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Identification of NIX-GST and BNIP3-GST interactors

ABSTRACT: We aimed to identify proteins that interact with the mitophagy receptors NIX or BNIP3. To this end, we incubated recombinantly purified NIX-GST or BNIP3-GST with HeLa cell lysate to identify proteins that would bind to NIX and BNIP3.

INSTRUMENT(S): Orbitrap Exploris 480

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Markus Hartl

LAB HEAD: Sascha Martens

PROVIDER: PXD060351 | Pride | 2025-01-30

REPOSITORIES: pride

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			Action	DRS
	20230417_E4_NEO1_Adriaenssens_Martens_MPL_UniWien_MPLID23069_BCL_2p.raw	Raw
	20230417_E4_NEO1_Adriaenssens_Martens_MPL_UniWien_MPLID23069_FUN_2p.raw	Raw
	20230417_E4_NEO1_Adriaenssens_Martens_MPL_UniWien_MPLID23069_GST_5p.raw	Raw
	20230417_E4_NEO1_Adriaenssens_Martens_MPL_UniWien_MPLID23069_NIX_2p.raw	Raw
	20230509_E4_NEO1_Adriaenssens_Martens_MPL_UniWien_MPLID23095_WIPI_5p.raw	Raw

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Identification of global proteome changes upon DFP treatment of HeLa cells

Project description:We aimed to identify proteins that would be turned over upon DFP treatment, a small molecule that mimicks hypoxia treatment and which induces NIX/BNIP3 mitophagy. We aimed to identify which proteins are degraded upon 24 h DFP treatment and verified whether there was an enrichment of mitochondrial proteins being selectively turned over by mitophagy under these conditions.

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Gene expression of wild-type and Nix-/-Bnip3-/- memory B cells

Project description:Memory B cells are long-lived lymphocytes essential for humoral immunological memory. Autophagy is required for the long-term survival of memory B cells, however, the molecular mechanisms for the protection by autophagy have not been fully elucidated. Here we show that mitochondrial autophagy mediated by Nix and Bnip3 prevents necroptosis in memory B cells by maintaining mitochondrial homeostasis and normal lipid metabolism. In mice with B cell-specific deletion of Nix and Bnip3, memory B cells showed significant increases in viable mitochondria and de novo fatty acid synthesis, with accumulation of lipid droplets in the cytoplasm and accelerated cell death. Inhibiting the mitochondrial citrate transporter Slc25a1 or silencing the necroptosis gene Ripk3 rescued Nix–/–Bnip3–/– memory B cells in vivo. These data indicate that Nix- and Bnip3-dependent mitochondrial autophagy in memory B cells is important for restricting de novo fatty acid synthesis and preventing necroptosis. Our results suggest a mechanism for autophagy in the maintenance of mitochondrial homeostasis for the protection of immunological memory.

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Identification of global proteome changes upon rapalog-induced tethering of WIPI2 to the mitochondrial outer membrane in wild-type or NIX/BNIP3 DKO HeLa cells

Project description:We aimed to identify proteins that would be turned over upon artificial tethering of WIPI2 to the mitochondrial surface upon rapalog treatment, using the FIS1-FRB plus FKBP-GFP-WIPI2 tethering system. We had previously observed that this induces mitophagy based on flow cytometry analysis of the mt-mKeima probe. Here, we aimed to identify which proteins are degraded upon 24 h Rapalog treatment and verified whether there was an enrichment of mitochondrial proteins being selectively turned over by mitophagy under these conditions in wild-type and NIX/BNIP3 double-knockout HeLa cells.

2025-01-30 | PXD060363 | Pride

Cytoplasmic mRNA decay controlling inflammatory gene expression is determined by pre-mRNA fate decision

Project description:The fidelity of immune responses depends on a timely controlled and selective mRNA degradation that is largely driven by RNA-binding proteins (RBPs). It remains unclear whether the selection of an individual mRNA molecule for degradation is governed by stochastic or directed processes. Here, we show that tristetraprolin (TTP, also known as ZFP36), an essential anti-inflammatory RBP, destabilizes target mRNAs via a hierarchical molecular assembly. The formation of the assembly strictly relies on the interaction of TTP with RNA. The TTP homolog ZFP36L1 exhibits similar requirements, indicating a broader relevance of this regulatory program. Unexpectedly, the assembly of the cytoplasmic mRNA-destabilization complex is licensed in the nucleus by TTP binding to pre-mRNA, while cytoplasmic mRNA does not constitute a de novo TTP target. Hence, the fate of an inflammation-induced mRNA is decided concomitantly with its synthesis. This mechanism prevents the translation of excessive and potentially harmful inflammation mediators, irrespective of transcription.

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PPTC7 integrates homeostatic and physiological signals to regulate mitophagy and mitochondrial mass

Project description:Here we report that knockout of PPTC7, a mitochondrial matrix protein, hyperactivates BNIP3/NIX-mediated mitophagy in vitro and in vivo. Biochemically, the PPTC7 precursor is trapped by BNIP3 and NIX to mitochondrial outer-membrane, where PPTC7 scaffolds the assembly of the substrate-PPTC7- SCFFBXL4 holocomplex to degrade BNIP3 and NIX, forming a homeostatic regulatory loop. PPTC7 possesses an unusually weak mitochondrial targeting sequence to facilitate its outer-membrane retention and mitophagy control. Upon starvation, PPTC7 is transcriptionally upregulated in mouse liver to repress mitophagy, which critically maintains hepatic mitochondrial mass, bioenergetics and gluconeogenesis. Collectively, PPTC7 functions as a mitophagy sensor that integrates homeostatic and physiological signals to dynamically control BNIP3 and NIX degradation, thereby maintaining proper mitochondrial mass and cellular homeostasis.

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Gene expression of wild-type and Nix-/-Bnip3-/- memory B cells

Project description:Gene expression of wild-type and Nix-/-Bnip3-/- memory B cells

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The proteins interacting with GST-betaTub85D from the GST pulldown

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Opposing roles for AMPK in regulating distinct mitophagy pathways

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2024-11-29 | PXD056956 | Pride

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The molecular consequences of Nix ablation on apoptosis and erythropoiesis

Project description:Normal erythropoiesis requires a critical balance between proapoptotic and antipaoptotic pathways. Bcl-xl, an antiapoptotic protein is induced at end-stages of differentiation of erythroid precursors in response to erythropoietin. The details of the proapoptotic pathway and the critical proapoptotic proteins inhibited by Bcl-xl in erythropoiesis are not well understood. We employed gene targeting to ablate Nix, a proapoptotic BH3-domain only Bcl2 family protein, which is known to be transcriptionally induced during erythropoiesis. Nix null mice exhibited reticulocytosis and thrombocytosis in the peripheral blood; and profound splenomegaly with erythroblastosis in the spleen and bone marrow despite normal erythropoietin levels and blood oxygen tension. In vivo apoptosis was diminished in erythroblast precursors from Nix null spleens. To define the molecular consequences of Nix ablation on apoptosis and erythropoiesis, we conducted a detailed comparative analysis of gene expression in spleens from 8 week old Nix null mice and wild type controls. Of 45,101 genes analyzed, 514 were significantly upregulated and 386 down-regulated in Nix-/- splenocytes. Functional cluster analysis delineated the ten most highly regulated gene sets, revealing increased levels of cell cycle and erythroid genes, with decreased levels of cell death and B-cell genes. Keywords: strain comparison

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