TY - GEN A1 - Petrov, Veselin A1 - Hille, Jacques A1 - Müller-Röber, Bernd A1 - Gechev, Tsanko S. T1 - ROS-mediated abiotic stress-induced programmed cell death in plants T2 - Postprints der Universität Potsdam : Humanwissenschaftliche Reihe N2 - 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. T3 - Zweitveröffentlichungen der Universität Potsdam : Humanwissenschaftliche Reihe - 425 KW - abiotic stress KW - programmed cell death KW - reactive oxygen species KW - signal transduction KW - stress adaptation Y1 - 2018 UR - https://publishup.uni-potsdam.de/frontdoor/index/index/docId/40648 UR - https://nbn-resolving.org/urn:nbn:de:kobv:517-opus4-406481 IS - 425 ER -