Infection by necrotrophs is a complex process that starts with the breakdown of the cell wall (CW) matrix initiated by CW-degrading enzymes and results in an extensive tissue maceration. Plants exploit induced defense mechanisms based on biochemical modification of the CW components to protect themselves from enzymatic degradation. The pectin matrix is the main CW target of , and pectin methylesterification status is strongly altered in response to infection. The methylesterification of pectin is controlled mainly by pectin methylesterases (PMEs), whose activity is posttranscriptionally regulated by endogenous protein inhibitors (PMEIs). Here, AtPMEI10, AtPMEI11, and AtPMEI12 are identified as functional PMEIs induced in Arabidopsis () during infection. AtPMEI expression is strictly regulated by jasmonic acid and ethylene signaling, while only AtPMEI11 expression is controlled by PME-related damage-associated molecular patterns, such as oligogalacturonides and methanol. The decrease of pectin methylesterification during infection is higher and the immunity to is compromised in ,, and mutants with respect to the control plants. A higher stimulation of the fungal oxalic acid biosynthetic pathway also can contribute to the higher susceptibility of mutants. The lack of expression does not affect hemicellulose strengthening, callose deposition, and the synthesis of structural defense proteins, proposed as CW-remodeling mechanisms exploited by Arabidopsis to resist CW degradation upon infection. We show that PME activity and pectin methylesterification are dynamically modulated by PMEIs during infection. Our findings point to AtPMEI10, AtPMEI11, and AtPMEI12 as mediators of CW integrity maintenance in plant immunity.

BackgroundFusarium graminearum, one of the causal agents of Fusarium Head Blight (FHB, scab), leads to severe losses in grain yield and quality due to the production of mycotoxins which are harmful to human and livestock. Different traits for FHB resistance in wheat were identified for common wheat (Triticum aestivum L.) while the sources of FHB resistance in durum wheat (Triticum turgidum ssp. Durum), one of the cereals most susceptible to F. graminearum infection, have not been found. New lines of evidence indicate that content and composition of cell wall polymers affect the susceptibility of the wall to degrading enzymes produced by pathogens during infection and can play a role in the outcome of host-pathogen interactions. The objective of our research is to identify potential cell wall biochemical traits linked to Fusariosis resistance to be transferred from a resistant common wheat to a susceptible durum wheat line.ResultsA detailed analysis of cell wall composition in spikes isolated from a highly resistant common wheat accession “02-5B-318”, a breeding line derived from the FHB-resistant Chinese cv. Sumai-3 and a high susceptible durum wheat cv. Saragolla was performed. Significant differences in lignin monolignols composition, arabinoxylan (AX) substitutions and pectin methylesterification were found between resistant and susceptible plants. We isolated and characterized a pectin methylesterase gene WheatPME1, which we found being down regulated in the FHB-resistant line and induced by fungal infection in the susceptible wheat.ConclusionsOur results indicate cell wall traits differing between the FHB sensitive and resistant wheat genotypes, possibly related to FHB-resistance, and identify the line 02-5B-318R as a potential resource of such traits. Evidence suggests that WheatPME1 is involved in wheat response to F. graminearum.Electronic supplementary materialThe online version of this article (doi:10.1186/s12870-014-0369-1) contains supplementary material, which is available to authorized users.

No abstract