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Investigating the impact of SopB on the gut epithelium – proteome and phosphoproteome

ABSTRACT: In this study, the impact of the Salmonella SPI1 effector SopB on the gut epithelium was investigated based on a proteome and a phosphoproteome.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Culture

SUBMITTER: Kristin Schubert

LAB HEAD: Kristin Schubert

PROVIDER: PXD046081 | Pride | 2026-07-07

REPOSITORIES: Pride

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			Action	DRS
	2_result_all_together.pdStudy	Other
	CP_B1_f1.raw	Raw
	CP_B1_f2.raw	Raw
	CP_B2_f1.raw	Raw
	CP_B2_f2.raw	Raw

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Publications

Salmonella SopB suppresses post-transcriptionally regulated cytokine release to reduce early tissue inflammation and delay disease progression.

Diab Nour N Yong Chiun Huei CH Stange Eva-Lena EL Birk Marlène S MS Schmitz Matthias A MA Düsterhöft Stefan S Pes Jonas J Ferle Kira Noemi KN Karkossa Isabel I Schubert Kristin K Deiwick Jörg J Vucur Mihael M Luedde Tom T Torow Natalia N Ludwig Andreas A Dupont Aline A Selkrig Joel J von Bergen Martin M Hensel Michael M Zhang Kaiyi K Hornef Mathias W MW

Nature communications 20260706 1

Salmonella enterica subsp. enterica serovar Typhimurium (S. Typhimurium) manipulates cellular processes through the translocation of effector molecules into the host cell cytosol. Using a recently established neonatal S. Typhimurium infection model, we provide functional insights into how Salmonella outer protein B (SopB) suppresses early mucosal tissue inflammation and prolongs host survival. Mechanistically, SopB prevents a disintegrin and metalloprotease 17 (ADAM17) activation, plasma membran ...[more]

PMID: 42409845

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Phosphoproteome dynamics during differentiation of 3T3-L1 adipocytes

Project description:Here, we identified temporal dynamics of the phosphoproteome during adipocyte differentiation in the murine 3T3-L1 cells, applying untargeted proteomics in combination with enrichment strategies for phosphorylated peptides. Samples were taken at initiation of differentiation, at an intermediate and terminal time point.

2024-06-13 | PXD045778 | Pride

Phosphoproteome dynamics during differentiation of SGBS adipocytes

Project description:Here, we identified temporal dynamics of the phosphoproteome during adipocyte differentiation in the human SGBS cells, applying untargeted proteomics in combination with enrichment strategies for phosphorylated peptides. Samples were taken at initiation of differentiation, at an intermediate and terminal time point.

2024-06-13 | PXD045770 | Pride

Effects of high molecular weight phthalates on LPS-stimulated THP-1 macrophages - phosphoproteome

Project description:In this study, the effects of three high molecular weight phthalates (DINP, DIDP, DPHP) and their metabolites (MHINP, MCINP, OHMPHP) were investigated in THP-1 macrophages. For this purpose, the phosphoproteome was evaluated.

2023-09-13 | PXD042912 | Pride

Redundancy and Specialisation of Cyclin Dependent Kinases

Project description:Cyclin dependent kinases (CDKs) lie at the heart of eukaryotic cell division, with different CDK complexes initiating DNA replication (S-CDKs) and mitosis (M-CDKs)1-3. However, the principles on which cyclin-CDKs organise the cell cycle are still contentious, with current theories suggesting that either M-CDKs and S-CDKs are redundant with each other, and simply serve as a source of CDK activity, or that they are functionally specialised and execute distinct tasks. Here we reconcile these two views, showing that although S-CDKs are unable to drive mitosis, global CDK phosphorylation in vivo between S-CDK and M-CDK is surprisingly similar. Remarkably, S-CDK has cryptic mitotic activity which can be exposed by the removal of Protein Phosphatase 1 (PP1). In particular, removal of centrosomal PP1 allows S-CDK to execute mitosis indistinguishably from M-CDK, demonstrating their functional redundancy. Thus, we reconcile the two opposing views of cell cycle control, showing that although there is a minor level of specialisation between S-CDKs and M-CDKs, that the core cell cycle engine is based upon modulation of CDK activity, with cyclins providing refinements to this core system.

2022-03-22 | PXD029073 | Pride

Phosphatase specificity influences the phosphorylation timing of CDK substrates during the cell cycle

Project description:Cell cycle events are ordered by cyclin-dependent kinases (CDKs), which phosphorylate hundreds of substrates. Multiple phosphatases oppose these CDK substrates, yet their collective role in regulating phosphorylation timing in vivo remains unclear. Here, we show that four phosphatases (PP2A-B55, PP2A-B56, CDC14, and PP1) each target distinct subsets of CDK substrate sites in vivo in fission yeast, influencing when phosphorylation occurs during G2 and mitosis. On average, sites dephosphorylated by CDC14 and PP2A-B56 are phosphorylated earlier during G2, followed by sites dephosphorylated by PP1 and PP2A-B55. This suggests that these phosphatases set different phosphorylation thresholds at the G2/M transition. Consistent with this, depleting PP2A-B55 or CDC14 accelerates mitotic onset, likely by advancing phosphorylation of their respective CDK substrates, suggesting these phosphorylation thresholds are important for regulating mitotic onset. Our findings establish in vivo phosphatase substrate specificity as a key factor regulating the timing of CDK substrate phosphorylation throughout the cell cycle.

