The intersection between cell wall disassembly, ripening, and fruit susceptibility to
            <i>Botrytis cinerea</i>

Cantu, Dario; Vicente, Ariel Roberto; Greve, L. Carl; Dewey, F. M.; Bennett, A. B.; Labavitch, John M.; Powell, Ann

doi:10.1073/pnas.0709813105

Cited by 265 publications

(246 citation statements)

References 48 publications

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“…Plant developmental processes that facilitate susceptibility are an integral part of the host-pathogen interaction and must be considered, as they can offset the defenses deployed or reduce their effectiveness. Tomato fruit ripening includes the progressive and extensive loss of firmness that is largely a result of metabolism of the cell wall polysaccharides (Brummell, 2006;Cantu et al, 2007Cantu et al, , 2008a. The ripeningassociated disassembly of hemicellulosic and pectic cell wall polysaccharides is known to be severely reduced in rin fruit and apparently is diminished in nor and 1-MCP-treated fruit, since they also have only limited softening (Seymour et al, 1987;Giovannoni et al, 1989;DellaPenna et al, 1990;Maclachlan and Brady, 1994).…”

Section: Discussionmentioning

confidence: 99%

“…The simultaneous expression of LePG and LeExp1 and the subsequent action of the encoded proteins on cell wall polysaccharide networks is critical for fruit susceptibility (Cantu et al, 2008a), and expression of both genes was induced by B. cinerea in wild-type MG fruit (Figs. 8 and 9).…”

Section: B Cinerea Induced Transcript Changes In Ripening Mutantsmentioning

confidence: 99%

“…The interaction of tomato fruit with the ascomycete Botrytis cinerea (teleomorph Botryotinia fuckeliana) is a model pathosystem for investigating necrotrophic microorganisms (Powell et al, 2000;Company and Gonzalez-Bosch, 2003;Flors et al, 2007;Cantu et al, 2008aCantu et al, , 2008b. B. cinerea is an opportunistic pathogen with a broad host range and is notoriously aggressive on fleshy fruit.…”

mentioning

confidence: 99%

“…During B. cinerea infections of plant tissues, cell wall-degrading enzymes are secreted by the fungus. Although some of these enzymes are required for virulence (ten Have et al, , 2001Kars et al, 2005), the fungus fails to infect ripe fruit in the absence of endogenous fruit cell wall disassembly (Cantu et al, 2008a).…”

mentioning

confidence: 99%

“…susceptibility (Cantu et al, 2008a). Ripening in tomato fruit is regulated by ethylene and transcription factors, including NON-RIPENING (NOR or NAC-NOR), RIPENING-INHIBITOR (RIN; Vrebalov et al, 2002), and COLORLESS NON-RIPENING (Manning et al, 2006).…”

mentioning

confidence: 99%

See 4 more Smart Citations

Ripening-Regulated Susceptibility of Tomato Fruit toBotrytis cinereaRequiresNORBut NotRINor Ethylene

Cantu

Blanco‐Ulate

Long³

et al. 2009

Plant Physiology

148

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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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