Oligosaccharins: structures and signal transduction

Côté, François; Hahn, Michael G.

doi:10.1007/978-94-011-0239-1_9

Cited by 66 publications

(80 citation statements)

References 229 publications

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“…The observation that TomQ'a expression is induced in unripe wild-type fruit and in all ripening mutants at both 31 and 42 dpa but is down-regulated by B. cinerea in wild-type ripe fruit supports the conclusion that ripening affects the way fruit respond to the pathogen and what defenses are deployed. How fruit cells perceive and respond to fungal toxins or elicitors, such as cell wall fragments generated by fungal digestion of host cell walls, may also change during ripening (Cô té and Hahn, 1994;Collado et al, 2000;An et al, 2005;van Kan, 2006;Staats et al, 2007). Although B. cinerea is a necrotroph and hypersensitive responses and cell death have been thought to increase its aggressiveness (Govrin and Levine, 2000;Dickman et al, 2001;van Baarlen et al, 2004van Baarlen et al, , 2007, the timely and localized accumulation of antimicrobial substances, hydrogen peroxide, and lignin, all features of a hypersensitive response, effectively prevent expanding infections; the responses are evident in resistant unripe fruit but not in susceptible ripe fruit.…”

Section: Discussionmentioning

confidence: 99%

Ripening-Regulated Susceptibility of Tomato Fruit toBotrytis cinereaRequiresNORBut NotRINor Ethylene

Cantu

Blanco‐Ulate

Long³

et al. 2009

Plant Physiology

152

163

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Fruit ripening is a developmental process that is associated with increased susceptibility to the necrotrophic pathogen Botrytis cinerea. Histochemical observations demonstrate that unripe tomato (Solanum lycopersicum) fruit activate pathogen defense responses, but these responses are attenuated in ripe fruit infected by B. cinerea. Tomato fruit ripening is regulated independently and cooperatively by ethylene and transcription factors, including NON-RIPENING (NOR) and RIPENING-INHIBITOR (RIN). Mutations in NOR or RIN or interference with ethylene perception prevent fruit from ripening and, thereby, would be expected to influence susceptibility. We show, however, that the susceptibility of ripe fruit is dependent on NOR but not on RIN and only partially on ethylene perception, leading to the conclusion that not all of the pathways and events that constitute ripening render fruit susceptible. Additionally, on unripe fruit, B. cinerea induces the expression of genes also expressed as uninfected fruit ripen. Among the ripening-associated genes induced by B. cinerea are LePG (for polygalacturonase) and LeExp1 (for expansin), which encode cell wall-modifying proteins and have been shown to facilitate susceptibility. LePG and LeExp1 are induced only in susceptible rin fruit and not in resistant nor fruit. Thus, to infect fruit, B. cinerea relies on some of the processes and events that occur during ripening, and the fungus induces these pathways in unripe fruit, suggesting that the pathogen itself can initiate the induction of susceptibility by exploiting endogenous developmental programs. These results demonstrate the developmental plasticity of plant responses to the fungus and indicate how known regulators of fruit ripening participate in regulating ripening-associated pathogen susceptibility.

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Section: Discussionmentioning

confidence: 99%

Ripening-Regulated Susceptibility of Tomato Fruit toBotrytis cinereaRequiresNORBut NotRINor Ethylene

Cantu

Blanco‐Ulate

Long³

et al. 2009

Plant Physiology

152

163

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“…For example, lack of callose might unmask fungal wall polysaccharides and/or secreted proteins. Certain branched (1→3,1→6)-␤-D-oligoglucosides and chitin/chitosan oligosaccharides released from these fungal wall polysaccharides (Bartnicki-Garcia, 1968) by partial endohydrolysis are highly active elicitors of plant defense responses, even at concentrations as low as 10 nM (Côté and Hahn, 1994). By contrast, linear (1→3)-␤-D-oligoglucosides of the type that would be released from callose itself by the (1→3)-␤-D-glucanases are not active in eliciting plant defense (Côté and Hahn, 1994).…”

