Cell wall traits as potential resources to improve resistance of durum wheat against Fusarium graminearum

Background: Fusarium 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. Results: A 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. Conclusions: Our 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

Three pectin methylesterase inhibitors protect cell wall integrity for arabidopsis immunity to Botrytis

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 Botrytis cinerea and pectin methylesterification status is strongly altered in response to infection. The methylesterification of pectin is mainly controlled by pectin methylesterases (PMEs) which activity is post-transcriptionally regulated by endogenous protein inhbibitors (PMEIs). Here, AtPMEI10, AtPMEI11 and AtPMEI12 are identified as functional pectin methylesterase inhibitors induced in Arabidopsis during Botrytis infection. AtPMEIs expression is strictly regulated by Jasmonic Acid and Ethylene signaling while only AtPMEI11 expression is controlled by PME-related DAMPs, such as oligogalacturonides and methanol. The decrease of pectin methylesterification during infection is higher and the immunity to Botrytis compromised in pmei10, pmei11 and pmei12 mutants respect to the control plants. A higher stimulation of the fungal oxalic acid bioshynthetic pathway can also contribute to the higher susceptibility of pmei mutants. The lack of PMEIs expression do not affect hemicellulose strengthening, callose deposition and synthesis of structural defence proteins, proposed as CW remodeling mechanisms exploited by Arabidopsis to resist to the CW degradation upon Botrytis infection. We showed that PME activity and pectin methylesterification are dynamically modulated by PMEIs during Botrytis infection. Our findings point to AtPMEI10, AtPMEI11 and AtPMEI12 as mediators of CW integrity maintenance in plant immunity

Cell wall traits as potential resources to improve resistance of durum wheat against Fusarium graminearum

Background Fusarium 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. Results A 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. Conclusions Our 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.This article is from BMC Plant Biology 15 (2015): 6, doi:10.1186/s12870-014-0369-1. Posted with permission.</p

Cell wall features transferred from common into durum wheat to improve Fusarium Head Blight resistance

Durum wheat is naturally more susceptible to Fusarium graminerum infection in comparison to common wheat. The improvement of durum wheat resistance against F. graminearum is a challenge due to the lack of resistance sources in its gene pool. FHB-resistance factors were introduced in durum wheat by generating recombinant inbred lines (RILs), obtained by crossing the hexaploid resistant accession 02-5B-318 with the susceptible durum wheat cv. Saragolla. In this work we explored the possible contribution of cell wall (CW) in RILs with improved FHB resistance. We thoroughly studied CW components, mycotoxins content and the expression of related genes in different RILs selected for their extremely high and low resistance to FHB. Differences were found in resistant and susceptible lines in the degree of pectin methylesterification and in deoxynivalenol (DON) accumulation after fungal infection. Genes involved in biochemical modification of CW structure (WheatPme-1, Glu-1) and mycotoxins accumulation (ns-LTP-1) were analyzed as putative candidates for FHB resistance. Our results indicate that durum wheat plants with cell wall structure and gene response acquired from common wheat displayed an increased resistance to FHB

Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356

non present