Arabidopsis FLOWERING LOCUS D influences systemic-acquired-resistance-induced expression and histone modifications of WRKY genes

Abstract

A plant that is in part infected by a pathogen is more resistant throughout its whole body to subsequent infections--a phenomenon known as systemic acquired resistance (SAR). Mobile signals are synthesized at the site of infection and distributed throughout the plant through vascular tissues. Mechanism of SAR development subsequent to reaching the mobile signal in the distal tissue is largely unknown. Recently we showed that flowering locus D (FLD) gene of Arabidopsis thaliana is required in the distal tissue to activate SAR. FLD codes for a homologue of human-lysine-specific histone demethylase. Here we show that FLD function is required for priming (SAR induced elevated expression during challenge inoculation) of WRKY29 and WRKY6 genes. FLD also differentially influences basal and SAR-induced expression of WRKY38, WRKY65 and WRKY53 genes. In addition, we also show that FLD partly localizes in nucleus and influences histone modifications at the promoters of WRKY29 and WRKY6 genes. The results altogether indicate to the possibility of FLD's involvement in epigenetic regulation of SAR.

Arabidopsis thaliana GLUTATHIONE‐S‐TRANSFERASE THETA 2 interacts with RSI1/FLD to activate systemic acquired resistance

“…PR1 expression in systemic tissue is often associated with the activation of SAR, and several SAR‐defective mutants, such as npr1 , sfd1 and dir1 , are compromised for PR1 expression in systemic tissues (Maldonado et al ., ; Nandi, ; Nandi et al ., ). SAR‐induced WT Arabidopsis plants also accumulate WRKY6 and WRKY29 transcripts in pathogen‐free distal tissues (Jaskiewicz et al ., ; Singh et al ., ). In agreement with the loss‐of‐SAR phenotype of the gstt2 mutant, we observed a lack of systemic induction of PR1 (Fig.…”

“…The discrepancies in WRKY promoter modification and expression pattern between the fld and gstt2 mutants suggest that, although FLD and GSTT2 interact with each other, they independently influence the expression of WRKY6 and WRKY29 . The results described here and reported earlier (Singh et al ., ) also raise the question of whether epigenetic modifications in these WRKY genes are essential for SAR activation. Nevertheless, together, the results suggest that FLD and GSTT2 form a complex that is necessary for SAR, and as both are structural homologues of established chromatin modifiers, they are likely to contribute to SAR development through epigenetic modifications of as yet unidentified genes.…”

“…Moreover, exogenous application of SAR elicitors, such as DA and AzA, could not produce SAR in rsi1 plants (Singh et al ., ). It has also been demonstrated that the histone demethylase activity of RSI1/FLD is required for the development of SAR (Singh et al ., ). FLD codes for an orthologue of human LYSINE‐SPECIFIC DEMETHYLASE 1 (LSD1) (Liu et al ., ).…”

“…Priming of SAR is associated with epigenetic modifications of defence-related genes. Pathogen inoculation or activation of SAR by chemicals leads to the altered occupancy of methylated and acetylated histones, in the promoter of SAR-associated WRKY genes (Banday and Nandi, 2015;Jaskiewicz et al, 2011;Luna et al, 2012;Singh et al, 2014b). Repeated induction of SAR causes the inheritance of stress-associated epigenetic modifications to the next generation and over a stress-free generation .…”

Signaling by small metabolites in systemic acquired resistance

“…As mentioned above, during the biological induction of SAR by inoculation with a pathogen, FLD is required in the distal leaves to respond to the SAR‐inducing factor (Figure ) (Singh et al ., ). FLD function is required for the SAR‐associated systemic accumulation of SA and priming of PR1 and the defense‐regulatory WRKY6 and WRKY29 genes (Singh et al ., , ). In contrast, FLD is not required for the accumulation of SA in pathogen‐treated leaves (Singh et al ., ).…”