Metabolism and detoxification of phytoalexins and analogs by phytopathogenic fungi

Pedras, M. Soledade C.; Ahiahonu, Pearson W. K.

doi:10.1016/j.phytochem.2004.12.032

Cited by 147 publications

(123 citation statements)

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“…The B. cinerea ABC transporter, atrB, exports camalexin in vitro and is required for pathogen tolerance to this phytoalexin (Stefanato et al, 2009). The mechanism of atrB camalexin detoxifi cation, cellular export or enzymatic modifi cation, is currently unknown however many necrotrophic fungi use different types of transporters to facilitate active removal of plant defense compounds (Stefanato et al, 2009);(Del Sorbo et al, 2000;Pedras and Ahiahonu, 2005;Stefanato et al, 2009). S. sclerotiorum glycosylates the indole ring of camalexin converting it to a less toxic form Ahiahonu, 2002, 2005).…”

Section: Modifi Cation Of Host Physiologymentioning

confidence: 99%

“…The variation in camalexin-based resistance to necrotrophs is likely a result of interplay between multiple defense factors and disparities in isolate sensitivity to camalexin (Kliebenstein et al, 2005;Rowe and Kliebenstein, 2008). The virulence of many fungal species has been linked to their ability to metabolize or detoxify phytoalexins (Pedras and Ahiahonu, 2005). This was recently confi rmed with identifi cation of the B. cinerea ABC transporter BcatrB, involved in the active export of camalexin from the fungal cell (Stefanato et al, 2009).…”

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confidence: 99%

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Necrotroph Attacks on Plants: Wanton Destruction or Covert Extortion?

Laluk

Mengiste

2010

The Arabidopsis Book

204

168

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Necrotrophic pathogens cause major pre-and post-harvest diseases in numerous agronomic and horticultural crops infl icting signifi cant economic losses. In contrast to biotrophs, obligate plant parasites that infect and feed on living cells, necrotrophs promote the destruction of host cells to feed on their contents. This difference underpins the divergent pathogenesis strategies and plant immune responses to biotrophic and necrotrophic infections. This chapter focuses on Arabidopsis immunity to necrotrophic pathogens. The strategies of infection, virulence and suppression of host defenses recruited by necrotrophs and the variation in host resistance mechanisms are highlighted. The multiplicity of intraspecifi c virulence factors and species diversity in necrotrophic organisms corresponds to variations in host resistance strategies. Resistance to host-specifi c necrotophs is monogenic whereas defense against broad host necrotrophs is complex, requiring the involvement of many genes and pathways for full resistance. Mechanisms and components of immunity such as the role of plant hormones, secondary metabolites, and pathogenesis-related proteins are presented. We will discuss the current state of knowledge of Arabidopsis immune responses to necrotrophic pathogens, the interactions of these responses with other defense pathways, and contemplate on the directions of future research.: e0136. of 34The Arabidopsis Book Infection by fungal necrotrophs generally involves stages of conidial attachment, germination, host penetration, primary lesion formation, lesion expansion, and tissue maceration followed by sporulation (Prins et al., 2000). Following germination, penetration may be achieved by active mechanisms such as appressoria formation and enzymatic degradation or passively through prior infection or wound sites as well as stomates (Prins et al., 2000). After entry, tissue is decomposed through further cellular dismantling using many of the lytic enzymes employed for initial penetration as well as toxic levels of reactive oxygen species (ROS). Many necrotrophs produce various low-molecular weight phytotoxic metabolites, ranging from host-specifi c to those having adverse effects on many diverse species (van Kan, 2006). Others secrete phytotoxic proteins known to induce necrosis, with the vast majority of broad host necrotrophs producing multiples of both (Pemberton and Salmond, 2004;Gijzen and Nurnberger, 2006;Choquer et al., 2007). Throughout infection, these fungi also actively manipulate host cellular machinery in order to suppress defenses and/or aid in disease progression. Some necrotrophs infl uence host phytohormone levels or employ their own hormone biosynthesis thereby disrupting defense signaling (Prins et al., 2000;Sharon et al., 2004). Others have adapted mechanisms to detoxify host metabolites that interfere with virulence (Morrissey and Osbourn, 1999).Overall, bacterial necrotrophs follow a similar mode of pathogenesis to their fungal counterparts, secreting virulence factors into host tissue to induc...

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Section: Modifi Cation Of Host Physiologymentioning

confidence: 99%

mentioning

confidence: 99%

Necrotroph Attacks on Plants: Wanton Destruction or Covert Extortion?

Laluk

Mengiste

2010

The Arabidopsis Book

204

168

View full text Add to dashboard Cite

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“…In addition, cyclin B/Cdc2 complex activation causes the breakdown of the nuclear envelope and the initiation of prophase and, subsequently, its deactivation causes the cell to exit mitosis (8,9). Phytoalexins are low-molecular-weight compounds that are synthesized by, and accumulated in plants after their exposure to microorganisms (10,11). Among them, momilactone B, a terpenoid phytoalexin commonly biosynthesized from geranylgeranyl diphosphate, was originally isolated from rice (Oryza sativa L.) hulls as a growth inhibitor involved in seed dormancy (12,13).…”

Section: Introductionmentioning

confidence: 99%

Momilactone B induces apoptosis and G1 arrest of the cell cycle in human monocytic leukemia U937 cells through downregulation of pRB phosphorylation and induction of the cyclin-dependent kinase inhibitor p21Waf1/Cip1

