Participation of the mitochondrial permeability transition pore in nitric oxide‐induced plant cell death

Abstract

In the present study, we investigated the involvement of the mitochondrial permeability transition pore (PTP) in nitric oxide (NO)-induced plant cell death. NO donors such as sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine inhibited growth and caused death in suspension-cultured cells of Citrus sinensis. Cells treated with SNP showed chromatin condensation and fragmentation, characteristic of apoptosis. SNP caused loss of the mitochondrial membrane electrical potential, which was prevented by cyclosporin A (CsA), a specific inhibitor of PTP formation. CsA also prevented the nuclear apoptosis and subsequent Citrus cell death induced by NO. These findings indicate that mitochondrial PTP formation is involved in the signaling pathway by which NO induces apoptosis in cultured Citrus cells. ß 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

Regulation of Plant Glycine Decarboxylase byS-Nitrosylation and Glutathionylation

“…The PTP depolarizes mitochondria, leading to mitochondrial swelling and subsequent release of cytochrome c from the intermembrane space (Goldstein et al, 2000). It has been demonstrated that the mitochondrial PTP participates in NO-induced cell death in plants (Saviani et al, 2002). In concurrence, our data show a 50% loss of membrane potential in Arabidopsis cells 30 min after treatment with AAN, whereas this loss is limited by the action of the alternative respiratory pathway (Fig.…”

“…9A). The depolarization observed in the control was most likely due to a stress condition of cells in the plate reader and was completely suppressed by pretreatment with cyclosporine A, which is an inhibitor of the mitochondrial transition pore (Saviani et al, 2002). In addition, catalase was able to reduce the DC m in untreated or AAN-treated cells, confirming that the oxidative burst is essential for the breakdown of the mitochondrial membrane potential (Fig.…”

“…Plant mitochondrial responses to stress signals are similar to those of animal mitochondria and include a collapse of the transmembrane potential (DC m ), release of cytochrome c, and decrease in ATP production (Saviani et al, 2002;Tiwari et al, 2002;Krause and Durner, 2004). Normally, the mitochondrial H 2 O 2 burst appears to precede the breakdown in the DC m , probably as a result of perturbation of the mitochondrial electron transport chain (Pellinen et al, 1999; Yao et al, Figure 5.…”

“…Among these identified proteins, we focused our attention on the P-subunit of the Gly decarboxylase complex (GDC), which is an integral part of the photorespiratory system. Since the release of apoptotic factors from mitochondria may be a result of inhibition of respiration, transition of mitochondrial permeability, and formation of reactive oxygen species (ROS; Saviani et al, 2002;Taylor et al, 2004;Chen and Gibson, 2008), Figure 1. Harpin-dependent NO production in mitochondria.…”

Substâncias antifúngicas constitutivas e induzidas em folhas e suspensões celulares de Rudgea jasminoides (Cham.) Müll. Arg. (Rubiaceae)

“…A inibição de crescimento correlacionada à morte celular por doadores de NO também foi observada em suspensões celulares de Citrus sinensis (L.) Osbeck após dez dias de incubação com SNP em concentrações que variaram de 0,01 a 100 μM (Saviani et al 2002). Segundo esses autores, a ausência de um mecanismo regulatório de controle da morte celular explicaria, parcialmente, a sensibilidade das células, como verifi cado também em R. jasminoides.…”