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Loss of FBXO11 establishes a stem cell program in acute myeloid leukemia by dysregulating LONP1 [RNA-seq]

ABSTRACT: Purpose: The goals of this study are to compare the transcriptome profile of human cord blood derived CD34+ cells expressing shRNA targeting FBXO1, LONP1 or non-targeting shRNA, combined with or without over-expression of FLAG-FBXO11 or LONP1 by RNAseq. Methods: mRNA profiles of CD34+ cord blood cells with combinations of FBXO11 or LONP1 knockdown or over-expression were generated by RNAseq.

ORGANISM(S): Homo sapiens

PROVIDER: GSE183843 | GEO | 2025/12/04

REPOSITORIES: GEO

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Loss of FBXO11 establishes a stem cell program in acute myeloid leukemia by dysregulating LONP1 [array]

Project description:Purpose: The goals of this study are to compare the transcriptome profile of human cord blood derived CD34+ cells expressing shRNA targeting FBXO11 or non-targeting shRNA by microarray. Methods: mRNA profiles of CD34+ cord blood cells expressing non-targeting shRNA or shRNA targeting FBXO11 were generated by microarray sequencing.

2025-10-21 | GSE182030 | GEO

Loss of FBXO11 establishes a stem cell program in acute myeloid leukemia by dysregulating LONP1

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Loss of FBXO11 establishes a stem cell program in acute myeloid leukemia by dysregulating LONP1 [array]

Project description:Loss of FBXO11 establishes a stem cell program in acute myeloid leukemia by dysregulating LONP1 [array]

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Loss of FBXO11 establishes a stem cell program in acute myeloid leukemia by dysregulating LONP1 [RNA-seq]

Project description:Loss of FBXO11 establishes a stem cell program in acute myeloid leukemia by dysregulating LONP1 [RNA-seq]

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RNAseq analysis of skeletal muscle transcriptomes from wild-type and LONP1 skeletal muscle specific knockout (LONP1-MKO) mice

Project description:Mitochondria serve diverse functions and are essential organelles that require continuous surveillance to maintaintheir integrity and function. LONP1 is an evolutionarily conservedserine peptidase that safeguards mitochondrial protein quality from yeast to human.To investigatethe physiological role of LONP1-mediated mitochondrial quality-control in skeletal musclein vivo, we generated skeletal muscle-specificLonp1-knockout mice (referred to as LONP1 MKO). We performedtranscriptome analysis by whole-genome gene expression profiling experiments in gastrocnemius (GC) muscle from both wild-type (WT) and LONP1-MKO mice. Knockout of LONP1 in skeletal muscle resulted in deregulation of 457 genes in 2-week-old mice and of 1922 genes in 6-week-old mice. Gene ontology analysis revealed that LONP1 deficiency triggers unfolded protein response (UPR) in skeletal muscle.Moreover, GSEA analysis of transcriptomic datain 6-week-old micefurther revealed that genes deregulated by LONP1 deficiency were significantly enriched during aging.Together, the transcriptional profiling results suggest a critical role of LONP1 in regulating skeletal muscle metabolism and health.

2022-01-05 | GSE166071 | GEO

Transcriptomic analysis on prostate tissues uncover the diverse gene expression features induced by Lonp1

Project description:Lon protease 1 (LONP1) is an ATP-dependent protease located in the mitochondrial matrix and plays a crucial role in regulating mitochondrial proteostasis, metabolism and cellular stress responses. Here we show that overexpression of LONP1 is closely related to adverse clinicopathological features and poor prognosis in prostate cancer (PCa) patients. Mechanistically, the findings reveal that LONP1 is implicated in modulating the metabolic switch from oxidative phosphorylation (OXPHOS) to aerobic glycolysis, thereby promoting tumor proliferation, invasion and metastasis both in vitro and in vivo. Meanwhile, we prove that LONP1 as a protease directly targets mitochondrial pyruvate carrier 1 (MPC1), a key metabolic protein in the process of glycolysis, and enhances its degradation, which in turn suppresses tricarboxylic acid (TCA) cycle and ultimately promotes the progression of PCa. Furthermore, using PCa in cancer-prone mice homozygous for a prostate-targeted conditional Pten knockout and Lonp1 knockin, we integrate transcriptomic and proteomic analyses of prostate tumors, upon which reveals that Lonp1 overexpression results in a significant downregulation of NADH: ubiquinone oxidoreductase activity, consequently impeding the electron transfer process and mitochondrial ATP synthesis, associated with metastasis of PCa. Collectively, our results highlight that metabolic reprogramming induced by LONP1 in PCa is closely coupled with disease progression, suggesting that targeting the LONP1-mediated cascade in the mitochondrial may provide therapeutic potential for PCa disease.