Park¹,

Jeong²,

Kim³

et al. 2014

Oncology Reports

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Abstract. Momilactone B, a terpenoid phytoalexin present in rice bran, has been shown to exhibit several biological activities. The present study was conducted using cultured human leukemia U937 cells to elucidate the possible mechanisms by which momilactone B exerts its anticancer activity, which to date has remained poorly understood. Momilactone B treatment of U937 cells resulted in a dose-dependent inhibition of cell growth and induced apoptotic cell death as detected by chromatin condensation, DNA fragmentation, the cleavage of poly(ADP-ribose) polymerase and Annexin V-FITC staining. Flow cytometric analysis revealed that momilactone B resulted in G1 arrest in cell cycle progression, which was associated with the dephosphorylation of retinoblastoma protein (pRB) and enhanced binding of pRB with the E2F transcription factor family proteins. Treatment with momilactone B also increased the expression of cyclin-dependent kinase (Cdk) inhibitor p21Waf1/Cip1 in a p53-independent manner, without any noticeable changes in G1 cyclins and cyclin-dependent kinases (Cdks), except a slight decrease in cyclin E. Moreover, in vitro kinase assay indicated that momilactone B significantly decreased Cdk4-and Cdk6-associated kinase activities through a notably increased binding of p21 to Cdk4 and Cdk6. Our results demonstrated that momilactone B caused G1 cell cycle arrest and apoptosis in U937 cells through the induction of p21 expression, inhibition of Cdk/cyclin-associated kinase activities, and reduced phosphorylation of pRB, which may be related to anticancer activity. IntroductionImpaired deregulated cell cycle progression and induction of apoptosis are the primary characteristics of cancer cells due to an imbalance between proliferation and cell death. In terms of cell cycle regulation, the cyclin-dependent kinases (Cdks) are the key regulators of eukaryotic cell cycle progression in cooperation with various endogenous cyclins and Cdks (1,2). An alteration in the cooperation may lead to increased or decreased cell growth and proliferation followed by differentiation and/or cell death by apoptosis (3,4). Therefore, the key regulators of cell cycle progression and apoptotic induction may be important molecular targets for therapeutic intervention, and inhibition of cell cycle regulation may be particularly useful in the treatment of diseases caused by uncontrolled cell proliferation, such as cancer.In general, passage through G1 into the S phase is regulated by the activities of D-type cyclin-and cyclin E-associated Cdks. D-type cyclins bind to existing Cdk4 and Cdk6, forming active complexes. The complexes in turn phosphorylate the retinoblastoma susceptibility protein (pRB). The hyperphosphorylated pRB dissociates from the E2F/DP1/pRB Momilactone B induces apoptosis and G1 arrest of the cell cycle in human monocytic leukemia U937 cells through downregulation of pRB phosphorylation and induction of the cyclin-dependent kinase inhibitor p21Waf1/Cip1

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“…The results showed momilactone A and sakuranetin were detectable only in the treatment group with pathogenic inoculation and not found in the non-inoculation or the control group. According to phytoalexin role as an antimicrobial substance, plant cell could generate phytoalexin to defense any intruder pathogen (Ahuja et al, 2012;Ejike et al, 2013;Jeandet et al, 2014;Pedras and Ahiahonu, 2005). Normally, the high amount of phytoalexin was found close to damaged area from the disease attack (Großkinsky et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Combining effects of ozone and Xanthomonas oryzae pv. oryzae on antioxidants and phytoalexins in rice (Oryza sativa L.)

Buawat¹,

Hasegawa²,

Umponstira³

2017

Aust J Crop Sci

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Ozone is the most oxidative air pollutant and considered as an abiotic stress which harm to vegetation and crop. Similarly, biological stressor such as plant pathogen could cause severe damage to crops. Combination effects from both stresses will potentially lead to economic loss. Basically, plants will response to both abiotic stress and pathogenic stressor by generate antioxidants and phytoalexins. The concentration of these chemical indicate stress level in plant and also defence system response. This research is aimed to investigate the combination effects of ozone and Xanthomonas oryzae pv. oryzae on antioxidants and phytoalexins in rice (Oryza sativa L. cv. KDML 105). In this study, 45-day-old rice plants were used. Ozone was elevated at concentrations of 100, 200 and 300 ppb in the fumigating chambers for 12 hours. Xanthomonas oryzae pv. oryzae which caused bacterial blight disease in rice was selected as plant pathogen. Combining effects of ozone and Xanthomonas oryzae pv. oryzae were examined using ozone at a concentration of 100 ppb and Xanthomonas oryzae pv. oryzae 1x10 8 cells/ml inoculation. The experimental design was a completely randomized design with 2×2 factorials treatment and three replications required. Temperature, relative humidity and light intensity in fumigating chambers were controlled. The results of the combining effects showed the amount of antioxidants and phytoalexins were higher than those in single treatment. The experimental data indicated that the combining effects will result in more stress in rice. This suggests that, in rice plantation area with experience of ozone episode, pathogenic resistance rice strain should be considered to reduce combining effects.

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Metabolism and detoxification of phytoalexins and analogs by phytopathogenic fungi

Cited by 147 publications

References 90 publications

Necrotroph Attacks on Plants: Wanton Destruction or Covert Extortion?

Necrotroph Attacks on Plants: Wanton Destruction or Covert Extortion?

Momilactone B induces apoptosis and G1 arrest of the cell cycle in human monocytic leukemia U937 cells through downregulation of pRB phosphorylation and induction of the cyclin-dependent kinase inhibitor p21Waf1/Cip1

Combining effects of ozone and Xanthomonas oryzae pv. oryzae on antioxidants and phytoalexins in rice (Oryza sativa L.)

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