02411nab a2200241 i 4500 publ6141 20180821123911.0 160202s2013 hu o 0|| zxx d 0033-183X 10.1007/s00709-012-0408-4 doi 1974033 mtmt SZTE Publicatio Repozitórium hun zxx Poór Péter Ethylene signaling in salt stress- and salicylic acid-induced programmed cell death in tomato suspension cells [elektronikus dokumentum] / Poór Péter Springer-Verlag 2013 273-284 PROTOPLASMA 250 No. 1 Salt stress- and salicylic acid (SA)-induced cell death can be activated by various signaling pathways including ethylene (ET) signaling in intact tomato plants. In tomato suspension cultures, a treatment with 250 mM NaCl increased the production of reactive oxygen species (ROS), nitric oxide (NO), and ET. The 10(-3) M SA-induced cell death was also accompanied by ROS and NO production, but ET emanation, the most characteristic difference between the two cell death programs, did not change. ET synthesis was enhanced by addition of ET precursor 1-aminocyclopropane-1-carboxylic acid, which, after 2 h, increased the ROS production in the case of both stressors and accelerated cell death under salt stress. However, it did not change the viability and NO levels in SA-treated samples. The effect of ET induced by salt stress could be blocked with silver thiosulfate (STS), an inhibitor of ET action. STS reduced the death of cells which is in accordance with the decrease in ROS production of cells exposed to high salinity. Unexpectedly, application of STS together with SA resulted in increasing ROS and reduced NO accumulation which led to a faster cell death. NaCl- and SA-induced cell death was blocked by Ca(2+) chelator EGTA and calmodulin inhibitor W-7, or with the inhibitors of ROS. The inhibitor of MAPKs, PD98059, and the cysteine protease inhibitor E-64 reduced cell death in both cases. These results show that NaCl induces cell death mainly by ET-induced ROS production, but ROS generated by SA was not controlled by ET in tomato cell suspension. Kovács Judit aut Szopkó Dóra aut Görgényi Miklósné Tari Irma aut http://publicatio.bibl.u-szeged.hu/6141/1/Article1_proof_u.PDF Dokumentum-elérés