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Proteomic analysis of FBXL6 interacting proteome

ABSTRACT: FBXL6 is a E3 ubiquitin ligase that we suspected to be involved in mitochondrial functions. We have investigated the specific interactome of this E3 by transfecting HEK cells with Flagged-FBXL6, or with b-gal (control). After flag immunoprecipiation, specific interacting proteome was identified by mass spectrometry and discriminate from control IP.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Dupuy Jean-William

LAB HEAD: Giovanni Benard

PROVIDER: PXD037248 | Pride | 2023-09-25

REPOSITORIES: Pride

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			Action	DRS
	F016093.dat	Other
	F016095.dat	Other
	F016096.dat	Other
	F016097.dat	Other
	F016098.dat	Other

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Publications

The E3 ubiquitin ligase FBXL6 controls the quality of newly synthesized mitochondrial ribosomal proteins.

Lavie Julie J Lalou Claude C Mahfouf Walid W Dupuy Jean-William JW Lacaule Aurélie A Cywinska Agata Ars AA Lacombe Didier D Duchêne Anne-Marie AM Raymond Anne-Aurélie AA Rezvani Hamid Reza HR Ngondo Richard Patryk RP Bénard Giovanni G

Cell reports 20230601 6

In mammals, about 99% of mitochondrial proteins are synthesized in the cytosol as precursors that are subsequently imported into the organelle. The mitochondrial health and functions rely on an accurate quality control of these imported proteins. Here, we show that the E3 ubiquitin ligase F box/leucine-rich-repeat protein 6 (FBXL6) regulates the quality of cytosolically translated mitochondrial proteins. Indeed, we found that FBXL6 substrates are newly synthesized mitochondrial ribosomal protein ...[more]

PMID: 37267103

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Proteomic analysis of FBXL6 Knockdown cells proteome

Project description:FBXL6 is E3 ubiquitin ligase that we suspected to be involved in mitochondrial functions. We have investigated how deletion of this E3s by CRSIPR/Cas in Hela cells affects the cellular proteome. We compared this proteome to cells treated with CRISPR Non-Targeting Control (control cells).

2023-09-25 | PXD037252 | Pride

Analyses of FBXL6 interaction with newly synthesized proteins.

Project description:HEK cells were grown in light media for two weeks. One day before experiments, cells were transfected with FBXL6-flag or B-gal (control). At t=0, cells were switched to heavy media for 3h and then Flag immunoprecipitation were performed. Pulled down protein were analyzed by mass spectrometry.

2023-09-25 | PXD037602 | Pride

Adaptation to pH and pH signaling in the phytopathogenic fungus Botrytis cinerea

Project description:The grey mould fungus Botrytis cinerea is capable of developing on a wide variety of host plants and different organs that differ greatly in their pH values. The strategy developed by this necrotrophic fungus is partly based on the acidification of the plant tissues via the secretion of several organic acids including oxalic acid. That’s why B.cinerea is considered as an “acidic” fungus. However, we have previously shown that it is also capable of alkalinizing its ambient environment during sunflower cotyledons or bean leaves infection and that the alkalinization is achieved by amino acids catabolism and ammonia secretion ( Billon-grand et al, 2012). This capacity to modulate the surrounding pH reveals also an ability to regulate the expression and the secretion of an arsenal of enzymes in order to produce virulence factors in accordance with the ambient pH and enzymes requirement for optimal activity. Expression of pH-regulated genes is controlled by the highly conserved signaling pathway Pal/Pac that leads to activation of the zinc finger transcription factor PACC under neutral or alkaline conditions. Investigations of the role of this pH regulator in the infectious process of B.cinerea are presented.

2021-09-13 | PXD004145 | Pride

Proteomic analysis of melanoma resistant cells transfected with siRNA targeting DDR2 or treated with DDR2 inhibitor or Dasatinib

Project description:Combined therapy with anti-BRAF plus anti-MEK is currently used as first-line treatment of patients with metastatic melanomas harboring the somatic BRAF V600E mutation. However, the main issue with targeted therapy is the acquisition of tumor cell resistance. In 70% of resistant melanoma cells, the resistant process consists in epithelial-to-mesenchymal transition (EMT). This process called phenotype switching makes melanoma cells more invasive. Its signature is characterized by MITF low, AXL high, and actin cytoskeleton reorganization through RhoA activation. In parallel of this phenotype switching phase, the resistant cells exhibit an anarchic cell proliferation due to hyper-activation of the MAP kinase pathway. We show that a majority of human melanoma overexpress discoidin domain receptor 2 (DDR2) after treatment. The same result was found in resistant cell lines presenting phenotype switching compared to the corresponding sensitive cell lines. We demonstrate that DDR2 inhibition induces a decrease in AXL expression and reduces stress fiber formation in resistant melanoma cell lines. In this phenotype switching context, we report that DDR2 control cell and tumor proliferation through the MAP kinase pathway in resistant cells in vitro and in vivo. Therefore, inhibition of DDR2 could be a new and promising strategy for countering this resistance mechanism.

2023-05-02 | PXD028292 | Pride

Enrichment and mass spectrometry analysis of TbTAX-1-interacting or TbTTC29-interacting proteins by co-immunoprecipitation

Project description:Study of Trypanosoma ZMYND12’s ortholog (TbTAX-1) confirmed an axonemal localization of the protein and knockdown of TbTAX-1 using RNAi induced dramatic flagellar motility defects as observed in human. Co-immunoprecipitation assays and ultra-structure expansion microscopy in Trypanosoma brucei then formally demonstrated that ZMYND12 and TTC29 directly interact and belong to the same axonemal complex. Subsequent comparative proteomics analysis in Trypanosoma and Ttc29 KO mice models also identified DNAH1 as a new interacting protein of both ZMYND12 and TTC29 proteins. These data evidenced the critical role of ZMYND12 for flagellum function and assembly in humans and Trypanosoma through its interaction with other axonemal partners such as TTC29 and DNAH1 in the same complex.

