {L{\"a}mke, J{\"o}rn and Brzezinka, Krzysztof and Altmann, Simone and B{\"a}urle, Isabel}, title = {A hit-and-run heat shock factor governs sustained histone methylation and transcriptional stress memory}, series = {The EMBO journal}, volume = {35}, journal = {The EMBO journal}, publisher = {Wiley-Blackwell}, address = {Hoboken}, issn = {0261-4189}, doi = {10.15252/embj.201592593}, pages = {162 -- 175}, year = {2016}, abstract = {In nature, plants often encounter chronic or recurring stressful conditions. Recent results indicate that plants can remember a past exposure to stress to be better prepared for a future stress incident. However, the molecular basis of this is poorly understood. Here, we report the involvement of chromatin modifications in the maintenance of acquired thermotolerance (heat stress [HS] memory). HS memory is associated with the accumulation of histone H3 lysine 4 di- and trimethylation at memory-related loci. This accumulation outlasts their transcriptional activity and marks them as recently transcriptionally active. High accumulation of H3K4 methylation is associated with hyper-induction of gene expression upon a recurring HS. This transcriptional memory and the sustained accumulation of H3K4 methylation depend on HSFA2, a transcription factor that is required for HS memory, but not initial heat responses. Interestingly, HSFA2 associates with memory-related loci transiently during the early stages following HS. In summary, we show that transcriptional memory after HS is associated with sustained H3K4 hyper-methylation and depends on a hit-and-run transcription factor, thus providing a molecular framework for HS memory.}, 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} } @article{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 = {International Journal of Molecular Sciences}, volume = {21}, journal = {International Journal of Molecular Sciences}, number = {2}, publisher = {Molecular Diversity Preservation International}, address = {Basel}, issn = {1422-0067}, doi = {10.3390/ijms21020474}, 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} }