Plant caspase-like proteases in plant programmed cell death

Xu, Qixian; Zhang, Lingrui

doi:10.4161/psb.4.9.9531

Cited by 31 publications

(19 citation statements)

References 28 publications

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“…1 (III)). These inhibitory effects are consistent with previous studies in human cells, suggesting that caspase-like proteases in plant cells (Xu and Zhang 2009) are activated by SO 2 stress and involved in the implementation of PCD in V. faba guard cells.…”

Section: So 2 Causes Cell Viability Decrease and Pcd Of V Faba Stomasupporting

confidence: 92%

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: So 2 Causes Cell Viability Decrease and Pcd Of V Faba Stomasupporting

confidence: 92%

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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“…The features of plant PCD include cytoplasmic shrinkage, chromatin condensation, mitochondrial swelling, generation of reactive oxygen species (ROS), and increased activity of cysteine proteases such as metacaspases (Coll et al ., ). Protease activity seems to be essential for PCD and defense in plants (Solomon et al ., ; Chichkova et al ., ; Xu and Zhang, ). Metacaspase genes are upregulated during PCD in tomato and during pathogen invasion in N. benthamiana and Arabidopsis (Hoeberichts et al ., ; Zimmermann et al ., ; Hao et al ., ).…”

Section: Introductionmentioning

confidence: 99%

Pepper pathogenesis‐related protein 4c is a plasma membrane‐localized cysteine protease inhibitor that is required for plant cell death and defense signaling

Kim

Hwang

2014

The Plant Journal

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SUMMARYXanthomonas campestris pv. vesicatoria (Xcv) type III effector AvrBsT triggers programmed cell death (PCD) and activates the hypersensitive response (HR) in plants. Here, we isolated and identified the plasma membrane localized pathogenesis-related (PR) protein 4c gene (CaPR4c) from pepper (Capsicum annuum) leaves undergoing AvrBsT-triggered HR cell death. CaPR4c encodes a protein with a signal peptide and a Barwin domain. Recombinant CaPR4c protein expressed in Escherichia coli exhibited cysteine proteaseinhibitor activity and ribonuclease (RNase) activity. Subcellular localization analyses revealed that CaPR4c localized to the plasma membrane in plant cells. CaPR4c expression was rapidly and specifically induced by avirulent Xcv (avrBsT) infection. Transient expression of CaPR4c caused HR cell death in pepper leaves, which was accompanied by enhanced accumulation of H 2 O 2 and significant induction of some defenseresponse genes. Deletion of the signal peptide from CaPR4c abolished the induction of HR cell death, indicating a requirement for plasma membrane localization of CaPR4c for HR cell death. CaPR4c silencing in pepper disrupted both basal and AvrBsT-triggered resistance responses, and enabled Xcv proliferation in infected leaves. H 2 O 2 accumulation, cell-death induction, and defense-response gene expression were distinctly reduced in CaPR4c-silenced pepper. CaPR4c overexpression in transgenic Arabidopsis plants conferred greater resistance against infection by Pseudomonas syringae pv. tomato and Hyaloperonospora arabidopsidis. These results collectively suggest that CaPR4c plays an important role in plant cell death and defense signaling.

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“…A correlation can be established between the reduced caspase-3-activity and the increased cell viability. Prior evidence suggests that several proteinases having caspase-like activity have been reported in plants (Xu and Zhang, 2009) and were involved in the regulation of plant cell death (Choi and Berges, 2013). Higher caspase-3-like activity has been associated with microspore cell death and has been reported after inductive stress in barley microspores and embryogenic suspension cultures (Rodríguez-Serrano et al, 2012) and in triticale microspore culture (Sinha and Eudes, 2015).…”

Section: Discussionmentioning

confidence: 99%

Bcl-2△21 and Ac-DEVD-CHO Inhibit Death of Wheat Microspores

et al. 2016

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Microspore cell death and low green plant production efficiency are an integral obstacle in the development of doubled haploid production in wheat. The aim of the current study was to determine the effect of anti-apoptotic recombinant human B-cell lymphoma-2 (Bcl-2△21) and caspase-3-inhibitor (Ac-DEVD-CHO) in microspore cell death in bread wheat cultivars AC Fielder and AC Andrew. Induction medium containing Bcl-2△21 and Ac-DEVD-CHO yielded a significantly higher number of viable microspores, embryo-like structures and total green plants in wheat cultivars AC Fielder and AC Andrew. Total peroxidase activity was lower in Bcl-2△21 treated microspore cultures at 96 h of treatment compared to control and Ac-DEVD-CHO. Electron paramagnetic resonance study of total microspore protein showed a different scavenging activity for Bcl-2△21 and Ac-DEVD-CHO. Bcl-2△21 scavenged approximately 50% hydroxyl radical (HO•) formed, whereas Ac-DEVD-CHO scavenged approximately 20% of HO•. Conversely, reduced caspase-3-like activities were detected in the presence of Bcl-2△21 and Ac-DEVD-CHO, supporting the involvement of Bcl-2△21 and Ac-DEVD-CHO in increasing microspore viability by reducing oxidative stress and caspase-3-like activity. Our results indicate that Bcl-2△21 and Ac-DEVD-CHO protects cells from cell death following different pathways. Bcl-2△21 prevents cell damage by detoxifying HO• and suppressing caspase-3-like activity, while Ac-DEVD-CHO inhibits the cell death pathways by modulating caspase-like activity.

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Plant caspase-like proteases in plant programmed cell death

Cited by 31 publications

References 28 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

Pepper pathogenesis‐related protein 4c is a plasma membrane‐localized cysteine protease inhibitor that is required for plant cell death and defense signaling

Bcl-2△21 and Ac-DEVD-CHO Inhibit Death of Wheat Microspores

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