Bacillus subtilis SL18r Induces Tomato Resistance Against Botrytis cinerea, Involving Activation of Long Non-coding RNA, MSTRG18363, to Decoy miR1918

Mounting evidence has indicated that beneficial rhizobacteria can suppress foliar pathogen invasion via elicitation of induced systemic resistance (ISR). However, it remains elusive whether long non-coding RNAs (lncRNAs) are involved in the mediation of the rhizobacteria-primed ISR processes in plants. Herein, we demonstrated the ability of the rhizobacterial strain Bacillus subtilis SL18r to trigger ISR in tomato plants against the foliar pathogen Botrytis cinerea. Comparative transcriptome analysis was conducted to screen differentially expressed lncRNAs (DELs) between the non-inoculated and SL18r-inoculated plants. Among these DELs, four variants of MSTRG18363 possessed conserved binding sites for miR1918, which negatively regulates immune systems in tomato plants. The expression of MSTRG18363 in tomato leaves was significantly induced by SL18r inoculation. The transcription of MSTRG18363 was negatively correlated with the expression of miR1918, but displayed a positive correlation with the transcription of the RING-H2 finger gene SlATL20 (a target gene of miR1918). Moreover, MSTRG18363-overexpressing plants exhibited the enhanced disease resistance, reduction of miR1918 transcripts, and marked increases of SlATL20 expression. However, the SL18r-induced disease resistance was largely impaired in the MSTRG18363-silenced plants. VIGS-mediated SlATL20 silencing also greatly weakened the SL18r-induced disease resistance. Collectively, our results suggested that induction of MSTRG18363 expression in tomato plants by SL18r was conducive to promoting the decoy of miR1918 and regulating the expression of SlATL20, thereby provoking the ISR responses against foliar pathogen infection.

Involvement of CsWRKY70 in salicylic acid-induced citrus fruit resistance against Penicillium digitatum

Penicillium digitatum causes serious losses in postharvest citrus fruit. Exogenous salicylic acid (SA) can induce fruit resistance against various pathogens, but the mechanism remains unclear. Herein, a transcriptome-based approach was used to investigate the underlying mechanism of SA-induced citrus fruit resistance against P. digitatum. We found that CsWRKY70 and genes related to methyl salicylate (MeSA) biosynthesis (salicylate carboxymethyltransferase, SAMT) were induced by exogenous SA. Moreover, significant MeSA accumulation was detected in the SA-treated citrus fruit. The potential involvement of CsWRKY70 in regulating CsSAMT expression in citrus fruit was studied. Subcellular localization, dual luciferase, and electrophoretic mobility shift assays and an analysis of transient expression in fruit peel revealed that the nucleus‐localized transcriptional activator CsWRKY70 can activate the CsSAMT promoter by recognizing the W-box element. Taken together, the findings from this study offer new insights into the transcriptional regulatory mechanism of exogenous SA-induced disease resistance in Citrus sinensis fruit.

Transcriptomic Profiling of Acute Cold Stress-Induced Disease Resistance (SIDR) Genes and Pathways in the Grapevine Powdery Mildew Pathosystem

Temperatures from 2 to 8°C transiently induce quantitative resistance to powdery mildew in several host species (cold stress-induced disease resistance [SIDR]). Although cold SIDR events occur in vineyards worldwide an average of 14 to 21 times after budbreak of grapevine and can significantly delay grapevine powdery mildew (Erysiphe necator) epidemics, its molecular basis was poorly understood. We characterized the biology underlying the Vitis vinifera cold SIDR phenotype—which peaks at 24 h post–cold (hpc) treatment and results in a 22 to 28% reduction in spore penetration success—through highly replicated (n = 8 to 10) RNA sequencing experiments. This phenotype was accompanied by a sweeping transcriptional downregulation of photosynthesis-associated pathways whereas starch and sugar metabolism pathways remained largely unaffected, suggesting a transient imbalance in host metabolism and a suboptimal target for pathogen establishment. Twenty-six cold-responsive genes peaked in their differential expression at the 24-hpc time point. Finally, a subset of genes associated with nutrient and amino acid transport accounted for four of the eight most downregulated transcripts, including two nodulin 1A gene precursors, a nodulin MtN21 precursor, and a Dynein light chain 1 motor protein precursor. Reduced transport could exacerbate localized nutrient sinks that would again be transiently suboptimal for pathogen growth. This study links the transient cold SIDR phenotype to underlying transcriptional changes and provides an experimental framework and library of candidate genes to further explore cold SIDR in several systems, with an ultimate goal of identifying novel breeding or management targets for reduced disease.