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Silhavy, D.

Publications and source records attributed to Silhavy, D..

3 recordsLinked to original sources

Ambivalent roles of nonsense-mediated mRNA decay in heat stress tolerance

RNA homeostasis is essential for gene regulation and cellular survival; however, how RNA degradation pathways contribute to stress adaptation remains incompletely understood. Here, we investigated the role of the nonsense-mediated mRNA decay (NMD) in regulating heat stress (HS) memory in a long-term acquired thermotolerance assay. NMD-deficient Arabidopsis thaliana mutants upf1-5 and upf3-1 exhibited a biphasic phenotype: they displayed transiently elevated heat tolerance during early recovery but became more sensitive to heat during late recovery. Genetic analysis of upf3;hsfa2 and upf3;hsfa3 double mutants demonstrated that the early heat tolerance occurs independently of both HsfA2 and HsfA3 HS-memory transcription factors. Under non-treated conditions, the upf3-1 transcriptome exhibited baseline priming of heat-shock responsive transcripts, likely accounting for the initial heat tolerance. Further transcriptome profiling revealed that upf3-1 mutants exhibited reduced levels of the functional HsfA2 isoform (HsfA2-I) and attenuated expression of the HsfA2-dependent thermomemory regulon following the triggering stress. NMD deficiency also upregulated immune-response genes while repressing developmental and cell-wall-associated pathways. Together, impaired HsfA2-dependent thermomemory and a compromised growth defense balance underlies the late heat sensitivity of NMD deficient plants. Overall, NMD acts as a dual-action post-transcriptional regulator that coordinates the transition from stress response to growth resumption.

plant biology↗

TFIIS is required for reproductive development and thermal adaptation in barley

Regulation of transcriptional machinery and its adaptive role under different stress conditions are studied extensively in the dicot model plant Arabidopsis, but our knowledge on monocot species remains elusive. TFIIS is an RNA polymerase II associated transcription elongation co-factor. Previously it was shown that TFIIS ensures efficient transcription elongation that is necessary for heat stress survival in A. thaliana. However, the function of TFIIS has not been analysed in monocots. In the present work, we have generated and studied independent tfIIscrispr mutant barley lines. We show that, TFIIS is needed for reproductive development and heat stress survival in barley. The molecular basis of HS-sensitivity of tfIIs mutants is the retarded expression of heat stress protein transcripts, that leads to late accumulation of HSP chaperones, enhanced proteotoxicity and ultimately to lethality. We also show that TFIIS is induced and autoregulated in response to heat, supporting a conserved adaptive function of these control elements for plant thermal adaptation. In sum, our results are a step forward for the better understanding of transcriptional machinery regulation in monocot crops.

plant biology↗

Nectar- and stigma-specific expression of a chitinase could partially protect against fire blight in certain apples

To attract pollinators many angiosperms secrete stigma exudate and nectar in their flowers. As these nutritious fluids are ideal infection points for pathogens, both secretions contain various antimicrobial compounds. Erwinia amylovora, the causing bacterium of the devastating fire blight apple disease, is the model pathogen that multiplies in flower secretions and infects through the nectaries. Although Erwinia resistant apples are not available, certain cultivars are tolerant. It was reported that in stigma infection assay, the Freedom cultivar was Erwinia tolerant while the Jonagold was susceptible. We hypothesized that differences in the nectar protein compositions lead to different susceptibility. Indeed we found that an acidic chitinase III protein (Machi3-1) selectively accumulates in the nectar and stigma of the Freedom cultivar. We demonstrate that MYB binding site containing repeats of the Freedom Machi3-1 promoter are responsible for the strong nectar- and stigma-specific expression. As we found that in vitro the Machi3-1 protein impairs growth and biofilm formation of Erwinia at physiological concentration, we propose that the Machi3-1 contribute to the tolerance by inhibiting Erwinia multiplication in the stigma exudate and in the nectar. We show that the Machi3-1 allele was introgressed from Malus floribunda 821 into different apple cultivars including the Freedom.\n\nHighlightCertain apple cultivars accumulate to high levels in their nectar and stigma an acidic chitinase III protein that can protect against pathogens including fire blight disease causing Erwinia amylovora

plant biology↗