Nitric oxide implication in cadmium-induced programmed cell death in roots and signaling response of yellow lupine plants

Arasimowicz‐Jelonek, Magdalena; Floryszak‐Wieczorek, Jolanta; Deckert, Joanna; Rucińska-Sobkowiak, Renata; Gzyl, Jarosław; Pawlak-Sprada, Sylwia; Abramowski, Dariusz; Jelonek, Tomasz; Gwóźdź, Edward A.

doi:10.1016/j.plaphy.2012.06.018

Cited by 113 publications

(79 citation statements)

References 67 publications

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“…Increased production of NO and/or H 2 O 2 in plants responding to abiotic stresses can cause cell death (Brüne 2003; Gao et al 2008;Breusegem and Dat 2006;Arasimowicz et al 2012;Domingos et al 2015). Our present study showed that SO 2 toxicity was decreased by scavengers of NO or H 2 O 2 and could be completely reversed when NO and H 2 O 2 scavengers were both present.…”

Section: Discussionsupporting

confidence: 56%

NO and H2O2 contribute to SO2 toxicity via Ca2+ signaling in Vicia faba guard cells

Bai

Xue

et al. 2017

Environ Sci Pollut Res

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NO and H 2 O 2 have been implicated as important signals in biotic and abiotic stress responses of plants to the environment. Previously, we have shown that SO 2 exposure increased the levels of NO and H 2 O 2 in plant cells. We hypothesize that, as signaling molecules, NO and H 2 O 2 mediate SO 2 -caused toxicity. In this paper, we show that SO 2 hydrates caused guard cell death in a concentration-dependent manner in the concentration range of 0.25 to 6 mmol L −1 , which was associated with elevation of intracellular NO, H 2 O 2 , and Ca 2+ levels in Vicia faba guard cells. NO donor SNP enhanced SO 2 toxicity, while NO scavenger c-PTIO and NO synthesis inhibitors L-NAME and tungstate significantly prevented SO 2 toxicity. ROS scavenger ascorbic acid (AsA) and catalase (CAT), Ca 2+ chelating agent EGTA, and Ca 2+ channel inhibitor LaCl 3 also markedly blocked SO 2 toxicity. In addition, both c-PTIO and AsA could completely block SO 2 -induced elevation of intracellular Ca 2+ level. Moreover, c-PTIO efficiently blocked SO 2 -induced H 2 O 2 elevation, and AsA significantly blocked SO 2 -induced NO elevation. These results indicate that extra NO and H 2 O 2 are produced and accumulated in SO 2 -treated guard cells, which further activate Ca 2+ signaling to mediate SO 2 toxicity. Our findings suggest that both NO and H 2 O 2 contribute to SO 2 toxicity via Ca 2+ signaling.

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Section: Discussionsupporting

confidence: 56%

NO and H2O2 contribute to SO2 toxicity via Ca2+ signaling in Vicia faba guard cells

Bai

Xue

et al. 2017

Environ Sci Pollut Res

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“…Rodríguez-Serrano et al [70] demonstrated that Cd toxicity strongly depressed the activity of NO-synthase dependent NO production in Pisum sativum seedlings; however, exogenous Ca supply ameliorated this efect due to enhanced JA and ET production. Interplay among NO, H 2 O 2 , and SA has also been reported in lupine seedlings [71] and ryegrass plants [72] under Cd stress. Application of putrescine (Put) and NO in combination was reported to alleviate Cd toxicity in Vigna radiate by triggering the activity of both enzymatic and nonenzymatic antioxidant machinery and a parallel increase in phytochelatin synthesis [73].…”

Section: No-phytohormone Cross Talk Under Heavy Metals Stressmentioning

confidence: 69%

Cross Talk between Nitric Oxide and Phytohormones Regulate Plant Development during Abiotic Stresses

Nawaz¹,

Shabbir²,

Shahbaz³

et al. 2017

Phytohormones - Signaling Mechanisms and Crosstalk in Plant Development and Stress Responses

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Plants, being sessile, are concurrently exposed to various biotic and abiotic stresses. The perception of stress signals in plants involves a wide spectrum of signal transduction pathways that interact to induce tolerance against adverse environmental conditions. This functional overlapping among various stress signaling cascades also leads to the expression of genes that regulate biosynthesis or action of other hormones. Phytohormonal signals, activated by both developmental and environmental responses, play a crucial role to develop stress tolerance in plants. Nitric oxide (NO) is one of the major players in plant signaling networks. Emerging evidence supports that NO interplays with signaling pathways of auxins, gibberellins, abscisic acid, ethylene, jasmonic acid, brassinosteroids, and other plant hormones to control metabolism, growth, and development in plants. This chapter focuses on the current state of knowledge of cross talk between signaling pathways of NO and phytohormones in plants exposed to various abiotic stresses.

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“…Moreover, it can react with superoxide generatinp toxic ONOO -tripllprlnnnf pf nl ?n n n u/hirh at h\oh rnnrenti-.itinn initiates cell death (Gupta and Igamberdiev 2011). Time-course experiments indicated that C>2~ rather than H2O2 functions in synergism with NO to trigger the PCD program (Blokhina and Fagerstedt 2010;Arasimowicz-Jelonek et al 2012).…”

Section: No-and Salt-induced Programmed Cell Deathmentioning

confidence: 99%

Role of Nitric Oxide in Salt Stress-induced Programmed Cell Death and Defense Mechanisms

Poór

Laskay

Tari

2015

Nitric Oxide Action in Abiotic Stress Responses in Plants

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Nitric oxide implication in cadmium-induced programmed cell death in roots and signaling response of yellow lupine plants

Cited by 113 publications

References 67 publications

NO and H2O2 contribute to SO2 toxicity via Ca2+ signaling in Vicia faba guard cells

NO and H2O2 contribute to SO2 toxicity via Ca2+ signaling in Vicia faba guard cells

Cross Talk between Nitric Oxide and Phytohormones Regulate Plant Development during Abiotic Stresses

Role of Nitric Oxide in Salt Stress-induced Programmed Cell Death and Defense Mechanisms

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