@article{MuenchHsinFerberetal.2016, author = {M{\"u}nch, Miriam and Hsin, Chih-Hsuan and Ferber, Elena and Berger, Susanne and M{\"u}ller, Martin J.}, title = {Reactive electrophilic oxylipins trigger a heat stress-like response through HSFA1 transcription factors}, series = {Journal of Experimental Botany}, volume = {67}, journal = {Journal of Experimental Botany}, number = {21}, doi = {10.1093/jxb/erw376}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-186766}, pages = {6139-6148}, year = {2016}, abstract = {Electrophilic oxylipins trigger a heat-shock-like response in the absence of heat through the canonical heat-shock transcription factor A1, thereby helping to cope with stresses associated with protein damage.Abiotic and biotic stresses are often characterized by an induction of reactive electrophile species (RES) such as the jasmonate 12-oxo-phytodienoic acid (OPDA) or the structurally related phytoprostanes. Previously, RES oxylipins have been shown massively to induce heat-shock-response (HSR) genes including HSP101 chaperones. Moreover, jasmonates have been reported to play a role in basal thermotolerance. We show that representative HSR marker genes are strongly induced by RES oxylipins through the four master regulator transcription factors HSFA1a, b, d, and e essential for short-term adaptation to heat stress in Arabidopsis. When compared with Arabidopsis seedlings treated at the optimal acclimation temperature of 37 A degrees C, the exogenous application of RES oxylipins at 20 A degrees C induced a much weaker induction of HSP101 at both the gene and protein expression levels which, however, was not sufficient to confer short-term acquired thermotolerance. Moreover, jasmonate-deficient mutant lines displayed a wild-type-like HSR and were not compromised in acquiring thermotolerance. Hence, the OPDA- and RES oxylipin-induced HSR is not sufficient to protect seedlings from severe heat stress but may help plants to cope better with stresses associated with protein unfolding by inducing a battery of chaperones in the absence of heat.}, language = {en} } @article{ZinnerKruegerReedetal.2016, author = {Zinner, C. and Krueger, M. and Reed, J. L. and Kohl-Bareis, M. and Holmberg, H. C. and Sperlich, B.}, title = {Exposure to a combination of heat and hyperoxia during cycling at submaximal intensity does not alter thermoregulatory responses}, series = {Biology of Sport}, volume = {33}, journal = {Biology of Sport}, number = {1}, doi = {10.5604/20831862.1192041}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-160993}, pages = {71-76}, year = {2016}, abstract = {In this study, we tested the hypothesis that breathing hyperoxic air (F\(_{in}\)O\(_2\) = 0.40) while exercising in a hot environment exerts negative effects on the total tissue level of haemoglobin concentration (tHb); core (T\(_{core}\)) and skin (T\(_{skin}\)) temperatures; muscle activity; heart rate; blood concentration of lactate; pH; partial pressure of oxygen (P\(_a\)O\(_2\)) and carbon dioxide; arterial oxygen saturation (S\(_a\)O\(_2\)); and perceptual responses. Ten well-trained male athletes cycled at submaximal intensity at 21°C or 33°C in randomized order: first for 20 min while breathing normal air (FinO\(_2\) = 0.21) and then 10 min with F\(_{in}\)O\(_2\) = 0.40 (HOX). At both temperatures, S\(_a\)O\(_2\) and P\(_a\)O\(_2\), but not tHb, were increased by HOX. Tskin and perception of exertion and thermal discomfort were higher at 33°C than 21°C (p < 0.01), but independent of F\(_{in}\)O\(_2\). T\(_{core}\) and muscle activity were the same under all conditions (p > 0.07). Blood lactate and heart rate were higher at 33°C than 21°C. In conclusion, during 30 min of submaximal cycling at 21°C or 33°C, T\(_{core}\), T\(_{skin}\) and T\(_{body}\), tHb, muscle activity and ratings of perceived exertion and thermal discomfort were the same under normoxic and hyperoxic conditions. Accordingly, breathing hyperoxic air (F\(_{in}\)O\(_2\) = 0.40) did not affect thermoregulation under these conditions.}, language = {en} }