ORCID Profile
0000-0001-6138-7454
Current Organisation
Westfälische Wilhelms-Universität Münster
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Publisher: Scientific Societies
Date: 02-2023
DOI: 10.1094/PHYTO-02-22-0051-R
Abstract: Ascochyta blight is a damaging disease that affects the stems, leaves, and pods of field pea ( Pisum sativum) and impacts yield and grain quality. In Australia, field pea Ascochyta blight is primarily caused by the necrotrophic fungal species Peyronellaea pinodes and Ascochyta koolunga. In this study, we screened 1,276 Pisum spp. germplasm accessions in seedling disease assays with a mix of three isolates of P. pinodes and 641 accessions with three mixed isolates of A. koolunga (513 accessions were screened with both species). A selection of three P. sativum accessions with low disease scores for either pathogen, or in some cases both, were crossed with Australian field pea varieties PBA Gunyah and PBA Oura, and recombinant inbred line populations were made. Populations at the F 3:4 and F 4:5 generation were phenotyped for their disease response to P. pinodes and A. koolunga, and genotypes were determined using the ersity arrays technology genotyping method. Marker-trait associations were identified using a genome-wide association study approach. Trait-associated loci were mapped to the published P. sativum genome assembly, and candidate resistance gene analogues were identified in the corresponding genomic regions. One locus on chromosome 2 (LG1) was associated with resistance to P. pinodes, and the 8 Mb genomic region contains 156 genes, two of which are serine/threonine protein kinases, putatively contributing to the resistance trait. A second locus on chromosome 5 (LG3) was associated with resistance to A. koolunga, and the 35 Mb region contains 488 genes, of which five are potential candidate resistance genes, including protein kinases, a mitogen-activated protein kinase, and an ethylene-responsive protein kinase homolog.
Publisher: Scientific Societies
Date: 08-2023
DOI: 10.1094/PHYTO-10-22-0397-R
Abstract: Ascochyta lentis, the causal organism of ascochyta blight of lentil (Lens culinaris L.), has been shown to produce an avirulence effector protein that mediates ascochyta blight (AB) resistance in certain lentil cultivars. The two known forms of the effector protein were identified from a biparental mapping population between isolates that have reciprocal virulence on PBA Hurricane XT and Nipper. The effector AlAvr1–1 was described for the PBA Hurricane XT–avirulent isolate P94–24 and AlAvr1–2 characterised in the PBA Hurricane XT-virulent isolate AlKewell. Here, we performed a genome-wide association study (GWAS) to identify other loci associated with AB for a differential set of lentil cultivars from a erse panel of isolates collected in the Australian lentil growing regions from 2013 to 2020. The chromosome 3 AlAvr1 locus was strongly associated with the PBA Hurricane XT, Indianhead and Nipper disease responses but one other genomic region on chromosome 11 was also associated with the Nipper disease trait. Our results corroborate the earlier work that identified the AlAvr1 locus, for field-collected isolates that span the period prior to release and after widespread adoption of PBA Hurricane XT. A multiplex PCR assay was developed to differentiate the respective genes AlAvr1–1 and AlAvr1–2, to predict PBA Hurricane XT avirulence and pathotype designation in the ersity panel. Increasing numbers of the PBA Hurricane XT–virulent pathotype 2 isolates across that time indicates strong selection for isolates with the AlAvr1–2 allele. Furthermore, one other region of the A. lentis genome may contribute to the pathogen-host interaction for lentil AB.
Publisher: Public Library of Science (PLoS)
Date: 23-09-2021
DOI: 10.1371/JOURNAL.PPAT.1009943
Abstract: Regulation of cellular metabolism is now recognized as a crucial mechanism for the activation of innate and adaptive immune cells upon erse extracellular stimuli. Macrophages, for instance, increase glycolysis upon stimulation with pathogen-associated molecular patterns (PAMPs). Conceivably, pathogens also counteract these metabolic changes for their own survival in the host. Despite this dynamic interplay in host-pathogen interactions, the role of immunometabolism in the context of intracellular bacterial infections is still unclear. Here, employing unbiased metabolomic and transcriptomic approaches, we investigated the role of metabolic adaptations of macrophages upon Salmonella enterica serovar Typhimurium ( S . Typhimurium) infections. Importantly, our results suggest that S . Typhimurium abrogates glycolysis and its modulators such as insulin-signaling to impair macrophage defense. Mechanistically, glycolysis facilitates glycolytic enzyme aldolase A mediated v-ATPase assembly and the acidification of phagosomes which is critical for lysosomal degradation. Thus, impairment in the glycolytic machinery eventually leads to decreased bacterial clearance and antigen presentation in murine macrophages (BMDM). Collectively, our results highlight a vital molecular link between metabolic adaptation and phagosome maturation in macrophages, which is targeted by S . Typhimurium to evade cell-autonomous defense.
Publisher: The American Association of Immunologists
Date: 11-2020
Abstract: Salmonella enterica serovar Typhimurium (S. Typhimurium) is a Gram-negative bacterium that induces cell death of macrophages as a key virulence strategy. We have previously demonstrated that the induction of macrophage death is dependent on the host’s type I IFN (IFN-I) response. IFN-I signaling has been shown to induce tripartite motif (TRIM) 21, an E3 ubiquitin ligase with critical functions in autoimmune disease and antiviral immunity. However, the importance and regulation of TRIM21 during bacterial infection remains poorly understood. In this study, we investigated the role of TRIM21 upon S. Typhimurium infection of murine bone marrow–derived macrophages. Although Trim21 expression was induced in an IFN-I–dependent manner, we found that TRIM21 levels were mainly regulated posttranscriptionally. Following TLR4 activation, TRIM21 was transiently degraded via the lysosomal pathway by chaperone-mediated autophagy (CMA). However, S. Typhimurium–induced mTORC2 signaling led to phosphorylation of Akt at S473, which subsequently impaired TRIM21 degradation by attenuating CMA. Elevated TRIM21 levels promoted macrophage death associated with reduced transcription of NF erythroid 2–related factor 2 (NRF2)–dependent antioxidative genes. Collectively, our results identify IFN-I–inducible TRIM21 as a negative regulator of innate immune responses to S. Typhimurium and a previously unrecognized substrate of CMA. To our knowledge, this is the first study reporting that a member of the TRIM family is degraded by the lysosomal pathway.
Publisher: Cold Spring Harbor Laboratory
Date: 28-02-2023
DOI: 10.1101/2023.02.27.530219
Abstract: TFEB is a master regulator of autophagy, lysosome biogenesis and mitochondrial metabolism that works, and immunity, primarily through transcription controlled by cytosol-to-nuclear translocation. Emerging data indicate additional regulatory interactions at the surface of organelles such as lysosomes. Here we show that TFEB has a non-transcriptional role in mitochondria, regulating the electron transport chain complex I to down-modulate inflammation. Proteomic analysis revealed extensive TFEB co-precipitation with several mitochondrial proteins, whose interactions are disrupted upon infection with S. Typhimurium. Localization of TFEB in the mitochondrial matrix was confirmed by high resolution confocal microscopy and biochemistry with translocation dependent on a conserved N-terminal TOMM20-binding motif enhanced by mTOR inhibition. Within the mitochondria, TFEB and protease LONP1 antagonistically co-regulate complex I, reactive oxygen species and the inflammatory response. Consequently, during infection, lack of TFEB specifically in the mitochondria exacerbates the expression of pro-inflammatory cytokines, contributing to innate immune pathogenesis.
Location: No location found
No related grants have been discovered for Julia Fischer.