2025-02-26 | GSE268736 | GEO

Genome-wide mapping of H3K4me1 status in primary adipocytes isolated from wild-type (WT) and Lonp1-knockout (LONP1 AKO) mice

Project description:Mitochondrial proteases are emerging as key regulators of mitochondrial plasticity acting both as protein quality surveillance and regulatory enzymes by performing highly regulated proteolytic reactions. It remains unclear, however, whether the regulated mitochondrial proteolysis is mechanistically linked to cell identity switch such as white-to-beige conversion of adipocytes. We found that disruption of LONP1-dependent proteolysis substantially impairs thermogenic molecular program and cellular respiration in in vitro differentiated primary adipocytes. qPCR analysis showed that expression levels of Ucp1 and other beige adipocyte thermogenic genes were remarkably downregulated in LONP1 AKO adipocytes. We took a deeper dive into the characterization of histone modifications in LONP1 AKO adipocytes using the global enhancer marker H3K4me1 ChIP-Seq. These unbiased ChIP seq data are strong evidence of that LONP1 loss results in decreased H3K4me1 on a broad array of thermogenic genes. These results collectively indicate that LONP1 is crucial to maintain proper epigenetic homeostasis and beige thermogenic gene expression.

2023-04-08 | GSE222490 | GEO

RNAseq analysis of skeletal muscle transcriptomes from wild-type, LONP1 skeletal muscle specific knockout (LONP1 mKO) and LONP1ATF4 skeletal muscle double-knockout (LONP1ATF4 DmKO) mice.

Project description:Studying the molecular basis for the skeletal muscle mitochondrial stress response could potentially be targeted to counteract metabolic disorders such as obesity. We uncovered a crucial role for the mitochondrial protease LONP1 in controlling the muscle mitochondrial proteostasis stress response that governs systemic metabolic homeostasis. Skeletal muscle-specific ablation of LONP1 led to broad genomic reprogramming of muscle and protected the mice from HFD-induced obesity. To thoroughly analyze pathways that are affected by ATF4 deficiency in the context of LONP1 mKO, we performed RNA-Seq transcriptome analysis of skeletal muscles from WT, LONP1 mKO and LONP1ATF4 DmKO mice. We identified a total of 3017 differentially expressed genes with a cutoff of 1.5-fold, and p < 0.05. Surprisingly, we found that ATF4 loss blunted a subset of regulated genes in LONP1 mKO muscles, whereas the majority of differentially regulated genes in LONP1 mKO muscles were not affected by ATF4 ablation. GO analysis of ATF4-dependent genes regulated by LONP1 ablation revealed significant enrichment in amino acid metabolic processes, Interestingly, however, LONP1 deficiency induced activation of muscle UPR and UPR-related RNA processing as well as myokine pathways were not affected by ATF4 ablation. Therefore, our results highlight a ATF4-independent mechanism in mediating the UPRmt in mammals.

2022-07-28 | GSE192990 | GEO

Proteomic profiling of FBXO11 protein complexes

Project description:FBXO11, a member of the F-box protein family, plays a critical role in cellular processes such as protein degradation, cell cycle regulation, and signaling pathways by serving as a substrate recognition component of the SKP1-Cullin-F-box (SCF) ubiquitin ligase complex. Dysregulation of FBXO11 has been implicated in various diseases, including cancer and developmental disorders, yet its full spectrum of interactions and functional roles remains poorly understood. This project aims to perform a comprehensive proteomic profiling of FBXO11-associated protein complexes to uncover its interaction network and better understand its biological functions. Using advanced mass spectrometry-based proteomics, we will identify and characterize the proteins that interact with FBXO11 under different cellular conditions. Additionally, bioinformatics tools will be employed to analyze the identified interactome and explore their functional enrichment in specific pathways and biological processes.

2025-11-14 | PXD059844 | Pride

FBXO11-Mediated Proteolysis of BAHD1 Relieves PRC2-dependent Transcriptional Repression in Erythropoiesis

Project description:The histone mark H3K27me3 and its reader/writer Polycomb repressive complex 2 (PRC2) mediate widespread transcriptional repression in stem and progenitor cells. Mechanisms that regulate this activity are critical for tissue development but poorly understood. Here we show that the E3 ubiquitin ligase FBXO11 relieves PRC2-mediated repression during erythroid maturation by targeting its newly identified substrate BAHD1, an H3K27me3 reader that recruits transcriptional co-repressors. Erythroblasts lacking FBXO11 are developmentally delayed, with reduced expression of maturation-associated genes, most of which harbor bivalent histone marks (activating H3K4me3 and repressive H3K27me3), bind BAHD1, and fail to recruit the erythroid transcription factor GATA1. The BAHD1 complex interacts physically with PRC2 and depletion of either component restores FBXO11-deficient erythroid gene expression. Previous studies showed that FBXO11 promotes B-cell development and inhibits lymphomagenesis by degrading the transcriptional repressor BCL6. We show that in aggressive B-cell lymphoma lines, depletion of FBXO11 causes the accumulation of both BCL6 and BAHD1, and that suppression of BAHD1 slows cell expansion. Our studies identify BAHD1 as a novel effector of PRC2-mediated repression and reveal how a single E3 ubiquitin ligase eliminates PRC2 repression at developmentally poised bivalent genes during erythropoiesis. The FBXO11-BAHD1 regulatory axis may function in other developmental pathways, including B-lymphopoiesis and lymphomagenesis.

2020-12-31 | GSE115357 | GEO

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