Verticillium longisporum Infection Affects the Leaf Apoplastic Proteome, Metabolome, and Cell Wall Properties in Arabidopsis thaliana

Abstract

Verticillium longisporum (VL) is one of the most devastating diseases in important oil crops from the family of Brassicaceae. The fungus resides for much time of its life cycle in the extracellular fluid of the vascular system, where it cannot be controlled by conventional fungicides. To obtain insights into the biology of VL-plant interaction in the apoplast, the secretome consisting of the extracellular proteome and metabolome as well as cell wall properties were studied in the model Brassicaceae, Arabidopsis thaliana. VL infection resulted in increased production of cell wall material with an altered composition of carbohydrate polymers and increased lignification. The abundance of several hundred soluble metabolites changed in the apoplast of VL-infected plants including signalling and defence compounds such as glycosides of salicylic acid, lignans and dihydroxybenzoic acid as well as oxylipins. The extracellular proteome of healthy leaves was enriched in antifungal proteins. VL caused specific increases in six apoplast proteins (three peroxidases PRX52, PRX34, P37, serine carboxypeptidase SCPL20, α-galactosidase AGAL2 and a germin-like protein GLP3), which have functions in defence and cell wall modification. The abundance of a lectin-like, chitin-inducible protein (CILLP) was reduced. Since the transcript levels of most of the induced proteins were not elevated until late infection time points (>20 dpi), whereas those of CILLP and GLP3 were reduced at earlier time points, our results may suggest that VL enhances its virulence by rapid down-regulation and delay of induction of plant defence genes.

Verticillium Infection Triggers VASCULAR-RELATED NAC DOMAIN7–Dependent de Novo Xylem Formation and Enhances Drought Tolerance in Arabidopsis

“…Autofluorescence of the newly formed xylem indicates lignification of the secondary cell wall structures ( Figure 2F; see Supplemental Figure 5F online). Together, our data fit with recent findings suggesting that cell wall metabolism, production of lignin precursors, and lignification were increased in V. longisporum-infected Arabidopsis plants (Floerl et al, 2012).…”

“…These toxins may affect membrane permeability or induce the formation of vascular gels. However, V. longisporum infection did not increase membrane permeability in Arabidopsis or in oilseed rape (B. napus) (Floerl et al 2008;Floerl et al 2012). Instead, the water status of infected Arabidopsis was increased, and the concentrations of osmolytes were decreased (Floerl et al 2010).…”

Lipoxygenases and their metabolites in formation of plant stress tolerance

“…arabidopsis thaliana (L.) Heynh. infected by a pathogenic fungus Verticillium longisporum (C. Stark) Karapapa showed an increase in the content of some compounds among which there were oxo-phytodienoic acid (OPDA), dinor-OPDA, 9,12,13-threehydroxy-10,15-octadecadienoic and 9,12,13-threehydroxy-10-octadecanoic acids involved in the immunity formation [37]. Physiologically active plant oxylipins (2Е)-dodecene-1,12-dicarboxylic acid (traumatic acid) and 12-oxo-trans-10-dodecenoic acid (traumatin) are also able to induce cell division and formation of callus in damaged sites [1,8].…”

Small Glycosylated Lignin Oligomers Are Stored in Arabidopsis Leaf Vacuoles

“…Furthermore, this preexisting battery of combinatorially coupled phenylpropanoids in the vacuole can be viewed as a "chemical library" helping to fight off pathogens, i.e., producing such a high number of phenolic compounds making it likely that at least one of them is toxic to the invading pathogen. In addition to this preexisting battery of defense molecules, Arabidopsis might also produce some of them as (neo)lignans in response to pathogen attack (Floerl et al, 2012). It is noteworthy that to produce such a "chemical library," evolution has apparently made beneficial use of the oligolignol coupling products that are formed as a consequence of the oxidative environment in the cell.…”