Calcium-mediated apoptosis in a plant hypersensitive disease resistance response

Levine, Alex; Pennell, Roger I.; Alvarez, María Elena; Palmer, R. Kyle; Lamb, Chris

doi:10.1016/s0960-9822(02)00510-9

Cited by 551 publications

(428 citation statements)

References 47 publications

(72 reference statements)

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“…Included are self-incompatibility of pollen, aleurone differentiation, aerenchyma formation, HR and leaf senescence. [51][52][53][54] Additional data confirm a role of CaMBP or channel in pathogen defense. The Arabidopsis Dnd1 gene, that encodes a cyclic nucleotidedependent calcium channel, is required for the activation of HR-induced cell death.…”

Section: Discussionmentioning

confidence: 82%

AtBAG6, a novel calmodulin-binding protein, induces programmed cell death in yeast and plants

et al. 2005

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Calmodulin (CaM) influences many cellular processes by interacting with various proteins. Here, we isolated AtBAG6, an Arabidopsis CaM-binding protein that contains a central BCL-2-associated athanogene (BAG) domain. In yeast and plants, overexpression of AtBAG6 induced cell death phenotypes consistent with programmed cell death (PCD). Recombinant AtBAG6 had higher affinity for CaM in the absence of free Ca 2 þ than in its presence. An IQ motif (IQXXXRGXXXR, where X denotes any amino-acid) was required for Ca 2 þ -independent CaM complex formation and single amino-acid changes within this motif abrogated both AtBAG6-activated CaM-binding and cell death in yeast and plants. A 134-amino-acid stretch, encompassing both the IQ motif and BAG domain, was sufficient to induce cell death. Agents generating oxygen radicals, which are known to be involved in plant PCD, specifically induced the AtBAG6 transcript. Collectively, these results suggest that AtBAG6 is a stress-upregulated CaM-binding protein involved in plant PCD.

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Section: Discussionmentioning

confidence: 82%

AtBAG6, a novel calmodulin-binding protein, induces programmed cell death in yeast and plants

et al. 2005

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“…In several species of cyanobacteria and unicellular algae, the production of H 2 O 2 can coordinate a series of cellular responses including the induction of programmed cell death or apoptosis (Korsmeyer et al, 1995;Levine et al, 1996;Vardi et al, 1999). For example, ultraviolet radiation (particularly UV-B: 280-320 nm) has a detrimental effect on the development and general metabolism of cyanobacteria (Tyagi et al, 1992;Hader, 1998, 2002).…”

Section: Discussionmentioning

confidence: 99%

Toxin release in response to oxidative stress and programmed cell death in the cyanobacterium Microcystis aeruginosa

2006

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“…Indeed, several groups have reported that extracellular EGTA can inhibit the mobilization of selected disease resistance mechanisms (52,53). Other workers have shown that introduction of exogenous Ca 2ϩ into resting cells can initiate a defense response in the absence of the usually required elicitors (16,54). Still other laboratories have demonstrated that Ca 2ϩ channel blockers such as La 3ϩ can prevent expression of a normal pathogen resistance mechanism when conditions are otherwise designed to stimulate its induction (52,54).…”

Section: Fig 2 Effect Of Plant Defense Elicitors On Intracellular Cmentioning

confidence: 99%

“…Other workers have shown that introduction of exogenous Ca 2ϩ into resting cells can initiate a defense response in the absence of the usually required elicitors (16,54). Still other laboratories have demonstrated that Ca 2ϩ channel blockers such as La 3ϩ can prevent expression of a normal pathogen resistance mechanism when conditions are otherwise designed to stimulate its induction (52,54). Nevertheless, it has never been determined wherein Ca 2ϩ actually exerts control over processes leading to disease resistance.…”

Section: Fig 2 Effect Of Plant Defense Elicitors On Intracellular Cmentioning

confidence: 99%

Measurement of Ca2+ Fluxes during Elicitation of the Oxidative Burst in Aequorin-transformed Tobacco Cells

Chandra

Low

1997

Journal of Biological Chemistry

147

117

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We have employed suspension cultured aequorintransformed tobacco cells to examine the involvement of Ca 2؉ in signal transduction of the oxidative burst. Use of cultured cells for this purpose was validated by demonstrating that the cells responded to cold shock quantitatively and qualitatively similarly to the intact transgenic plants from which they were derived. Stimulation of the oxidative burst in the cell suspension was achieved by administration of oligogalacturonic acid, Mas-7 (a peptide known to activate G proteins and Ca 2؉ fluxes), hypo-osmotic stress, or harpin (a protein from the pathogenic bacterium Erwinia amylovora). The latter failed to promote any detectable increase in cytoplasmic Ca 2؉ concentration, whereas each of the former three triggered a rapid rise in cytosolic Ca 2؉ followed by a return within seconds to basal Ca 2؉ levels. Peak Ca 2؉ concentrations induced by the former three elicitors were ϳ0.7, 1.4, and 1.3 M, respectively. Three lines of evidence suggest that the observed Ca 2؉ pulses are essential to transduction of the oxidative burst signals by their respective elicitors: (i) inhibition of the Ca 2؉ transients with Ca 2؉ chelators or Ca 2؉ channel blockers prevented expression of the oxidative burst, (ii) introduction of exogenous Ca 2؉ into the same cells initiated the burst even in the absence of other inducers of the response, and (iii) the observed Ca 2؉ transients often returned to near basal levels well before any H 2 O 2 synthesis could be detected, suggesting that the Ca 2؉ influx is required to communicate the burst signal but not maintain the defense response. These data suggest that Ca 2؉ pulses serve frequently, but not invariably, to transduce an oxidative burst signal.The oxidative burst constitutes one of the more rapid responses of a plant cell to pathogen attack (1). Within minutes of pathogen recognition, reactive oxygen species are generated that may promote cross-linking and lignification of the cell wall (2, 3), transcription of defense-related genes (4, 5), secondary metabolite biosynthesis (6), the hypersensitive response (4,7,8), and direct pathogen cytotoxicity (9, 10), depending on the plant species examined. In cultured cell systems, the oxidative burst can be promoted by isolated elicitors including harpin (11, 12), oligouronides (13), elicitins (14), purified fungal peptides (15), and other molecules from the extracts of pathogens (7,16). Abiotic stimuli such as mechanical stress (17), the pesticide fenthion (18), cold shock (19), phosphatase inhibitors (4, 20), and hypo-osmotic stress (17) can also induce biosynthesis of reactive oxygen species in plant cells.Because of its rapid expression, ease of assay, and similarity to the analogous defense response in human neutrophils (21), the oxidative burst has recently served as a model for exploring signal transduction pathways in plants. As the numbers of elicitors examined have risen, it has become increasingly clear that different elicitors may inaugurate independent signal transduction pathways that...

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Calcium-mediated apoptosis in a plant hypersensitive disease resistance response

Cited by 551 publications

References 47 publications

AtBAG6, a novel calmodulin-binding protein, induces programmed cell death in yeast and plants

AtBAG6, a novel calmodulin-binding protein, induces programmed cell death in yeast and plants

Toxin release in response to oxidative stress and programmed cell death in the cyanobacterium Microcystis aeruginosa

Measurement of Ca2+ Fluxes during Elicitation of the Oxidative Burst in Aequorin-transformed Tobacco Cells

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