Ergosterol treatment leads to the expression of a specific set of defence-related genes in tobacco

Abstract

Ergosterol is the main sterol of most fungi. Production of reactive oxygen species after the treatment of tobacco and tomato cells by nano-molar concentrations of ergosterol was previously observed as well as the activation of some stress activated mitogen-activated protein kinases on alfalfa cells. In this paper, the expression of some defence-related genes after the ergosterol treatment of tobacco Nicotiana tabacum plants is reported. The gene expression of pathogenesis related proteins of families PR1, PR3, PR5 and proteinase inhibitors of class I and II together with enzymes participating in the defence response, such as phenylalanine-ammonia lyase and sesquiterpene cyclase, were monitored by RT-qPCR. In addition, the concentrations of salicylic acid, an important signalling molecule, increased in time due to the enzyme activation. On the other hand, ergosterol did not provoke tissue necrosis and the possible cross-talk between the signalling pathways of salicylate and jasmonate was observed. Collected data shows that ergosterol is able to activate the expression of a number of defence genes and could increase resistance against pathogens.

Multi-Platform Metabolomic Analyses of Ergosterol-Induced Dynamic Changes in Nicotiana tabacum Cells

“…Under normal conditions, the FPP is channelled toward the biosynthesis of sterol and prenyl-lipid moieties [94], [99]. Moreover, the enhanced expression of sesquiterpene cyclase, a key enzyme in the biosynthesis of sesquiterpenoids in response to treatment with tobacco mosaic virus or cell wall fragments from Phytophthora species, was accompanied by the suppression of squalene synthase activity in tobacco and potato cells/tissues [32], [94], [123], [124]. Thus, the detection of both sesquiterpenoids and phytosterols in response to ergosterol suggests a complex regulation of the terpenoid pathway, permitting the production of both the sesquiterpenoid phytoalexins (fungitoxicity) and the increase of the levels of phytosterols (to restrict cell membrane permeability).…”

“…It is thus recognised by such cells as ‘non-self’ [28], thereby acting as a MAMP molecule in the lipophilic class of biotic elicitors [29]. The effect of ergosterol on plant secondary metabolism has not been thoroughly investigated [30]–[32]. Following our previous report [33], here we present a multi-platform metabolomics-based elucidation and analysis of changes in the metabolism of tobacco ( Nicotiana tabacum ) cells following ergosterol treatment.…”

Boosting Crop Yields with Plant Steroids

“…This sterolenhanced pathogen resistance may be of a physical nature because cell membranes are an important physical barrier against pathogen infection and sterols are known to play a role in membrane rigidity and permeability (Hartmann, 1998). It is also interesting to note that treatment with exogenous ergosterol, the main sterol of most fungi, promoted the expression of a number of defense genes in tobacco and grape and enhanced the production of resveratrol and the tolerance against the fungal pathogen B. cinerea in grape (Laquitaine et al, 2006;Lochman and Mikes, 2006).…”

Exogenous spermidine, arsenic and β-aminobutyric acid modulate tobacco resistance to tobacco mosaic virus, and affect local and systemic glucosylsalicylic acid levels and arginine decarboxylase gene expression in tobacco leaves

“…Tobacco PR-1a, PR-2 and ADC coding sequences were amplified by PCR from tobacco genomic DNA using oligonucleotide primers derived from published sequences as follows: PR-1a, sense 5 0 -CCTCGTACATTCT-CATGGTCAAT-3 0 , antisense 5 0 -CCATTGTTACACTGAACC-CTAGC-3 0 (Lochman and Mikes, 2006); PR-2, sense 5 0 -CATGCAAACAATTTACCATCAGACC-3 0 , antisense 5 0 -CCAG-GTTTCTTTGGAGTTCCTGCC-3 0 (Mayer et al, 2001); ADC, sense 5 0 -ATGCCGGCCTTAGGTTGTTGTGTAG-3 0 , antisense 5 0 -ACAACTTCAAGGGGTGCAATAGGACCA-3 0 (Marini et al, 2001). These primers were used to amplify poplar genomic DNA under the following thermocycling conditions: one cycle at 94 1C for 5 min, then 35 cycles at 94 1C for 30 s, at 56.5 1C (PR-1a) or 57.5 1C (PR-2) or 62 1C (ADC) for 30 s and 72 1C for 1 min, then at 72 1C for 5 min.…”