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ERK-Mediated Phosphorylation of OLA1 Controls Adaptive Mitochondria to Nucleus Communication Regulating Cellular Homeostasis [ChIP-seq]

ABSTRACT: ERK-Mediated Phosphorylation of OLA1 Controls Adaptive Mitochondria to Nucleus Communication Regulating Cellular Homeostasis [ChIP-seq]

PROVIDER: PRJNA795788 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17514595_1.fastq.gz	Fastqsanger.gz
	SRR17514595_2.fastq.gz	Fastqsanger.gz
	SRR17514596_1.fastq.gz	Fastqsanger.gz
	SRR17514596_2.fastq.gz	Fastqsanger.gz
	SRR17514597_1.fastq.gz	Fastqsanger.gz

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ERK-Mediated Phosphorylation of OLA1 Controls Adaptive Mitochondria to Nucleus Communication Regulating Cellular Homeostasis

Project description:ERK-Mediated Phosphorylation of OLA1 Controls Adaptive Mitochondria to Nucleus Communication Regulating Cellular Homeostasis

| PRJNA795850 | ENA

ERK-Mediated Phosphorylation of OLA1 Controls Adaptive Mitochondria to Nucleus Communication Regulating Cellular Homeostasis [RNA-seq]

Project description:ERK-Mediated Phosphorylation of OLA1 Controls Adaptive Mitochondria to Nucleus Communication Regulating Cellular Homeostasis [RNA-seq]

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ERK-Mediated Phosphorylation of OLA1 Controls Adaptive Mitochondria to Nucleus Communication Regulating Cellular Homeostasis [RNA-seq]

Project description:We found that changes in mitochondrial membrane potential or ROS generation trigger the translocation of OLA1 from mitochondria and cytoplasm to the nucleus, regulated by ERK1-mediated phosphorylation of OLA1 on Ser232/Tyr236. Subsequent phosphorylation of nuclear-OLA1 on Thre325 by ERK2 activates its function as a genetic factor regulating cellular homeostasis by modulating HDAC9 expression. Disruption of OLA1 phosphorylation blocks its nuclear translocation, compromised the expression of nuclear-encoded mitochondrial proteins, DNA damage response, and multiple stress-response-related-genes, leading to cellular dysfunction. Our findings reveal that OLA1 is a crucial component of mitonuclear response regulatory hubs essential for regulating cellular adaptation to stress.

2022-01-14 | GSE193318 | GEO

ERK-Mediated Phosphorylation of OLA1 Controls Adaptive Mitochondria to Nucleus Communication Regulating Cellular Homeostasis [ChIP-seq]

2022-01-14 | GSE193317 | GEO

ERK-Mediated Phosphorylation of OLA1 Controls Adaptive Mitochondria to Nucleus Communication Regulating Cellular Homeostasis [CHIP-seq]

2023-11-21 | GSE218381 | GEO

ERK-Mediated Phosphorylation of OLA1 Controls Adaptive Mitochondria to Nucleus Communication Regulating Cellular Homeostasis

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-01-14 | GSE193319 | GEO

Communication between mitochondria and nucleus: defining a retrograde response in fission yeast

Project description:Retrograde response was widely studied in budding yeast but the main transcription factors that transmit it (RTG1,2 and 3) are not conserved in other organisms, thus it is interesting to study how communication between mitochondria and nucleus evolved in distantly related fission yeast, and which are the common aspects of this conserved pathway between yeast and higher organisms.To analyse any retrograde response in fission yeast, we inhibited the electron transport chain activity by antimycin A and studied cellular gene expression changes by microarrays. Cells treated with antimycin A in fermentative medium (YE with 3% glucose), showed the same growth rate as untreated cells, but they reached a lower biomass in stationary phase. Antimycin A treated cells consumed glucose at a faster rate and produced more ethanol, indicating that the energy metabolism was shifted even more towards fermentation. We analyzed the transcriptomes of antimycin A-treated cells to untreated control cells during early exponential growth phase (OD 0.5).