Section: Discussionmentioning

confidence: 99%

An Arabidopsis Callose Synthase, GSL5, Is Required for Wound and Papillary Callose Formation

et al. 2003

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Arabidopsis was transformed with double-stranded RNA interference (dsRNAi) constructs designed to silence three putative callose synthase genes: GLUCAN SYNTHASE-LIKE5 ( GSL5 ), GSL6 , and GSL11 . Both wound callose and papillary callose were absent in lines transformed with GSL5 dsRNAi and in a corresponding sequence-indexed GSL5 T-DNA insertion line but were unaffected in GSL6 and GSL11 dsRNAi lines. These data provide strong genetic evidence that the GSL genes of higher plants encode proteins that are essential for callose formation. Deposition of callosic plugs, or papillae, at sites of fungal penetration is a widely recognized early response of host plants to microbial attack and has been implicated in impeding entry of the fungus. Depletion of callose from papillae in gsl5 plants marginally enhanced the penetration of the grass powdery mildew fungus Blumeria graminis on the nonhost Arabidopsis. Paradoxically, the absence of callose in papillae or haustorial complexes correlated with the effective growth cessation of several normally virulent powdery mildew species and of Peronospora parasitica .

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“…Secretion of cell wall-degrading enzymes can trigger the release of cell wall fragments, which can act as damage-associated molecular patterns that activate plant immune responses (Hahn et al, 1981;Ferrari et al, 2013). Similarly, pectin fragments known as oligogalacturonides (OGs) can trigger plant immune responses (Côté and Hahn, 1994;Ferrari et al, 2013). Such responses include the production of reactive oxygen species (ROS), activation of mitogen-activated protein kinase (MAPK) activation and enhanced expression of defense-related genes such as PAD3 (Ferrari et al, 2007;Denoux et al, 2008;Galletti et al, 2008;Galletti et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Pectin Biosynthesis Is Critical for Cell Wall Integrity and Immunity in Arabidopsis thaliana

et al. 2016

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(D.J.K.); 0000-0001-5167-736X (J.G.)Plant cell walls are important barriers against microbial pathogens. Cell walls of Arabidopsis thaliana leaves contain three major types of polysaccharides: cellulose, various hemicelluloses, and pectins. UDP-D-galacturonic acid, the key building block of pectins, is produced from the precursor UDP-D-glucuronic acid by the action of glucuronate 4-epimerases (GAEs). Pseudomonas syringae pv maculicola ES4326 (Pma ES4326) repressed expression of GAE1 and GAE6 in Arabidopsis, and immunity to Pma ES4326 was compromised in gae6 and gae1 gae6 mutant plants. These plants had brittle leaves and cell walls of leaves had less galacturonic acid. Resistance to specific Botrytis cinerea isolates was also compromised in gae1 gae6 double mutant plants. Although oligogalacturonide (OG)-induced immune signaling was unaltered in gae1 gae6 mutant plants, immune signaling induced by a commercial pectinase, macerozyme, was reduced. Macerozyme treatment or infection with B. cinerea released less soluble uronic acid, likely reflecting fewer OGs, from gae1 gae6 cell walls than from wild-type Col-0. Although both OGs and macerozyme-induced immunity to B. cinerea in Col-0, only OGs also induced immunity in gae1 gae6. Pectin is thus an important contributor to plant immunity, and this is due at least in part to the induction of immune responses by soluble pectin, likely OGs, that are released during plant-pathogen interactions.

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Oligosaccharins: structures and signal transduction

Cited by 66 publications

References 229 publications

Ripening-Regulated Susceptibility of Tomato Fruit toBotrytis cinereaRequiresNORBut NotRINor Ethylene

Ripening-Regulated Susceptibility of Tomato Fruit toBotrytis cinereaRequiresNORBut NotRINor Ethylene

An Arabidopsis Callose Synthase, GSL5, Is Required for Wound and Papillary Callose Formation

Pectin Biosynthesis Is Critical for Cell Wall Integrity and Immunity in Arabidopsis thaliana

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