2023-11-01 | PXD039470 | Pride

Comprehensive proteome profiling in Aedes albopictus to decipher Wolbachia-virus interference phenomenon

Project description:Cellular models have provided significant advances on molecular bases of bipartite interactions between either an arbovirus or a bacterial symbiont with a given arthropod vector. However, although an interference phenomenon was evidenced in tripartite interaction arbovirus-symbiont-mosquito vector very little is known regarding the mechanisms involved. Using large-scale proteome profiling, we characterized proteins differentially expressed in Aedes albopictus cells infected by the symbiotic bacterium Wolbachia and the Chikungunya virus (CHIKV). These proteins were mostly related to cellular processes involved in glycolysis process, protein metabolism, translation and amino acid metabolism. The presence of Wolbachia impacted significantly the protein profiles, including sequestration of proteins such as structural polyprotein and capsid viral proteins that may affect replication and assembly of CHIKV in cellulo. This study provides insights into the molecular pathways involved in the tripartite interaction mosquito-Wolbachia-virus and may help in defining targets for the better implementation of Wolbachia-based strategy for disease transmission control.

2018-03-14 | PXD005091 | Pride

Proteomic analysis of primary human microvascular endothelial cells (HMVECs) stimulated for 24â€‰h with either 50 ï�g/mL recombinant Fibrillin-1 C-terminal fragment or 25â€‰ng/ml VEGF-A compared to unstimulated cells.

Project description:Mutations in the fibrillin-1 gene result in cardiovascular, ocular, and skeletal abnormalities in Marfan syndrome. Here we show that a fibrillin-1 mutation also alters the neovessel formation. In the mouse retina vascularization model, fibrillin-1 is detected at the basement membrane underlying the angiogenic front and around arterioles. In Fbn1C1041G/+ mice, a model of Marfan disease, the microvasculature is altered at these sites. At the front, endothelial tip-cell sprouting and branching are decreased, and we show that mutant fibrillin-1 delays angiogenesis by affecting Notch signalling. Supplying the growing vasculature of Fbn1C1041G/+ mice with a C-terminal fragment of fibrillin-1 corrects all defects. In vitro, the C-terminal fragment of fibrillin-1 also displays pro-angiogenic activities on microvascular endothelial cell. Our data establish that fibrillin-1 performs essential functions in microvessel formation and integrity and that mutant fibrillin-1-induced defects can be rescued pharmacologically.

2023-05-31 | PXD029834 | Pride

Cell membrane proteome analysis in HEK293T cells challenged with α-Synuclein amyloids

Project description:Amyloids interact with plasma membranes. Extracellular amyloids cross the plasma membrane barrier. Internalized extracellular amyloids are reported to trigger amyloidogenesis of endogenous proteins in recipient cells. To what extent these extracellular and intracellular amyloids perturb the plasma membrane proteome is not investigated. Using α-Synuclein as a model amyloid protein, we performed membrane shaving followed by mass spectrometry experiment to identify the conformational changes in the cell surface proteins after extracellular amyloid challenge. We also performed membrane proteomics after the biogenesis of intracellular α-Synuclein amyloids. Our results suggest that promiscuous interaction with extracellular amyloids stochastically alter the conformation of plasma membrane proteins. This affects the biological process through the plasma membrane and result in loss in cell viability. Cells that survive the extracellular amyloid shock can grow normally and gradually develop intracellular amyloids which do not directly impact the plasma membrane proteome and associated biological processes. Thus, α-Synuclein amyloids can damage the plasma membrane and related processes only during cell to cell transfer and not during their intracellular biogenesis.

2024-07-09 | PXD046280 | Pride

Combining laser capture micro-dissection and proteomics reveals an active translation machinery controlling invadosome formation

Project description:We developed a method that combines laser micro-dissection and mass spectrometry, enabling the analysis of subcellular structures in their native state based on low amounts of input material. Using this combinatorial method, we showed that invadosomes contain specific components of the translational machinery, in addition to known marker proteins.

2018-10-19 | PXD009390 | Pride

PPARgamma ubiquitination sites in HEK293T cells

Project description:Peroxisome proliferator–activated receptor γ (PPARγ) is the central regulator of adipogenesis, and its dysregulation is linked to obesity and metabolic diseases. Identification of the factors that regulate PPARγ expression and activity is therefore crucial for combating obesity. Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor with a known role in xenobiotic detoxification. Recent studies have suggested that AhR also plays essential roles in energy metabolism. However, the detailed mechanisms remain unclear. We previously reported that experiments with adipocyte-specific Cullin 4b (Cul4b)-knockout mice showed that CUL4B suppresses adipogenesis by targeting PPARγ. Here, using immunoprecipitation, ubiquitination, real-time PCR and Gst-pulldown assays, we report that AhR functions as the substrate receptor in CUL4B–RING E3 ubiquitin ligase (CRL4B) complex and is required for recruiting PPARγ. AhR overexpression reduced PPARγ stability and suppressed adipocyte differentiation, and AhR knockdown stimulated adipocyte differentiation in 3T3-L1 cells. Furthermore, we found that two lysine sites on residues 268 and 293 in PPARγ are targeted for CRL4B-mediated ubiquitination, indicating cross-talk between acetylation and ubiquitination. Our findings establish a critical role of AhR in regulating PPARγ stability and suggest that the AhR–PPARγ interaction may represent a potential therapeutic target for managing metabolic diseases arising from PPARγ dysfunction.

2019-11-01 | PXD015830 | Pride

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