Infection Strategies of Botrytis cinerea and Related Necrotrophic Pathogens

Prins, T.W.; Tudzynski, Paul; Tiedemann, Andreas von; Tudzynski, Bettina; Have, Arjen ten; Hansen, Merili; Tenberge, Klaus B.; Kan, J.A.L. van

doi:10.1007/978-94-015-9546-9_2

Cited by 139 publications

(112 citation statements)

References 154 publications

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“…Whereas necrotrophic pathogens induce cell death in their hosts by secreting toxic substances into host tissue before and during colonization, biotrophic pathogens require living cells to complete their life cycle. The necrotroph Botrytis cinerea produces cell wall-degrading enzymes (Prins et al, 2000), toxic levels of reactive oxygen intermediates (Edlich et al, 1989;Deighton et al, 1999;Muckenschnabel et al, 2002), and toxins (Tiedemann, 1997;Colmenares et al, 2002) that result in the death and maceration of tissue, leading to plant decay. Evidence to date strongly suggests a limited role for SAR and gene-for-gene (race-specific) resistance against necrotrophic pathogens in Arabidopsis thaliana.…”

Section: Introductionmentioning

confidence: 99%

The Membrane-Anchored BOTRYTIS-INDUCED KINASE1 Plays Distinct Roles in Arabidopsis Resistance to Necrotrophic and Biotrophic Pathogens

et al. 2005

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Plant resistance to disease is controlled by the combination of defense response pathways that are activated depending on the nature of the pathogen. We identified the Arabidopsis thaliana BOTRYTIS-INDUCED KINASE1 (BIK1) gene that is transcriptionally regulated by Botrytis cinerea infection. Inactivation of BIK1 causes severe susceptibility to necrotrophic fungal pathogens but enhances resistance to a virulent strain of the bacterial pathogen Pseudomonas syringae pv tomato. The response to an avirulent bacterial strain is unchanged, limiting the role of BIK1 to basal defense rather than race-specific resistance. The jasmonate-and ethylene-regulated defense response, generally associated with resistance to necrotrophic fungi, is attenuated in the bik1 mutant based on the expression of the plant defensin PDF1.2 gene. bik1 mutants show altered root growth, producing more and longer root hairs, demonstrating that BIK1 is also required for normal plant growth and development. Whereas the pathogen responses of bik1 are mostly dependent on salicylic acid (SA) levels, the nondefense responses are independent of SA. BIK1 is membrane-localized, suggesting possible involvement in early stages of the recognition or transduction of pathogen response. Our data suggest that BIK1 modulates the signaling of cellular factors required for defense responses to pathogen infection and normal root hair growth, linking defense response regulation with that of growth and development.

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Section: Introductionmentioning

confidence: 99%

The Membrane-Anchored BOTRYTIS-INDUCED KINASE1 Plays Distinct Roles in Arabidopsis Resistance to Necrotrophic and Biotrophic Pathogens

et al. 2005

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“…Its ubiquitous occurrence and its lifestyle as a facultative necrotrophic pathogen imply that it has to cope with a variety of biotic and abiotic stresses. In fact, its ability to produce and to withstand high concentrations of reactive oxygen species during pathogenesis has been well documented (Prins et al, 2000;Rolke et al, 2004). In addition, the grey mould fungus is equipped with a set of membrane transport proteins including several ABC and MFS transporters which confer resistance to a variety of toxic compounds (de Waard et al, 2006;Hayashi et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Trehalose metabolism is important for heat stress tolerance and spore germination of Botrytis cinerea

2006

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To analyse the role of trehalose as stress protectant and carbon storage compound in the grey mould fungus Botrytis cinerea, mutants defective in trehalose-6-phosphate synthase (TPS1) and neutral trehalase (TRE1) were constructed. The Dtps1 mutant was unable to synthesize trehalose, whereas the Dtre1 mutant showed elevated trehalose levels compared to the wild-type and was unable to mobilize trehalose during conidial germination. Both mutants showed normal vegetative growth and were not affected in plant pathogenicity. Growth of the Dtps1 mutant was more heat sensitive compared to the wild-type. Similarly, Dtps1 conidia showed a shorter survival under heat stress, and their viability at moderate temperatures was strongly reduced. In germinating wild-type conidia, rapid trehalose degradation occurred only when germination was induced in the presence of nutrients. In contrast, little trehalose breakdown was observed during germination on hydrophobic surfaces in water. Here, addition of cAMP to conidia induced trehalose mobilization and accelerated the germination process, probably by activation of TRE1. In accordance with these data, both mutants showed germination defects only in the presence of sugars but not on hydrophobic surfaces in the absence of nutrients. The data indicate that in B. cinerea trehalose serves as a stress protectant, and also as a significant but not essential carbon source for germination when external nutrients are low. In addition, evidence was obtained that trehalose 6-phosphate plays a role as a regulator of glycolysis during germination.

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“…This pathogen shows extensive phenotypic variation and genetic evidence supports the existence of high levels of recombination and minimal species subdivision based on host or geography (Calpas et al 2001;Albertini et al 2002;Rowe and Kliebenstein 2007). Studies of defined genetic lesions affecting known A. thaliana defenses provide a valuable framework for the biology of B. cinerea-plant interactions, which can contribute to identification of candidate genes (Prins et al 2000;Glazebrook 2005;Robert-Seilaniantz et al 2007;Williamson et al 2007). Despite the documented genetic and phenotypic diversity of B. cinerea, many studies of molecular mechanisms of plant defense against B. cinerea are limited to single pathogen isolates.…”

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confidence: 99%

Complex Genetics Control Natural Variation inArabidopsis thalianaResistance toBotrytis cinerea

2008

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The genetic architecture of plant defense against microbial pathogens may be influenced by pathogen lifestyle. While plant interactions with biotrophic pathogens are frequently controlled by the action of large-effect resistance genes that follow classic Mendelian inheritance, our study suggests that plant defense against the necrotrophic pathogen Botrytis cinerea is primarily quantitative and genetically complex. Few studies of quantitative resistance to necrotrophic pathogens have used large plant mapping populations to dissect the genetic structure of resistance. Using a large structured mapping population of Arabidopsis thaliana, we identified quantitative trait loci influencing plant response to B. cinerea, measured as expansion of necrotic lesions on leaves and accumulation of the antimicrobial compound camalexin. Testing multiple B. cinerea isolates, we identified 23 separate QTL in this population, ranging in isolatespecificity from being identified with a single isolate to controlling resistance against all isolates tested. We identified a set of QTL controlling accumulation of camalexin in response to pathogen infection that largely colocalized with lesion QTL. The identified resistance QTL appear to function in epistatic networks involving three or more loci. Detection of multilocus connections suggests that natural variation in specific signaling or response networks may control A. thaliana-B. cinerea interaction in this population.

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Infection Strategies of Botrytis cinerea and Related Necrotrophic Pathogens

Cited by 139 publications

References 154 publications

The Membrane-Anchored BOTRYTIS-INDUCED KINASE1 Plays Distinct Roles in Arabidopsis Resistance to Necrotrophic and Biotrophic Pathogens

The Membrane-Anchored BOTRYTIS-INDUCED KINASE1 Plays Distinct Roles in Arabidopsis Resistance to Necrotrophic and Biotrophic Pathogens

Trehalose metabolism is important for heat stress tolerance and spore germination of Botrytis cinerea

Complex Genetics Control Natural Variation inArabidopsis thalianaResistance toBotrytis cinerea

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