2016-11-01 | E-MTAB-4520 | biostudies-arrayexpress

IQGAP1 mediates the communication between the nucleus and the mitochondria via NDUFS4 alternative splicing

Project description:A constant communication between mitochondria and nucleus ensures cellular homeostasis and adaptation to mitochondrial stress. Anterograde regulatory pathways involving a large number of nuclear-encoded proteins control mitochondrial biogenesis and functions. Such functions are deregulated in cancer, resulting in proliferative advantages for cancer cells, aggressive disease and therapeutic resistance. Transcriptional networks controlling the nuclear-encoded mitochondrial genes are known, however alternative splicing (AS) regulation has not been implicated in this communication. Here, we show that IQGAP1, a scaffold protein that regulates AS of distinct gene subsets in gastric cancer cells, participates in AS regulation that strongly affects mitochondrial respiration. Combined proteomic and RNA-seq analyses of IQGAP1KO and parental cells show that IQGAP1KO alters a specific AS event of the mitochondrial respiratory chain complex I (CI) subunit NDUFS4 and downregulates a subset of CI subunits. In IQGAP1KO cells, CI intermediates accumulate resembling assembly deficiencies observed in patients with Leigh syndrome bearing NDUFS4 mutations. Mitochondrial CI activity is significantly lower in KO compared to parental cells, while exogenous expression of IQGAP1 reverses mitochondrial defects of IQGAP1KO cells. Our work sheds light to a novel facet of IQGAP1 in mitochondrial quality control that involves fine-tuning of CI activity through AS regulation in gastric cancer.

2023-08-04 | GSE218220 | GEO

L-plastin Ser5 phosphorylation via RSKs, downstream effectors of the MAPK/ERK pathway, in (breast) cancer cells (and in vitro)

Project description:Deregulated cell migration and invasion, which are hallmarks of metastatic cancer cells, are correlated to structural and functional alterations of the actin cytoskeleton associated to a large panel of actin-binding proteins. Among these, the actin-bundling protein L-plastin, initially detected in leukocytes, is ectopically expressed in several solid tumours and is often considered as a metastatic marker. Phosphorylation of L-plastin on residue serine 5 (Ser5) has been shown to activate L-plastin and to be crucial for invasion and metastasis formation. Here, we investigate the signalling pathway leading to L-plastin Ser5 phosphorylation in four breast cancer cell lines. Whole genome microarray analysis comparing cell lines with different invasive capacities and corresponding L-plastin Ser5 phosphorylation levels revealed that genes of the MAPK/ERK pathway are differentially expressed. In line, in vitro kinase assays showed that MAPK/ERK pathway downstream kinases RSK1 and RSK2 are able to directly phosphorylate L-plastin on Ser5. In parallel to a knockdown approach, activation and inhibition studies of signalling molecules of the MAPK/ERK pathway, followed by computational modelling analysis, confirmed that RSK is an important activator of L-plastin in all four studied cell lines. Finally and rounding up our study, RSK knockdown significantly impaired migratory and invasive capacities of a selected invasive cell line, thus consolidating RSK as a promising therapeutic target in certain invasive carcinomas. Altogether, our data provide substantial evidence that the MAPK/ERK pathway is involved in L-plastin Ser5 phosphorylation in breast cancer cells with its downstream kinases RSK1 and RSK2 being able to directly phosphorylate L-plastin on Ser5.

2016-03-26 | E-MTAB-3487 | biostudies-arrayexpress

IQGAP1 mediates the communication between the nucleus and the mitochondria via NDUFS4 alternative splicing

Project description:A constant communication between mitochondria and nucleus ensures cellular homeostasis and adaptation to mitochondrial stress. Anterograde regulatory pathways involving a large number of nuclear-encoded proteins control mitochondrial biogenesis and functions. Such functions are deregulated in cancer, resulting in proliferative advantages for cancer cells, aggressive disease and therapeutic resistance. Transcriptional networks controlling the nuclear-encoded mitochondrial genes are known, however alternative splicing (AS) regulation has not been implicated in this communication. Here, we show that IQGAP1, a scaffold protein that regulates AS of distinct gene subsets in gastric cancer cells, participates in AS regulation that strongly affects mitochondrial respiration. Combined proteomic and RNA-seq analyses of IQGAP1 KO and parental cells show that IQGAP1 KO alters a specific AS event of the mitochondrial respiratory chain complex I (CI) subunit NDUFS4 and downregulates a subset of CI subunits. In IQGAP1 KO cells, CI intermediates accumulate resembling assembly deficiencies observed in patients with Leigh syndrome bearing NDUFS4 mutations. Mitochondrial CI activity is significantly lower in KO compared to parental cells, while exogenous expression of IQGAP1 reverses mitochondrial defects of IQGAP1 KO cells. Our work sheds light to a novel facet of IQGAP1 in mitochondrial quality control that involves fine-tuning of CI activity through AS regulation in gastric cancer.

2023-08-04 | PXD038314 | Pride

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