Biology subjects

Kracher, B.

Publications and source records attributed to Kracher, B..

5 recordsLinked to original sources

bioRxiv2021

Arabidopsis Topless-related 1 mitigates physiological damage and growth penalties of induced immunity

Transcriptional corepressors of the Topless family are important regulators of plant hormone and immunity signaling. The lack of a genome-wide profile of their chromatin associations limits understanding of transcriptional regulation in plant immune responses. Chromatin immunoprecipitation with sequencing (ChIP-seq) was performed on GFP-tagged Topless-related 1 (TPR1) expressed in Arabidopsis thaliana lines with and without constitutive immunity dependent on Enhanced Disease Susceptibility 1 (EDS1). RNA-seq profiling of pathogen-infected tpl/tpr mutants and assessments of growth and physiological parameters were employed to determine TPL/TPR roles in transcriptional immunity and defense homeostasis. TPR1 bound to promoter regions of ~1,400 genes and ~10% of the detected binding required EDS1 immunity signaling. A tpr1 tpl tpr4 (t3) mutant displayed mildly enhanced defense-related transcriptional reprogramming upon bacterial infection but not increased bacterial resistance. Bacteria or pep1 phytocytokine-challenged t3 plants exhibited, respectively, photosystem II dysfunction and exacerbated root growth inhibition. Transgenic expression of TPR1 restored the t3 physiological defects. We propose that TPR1 and TPL-family proteins function in Arabidopsis to reduce detrimental effects associated with activated transcriptional immunity.

plant biology↗

bioRxiv2020

Genome-wide chromatin binding of transcriptional corepressor Topless-related 1 in Arabidopsis

Timely and specific regulation of gene expression is critical for plant responses to environmental and developmental cues. Transcriptional coregulators have emerged as important factors in gene expression control, although they lack DNA-binding domains and the mechanisms by which they are recruited to and function at the chromatin are poorly understood. Plant Topless-related 1 (TPR1), belonging to a family of transcriptional corepressors found across eukaryotes, contributes to immunity signaling in Arabidopsis thaliana and wild tobacco. We performed chromatin immunoprecipitation and sequencing (ChIP-seq) on an Arabidopsis TPR1-GFP expressing transgenic line to characterize genome-wide TPR1-chromatin associations. The analysis revealed [~]1400 genes bound by TPR1, with the majority of binding sites located at gene upstream regions. Among the TPR1 bound genes, we find not only regulators of immunity but also genes controlling growth and development. To support further analysis of TPR1-chromatin complexes and other transcriptional corepressors in plants, we provide two ways to access the processed ChIP-seq data and enable their broader use by the research community.

plant biology↗

bioRxiv2018

An EDS1 EP-domain surface mediating timely transcriptional reprogramming of immunity genes

Plant intracellular NLR receptors recognize pathogen interference to trigger immunity. NLR signalling mechanisms have not been resolved. Enhanced disease susceptibility 1 (EDS1) heterodimers are recruited by Toll-interleukin1-receptor domain NLRs (TNLs) to transcriptionally mobilize resistance pathways. Using an Arabidopsis EDS1 heterodimer crystal structure we interrogate the conserved but functionally uncharacterized EDS1 -helical EP-domain. We identify EP-domain positively charged residues lining a cavity that are essential for TNL immunity signalling, beyond heterodimer formation. Mutating arginine (R493) to alanine creates a weak EDS1 allele which disables TNL immunity against bacteria producing a virulence factor, coronatine (COR). Arabidopsis plants expressing EDS1R493A are slow to mobilize defence gene expression changes, independently of COR. The transcriptional delay has severe consequences for pathogen resistance and for countering bacterial COR. We uncover a set of host immunity genes whose repression by COR is blocked by wild-type EDS1 but not by EDS1R493A in the TNL response. These data uncover an EDS1 signalling surface lining the heterodimer EP-domain cavity which confers timely transcriptional reprogramming of host defence pathways and blocks bacterial virulence in NLR receptor immunity.

plant biology↗

bioRxiv2018

Subfamily-specific functionalization of diversified immune receptors in wild barley

Gene-for-gene immunity between plants and host-adapted pathogens is often linked to population-level diversification of immune receptors encoded by disease resistance (R) genes. The complex barley (Hordeum vulgare L.) R gene locus Mildew Locus A (Mla) provides isolate-specific resistance against the powdery mildew fungus Blumeria graminis f. sp. hordei (Bgh) and has been introgressed into modern barley cultivars from diverse germplasms, including the wild relative H. spontaneum. Known Mla disease resistance specificities to Bgh appear to encode allelic variants of the R Gene Homolog 1 (RGH1) family of nucleotide-binding domain and leucine-rich repeat (NLR) proteins. To gain insights into Mla diversity in wild barley populations, we here sequenced and assembled the transcriptomes of 50 accessions of H. spontaneum representing nine populations distributed throughout the Fertile Crescent. The assembled Mla transcripts exhibited rich sequence diversity, which is linked neither to geographic origin nor population structure. Mla transcripts in the tested H. spontaneum accessions could be grouped into two similar-sized subfamilies based on two major N-terminal coiled-coil signaling domains that are both capable of eliciting cell death. The presence of positively selected sites, located mainly in the C-terminal leucine-rich repeats of both MLA subfamilies, together with the fact that both coiled-coil signaling domains mediate cell death, implies that the two subfamilies are actively maintained in the host population. Unexpectedly, known MLA receptor variants that confer Bgh resistance belong exclusively to one subfamily. Thus, signaling domain divergence, potentially to distinct pathogen populations, is an evolutionary signature of functional diversification of an immune receptor.

evolutionary biology↗

bioRxiv2018

Signatures of host specialization and a recent transposable element burst in the dynamic one-speed genome of the fungal barley powdery mildew pathogen

Powdery mildews are biotrophic pathogenic fungi infecting a number of economically important plants. The grass powdery mildew, Blumeria graminis, has become a model organism to study host specialization of obligate biotrophic fungal pathogens. We resolved the large-scale genomic architecture of B. graminis forma specialis hordei (Bgh) to explore the potential influence of its genome organization on the co-evolutionary process with its host plant, barley (Hordeum vulgare). The near-chromosome level assemblies of the Bgh reference isolate DH14 and one of the most diversified isolates, RACE1, enabled a comparative analysis of these haploid genomes, which are highly enriched with transposable elements (TEs). We found largely retained genome synteny and gene repertoires, yet detected copy number variation (CNV) of secretion signal peptide-containing protein-coding genes (SPs) and locally disrupted synteny blocks. Genes coding for sequence-related SPs are often locally clustered, but neither the SP clusters nor TEs are enriched in specific genomic regions. Extended comparative analysis with different host-specific B. graminis formae speciales revealed the existence of a core suite of SPs, but also isolate-specific SP sets as well as congruence of SP CNV and phylogenetic relationship. We further detected evidence for a recent, lineage-specific expansion of TEs in the Bgh genome. The characteristics of the Bgh genome (largely retained synteny, CNV of SP genes, recently proliferated TEs and a lack of compartmentalization) are consistent with a \"one-speed\" genome that differs in its architecture and (co-)evolutionary pattern from the \"two-speed\" genomes reported for several other filamentous phytopathogens.

genomics↗