A Plant Ca2+ Pump, ACA2, Relieves Salt Hypersensitivity in Yeast

Anil, Veena S.; Rajkumar, Premraj; Kumar, Prasoon; Mathew, M. K.

doi:10.1074/jbc.m700766200

Cited by 60 publications

(29 citation statements)

References 57 publications

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“…Interestingly, in the present study, susceptible plants showed an average low expression of TIP throughout pathogen progression, further validating oxidative injury that resulted in xylem clogging and water stress. ACAs are also thought to regulate salt stress along with calcium dependent protein kinases (CDPKs) and calmodulin, which act as negative regulators [81]–[82]. Present study showed enhanced expression of ACA in resistant plants, suggesting a role for CDPKs and calmodulin in host defense.…”

Section: Discussionmentioning

confidence: 56%

Fusarium oxysporum f.sp. ciceri Race 1 Induced Redox State Alterations Are Coupled to Downstream Defense Signaling in Root Tissues of Chickpea (Cicer arietinum L.)

et al. 2013

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Reactive oxygen species are known to play pivotal roles in pathogen perception, recognition and downstream defense signaling. But, how these redox alarms coordinate in planta into a defensive network is still intangible. Present study illustrates the role of Fusarium oxysporum f.sp ciceri Race1 (Foc1) induced redox responsive transcripts in regulating downstream defense signaling in chickpea. Confocal microscopic studies highlighted pathogen invasion and colonization accompanied by tissue damage and deposition of callose degraded products at the xylem vessels of infected roots of chickpea plants. Such depositions led to the clogging of xylem vessels in compatible hosts while the resistant plants were devoid of such obstructions. Lipid peroxidation assays also indicated fungal induced membrane injury. Cell shrinkage and gradual nuclear adpression appeared as interesting features marking fungal ingress. Quantitative real time polymerase chain reaction exhibited differential expression patterns of redox regulators, cellular transporters and transcription factors during Foc1 progression. Network analysis showed redox regulators, cellular transporters and transcription factors to coordinate into a well orchestrated defensive network with sugars acting as internal signal modulators. Respiratory burst oxidase homologue, cationic peroxidase, vacuolar sorting receptor, polyol transporter, sucrose synthase, and zinc finger domain containing transcription factor appeared as key molecular candidates controlling important hubs of the defense network. Functional characterization of these hub controllers may prove to be promising in understanding chickpea–Foc1 interaction and developing the case study as a model for looking into the complexities of wilt diseases of other important crop legumes.

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Section: Discussionmentioning

confidence: 56%

Fusarium oxysporum f.sp. ciceri Race 1 Induced Redox State Alterations Are Coupled to Downstream Defense Signaling in Root Tissues of Chickpea (Cicer arietinum L.)

et al. 2013

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“…PMC1 overexpression enhanced Al and Ca tolerance in wild-type yeast and the pmc1 mutant (Figure 3). Endomembrane Ca 2+ -ATPases appear to be important for intracellular Ca 2+ distribution [28], [40], [56]. Recent studies have shown that PMCA overexpression depletes intracellular Ca 2+ stores and induces apoptosis through the mitochondrial pathway in clonal β-cells [57].…”

Section: Discussionmentioning

confidence: 99%

“…Al toxicity strongly affects intracellular Ca homeostasis, which is another mechanism that is hypothesized to cause Al injury [1], [13]. The sensitivity and response of cells to various stresses, including Al, is dependent on the ability of cells to adequately sequester Ca 2+ into their internal stores [28], [29], [30]. Ca 2+ is stored in the cell wall and in intracellular organelles, including the endoplasmic reticulum (ER), mitochondria, and vacuoles.…”