2025-10-05 | PXD060298 | Pride

Genome-wide maps of ParBF (SopB) binding along DNA in E. coli

Project description:We report the genome-wide analysis from chromatin immunoprecipitated DNA (ChIP-sequencing) at very high resolution (about 50 millions reads) of the DNA binding pattern of ParBF (SopB) of plasmid F Differencial examination of ParBF binding by comparing input and IP (anti-SopB antibody) samples

2015-09-04 | E-GEOD-67869 | biostudies-arrayexpress

Salmonella SopB suppresses post-transcriptionally regulated cytokine release to reduce early tissue inflammation and delay disease progression

Project description:Salmonella enterica subsp. enterica serovar Typhimurium (S. Typhimurium) manipulates cellular processes through the translocation of effector molecules into the host cell cytosol. Using a recently established neonatal S. Typhimurium infection model, we provide functional insights into how Salmonella outer protein B (SopB) suppresses early mucosal tissue inflammation and prolongs host survival. Mechanistically, SopB prevents a disintegrin and metalloprotease 17 (ADAM17) activation, plasma membrane translocation and the release of membrane-bound TNFa from enterocytes and reduces epithelial secretion of IL-18 via mTOR-controlled secretory autophagy. This abolishes the early epithelial transcriptional response and reduces immune cell recruitment and programmed cell death-mediated mucosal barrier disruption delaying disease progression. The immunosuppressive effect of SopB is independent of the C-terminally encoded phosphatidylinositol phosphatase and phosphotransferase activity but requires an intact N-terminal domain. Thus, SopB suppresses the early, post-transcriptional regulation of epithelial cytokine release in an inositol phosphatase-independent manner likely promoting pathogen transmission.

2026-04-06 | GSE326693 | GEO

Liver phosphoproteomics in response to AgRP activated neurons in the presence/absence of NPY

Project description:Autophagy represents a key regulator of aging and metabolism upon cell autonomous sensing of energy deprivation. We find that fasting in mice activates autophagy in liver paralleled by activation of hypothalamic AgRP neurons. Optogenetic and chemogenetic activation of AgRP neurons induces autophagy, alters phosphorylation of autophagy regulators and promotes ß-oxidation in the liver. AgRP neuron dependent induction of liver autophagy relies on NPY expression in these neurons. AgRP neuron projections in the paraventricular nucleus of the hypothalamus (PVH) and the lateral hypothalamus (LHA) mediate AgRP neuron-dependent control of liver autophagy. Conversely, inhibiting AgRP neurons during energy deprivation abrogates induction of hepatic autophagy and re-wiring of metabolism. Finally, AgRP neuron activation increases circulating corticosterone concentrations, and reduction of hepatic glucocorticoid receptor expression attenuates AgRP neuron-dependent activation of hepatic autophagy. Collectively, our study reveals a fundamental regulatory principle of non-cell autonomous control of liver autophagy in control of metabolic adaptation during nutrient deprivation.

2023-04-18 | PXD029247 | Pride

Metaproteomic analysis of paired fresh, frozen and swab-collected/preservation medium-stored feces from four healthy human subjects

Project description:Metaproteomic analysis of paired fresh, frozen and swab-collected/preservation medium-stored feces from four healthy human subjects

2025-10-16 | PXD047278 | Pride

Screening privileged alkylguanidinium motifs under host-mimicking conditions reveals a novel antibiotic with an unconventional mode of action

Project description:Screening large molecule libraries against pathogenic bacteria is often challenged by a low hit rate due to limited uptake, underrepresentation of antibiotic structural motifs and assays which do not resemble the infection conditions. To address these limitations, we here screen a library focused on alkylguanidinium compounds, a structural motif associated with antibiotic activity and enhanced uptake, under host-mimicking infection conditions against a panel of disease-associated bacteria. Several hit molecules were obtained with activities against Gram-positive as well as Gram-negative bacteria highlighting the fidelity of the general concept. Based on the best antibiotic activity, we selected one compound (L15) for in-depth mode of action studies. L15 exhibited bactericidal activity against Staphylococcus aureus USA300 Lac (JE2) with a minimum inhibitory concentration of 1.5 µM whereby a structure-activity relationship study with 18 derivatives proved the necessity of the guanidinium motif for antibiotic activity. Electron microscopy studies and depolarization assays at high L15 concentrations showed an impact on the cell membrane and integrity which was absent at the MIC concentration. Sequencing of L15-resistant strains revealed a mutation in an efflux pump but did not provide hints for direct targets. We thus performed affinity-based protein profiling with a L15 probe and identified signal peptidase IB (SpsB) as the most promising hit. Validation by activity assays, binding site identification and molecular docking demonstrated SpsB overactivation by L15, similar to a previously reported activator molecule that dysregulates protein secretion of this essential enzyme. Overall, this study highlights the need for unconventional screening strategies to identify novel antibiotics.

2024-07-17 | PXD051986 | Pride

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