Section: Introductionmentioning

confidence: 99%

Regulating Cytoplasmic Calcium Homeostasis Can Reduce Aluminum Toxicity in Yeast

Qian

Wang

et al. 2011

PLoS ONE

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Our previous study suggested that increased cytoplasmic calcium (Ca) signals may mediate aluminum (Al) toxicity in yeast (Saccharomyces cerevisiae). In this report, we found that a yeast mutant, pmc1, lacking the vacuolar calcium ion (Ca2+) pump Ca2+-ATPase (Pmc1p), was more sensitive to Al treatment than the wild-type strain. Overexpression of either PMC1 or an anti-apoptotic factor, such as Bcl-2, Ced-9 or PpBI-1, decreased cytoplasmic Ca2+ levels and rescued yeast from Al sensitivity in both the wild-type and pmc1 mutant. Moreover, pretreatment with the Ca2+ chelator BAPTA-AM sustained cytoplasmic Ca2+ at low levels in the presence of Al, effectively making the cells more tolerant to Al exposure. Quantitative RT-PCR revealed that the expression of calmodulin (CaM) and phospholipase C (PLC), which are in the Ca2+ signaling pathway, was down-regulated under Al stress. This effect was largely counteracted when cells overexpressed anti-apoptotic Ced-9 or were pretreated with BAPTA-AM. Taken together, our results suggest that the negative regulation of Al-induced cytoplasmic Ca signaling is a novel mechanism underlying internal resistance to Al toxicity.

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“…Although double mutants lacking both Pmr1p and the vacuolar membrane Ca 2+ -ATPase Pmc1p are inviable irrespective of Ca 2+ concentration, triple mutants also defective in the Ca 2+ -binding subunit of calcineurin Cnb1p are viable but require exogenous Ca 2+ for growth (Cunningham and Fink, 1994; Sze et al, 2000). These pmr1 pmc1 cnb1 triple mutants are hypersensitive to high Na + levels but this salt hypersensitivity can be overcome by heterologous expression of an endoplasmic reticulum-located Ca 2+ -ATPase (Anil et al, 2008). In any consideration of calcium homeostasis, it is also important to remember that fungal vacuoles are a major site of Ca 2+ storage (Dunn et al, 1994; Klionsky et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

Analysis of a novel calcium auxotrophy in Aspergillus nidulans

Findon

Calcagno-Pizarelli

Martínez

et al. 2010

Fungal Genetics and Biology

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In Aspergillus nidulans a combination of null mutations in halA, encoding a protein kinase, and sltA, encoding a zinc-finger transcription factor having no yeast homologues, results in an elevated calcium requirement (‘calcium auxotrophy’) without impairing net calcium uptake. sltA− (±halA−) mutations result in hypertrophy of the vacuolar system. In halA−sltA− (and sltA−) strains, transcript levels for pmcA and pmcB, encoding vacuolar Ca2+-ATPase homologues, are highly elevated, suggesting a regulatory relationship between vacuolar membrane area and certain vacuolar membrane ATPase levels. Deletion of both pmcA and pmcB strongly suppresses the ‘calcium auxotrophy’. Therefore the ‘calcium auxotrophy’ possibly results from excessive vacuolar calcium sequestration, causing cytosolic calcium deprivation. Null mutations in nhaA, homologous to Saccharomyces cerevisiaeNHA1, encoding a plasma membrane Na+/H+ antiporter effluxing Na+ and K+, and a non-null mutation in trkB, homologous to S. cerevisiaeTRK1, encoding a plasma membrane high affinity K+ transporter, also suppress the calcium auxotrophy.

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A Plant Ca2+ Pump, ACA2, Relieves Salt Hypersensitivity in Yeast

Cited by 60 publications

References 57 publications

Fusarium oxysporum f.sp. ciceri Race 1 Induced Redox State Alterations Are Coupled to Downstream Defense Signaling in Root Tissues of Chickpea (Cicer arietinum L.)

Fusarium oxysporum f.sp. ciceri Race 1 Induced Redox State Alterations Are Coupled to Downstream Defense Signaling in Root Tissues of Chickpea (Cicer arietinum L.)

Regulating Cytoplasmic Calcium Homeostasis Can Reduce Aluminum Toxicity in Yeast

Analysis of a novel calcium auxotrophy in Aspergillus nidulans

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