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MOF and Ce-MOF improve soil

ABSTRACT: MOF and Ce-MOF improve soil Raw sequence reads

PROVIDER: PRJNA1175978 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31072900_1.fastq.gz	Fastqsanger.gz
	SRR31072900_2.fastq.gz	Fastqsanger.gz
	SRR31072901_1.fastq.gz	Fastqsanger.gz
	SRR31072901_2.fastq.gz	Fastqsanger.gz
	SRR31072902_1.fastq.gz	Fastqsanger.gz

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MOF and Ce-MOF for FS soil

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The histone acetyl-tranferase MOF is required for metabolic function in the liver .

Project description:Purpose: Conditional MOF deletion in mouse livers resulted in acute hepatic necrosis. The goal of this study was to identify transcriptomic changes in the livers of MOF-depeleted mice livers compared to WT. Methods: Transcriptomic profiles of MOF∆ and WT mouse livers were generated in triplicate. Sequenced reads were quality filtered using Trimmomatic. Quality reads were aligned to the mouse genome using TopHat2. Reads were counted using htseq-count and differentially expressed transcripts were identified using DESeq. Results: 1408 differentially expressed genes were identified between MOF∆ and WT livers. 774 genes were down-regulated in MOF∆ and primarilly associated with metabolic pathways. Branched chain amino acid and fatty acid metabolic pathways, which are deregulated in non-alcoholic fattly liver disease (NAFLD) prgression were down-regulated. 664 genes were upregulated and associated with increased proliferation. Conclusions: These data show that MOF is required for maintaining proper metabolic function in the liver and deregulation of MOF may be involved in progression of NAFLD.

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MOF regulates cell cycle progression

Project description:We utilized primary MEFs to further delineate the role of MOF in proliferating cells and demonstrate that MOF directly activates genes required for cell cycle progression.

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Analysis of MOF under stress conditions

Project description:We analyzed the role of MOF in primary MEFs and differentiated podocytes in response to Adriamycin. Mof was deleted in MEFs using the Cre-ERT2 trasgene, while Mof was knockdown in podocytes using shRNA infection. Samples were treated with Adriamycin for 24 hours and gene expression changes analysed.

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RNA-Seq Analysis to confirm Different Transcriptomic Profiles of Soil-Derived Functional Module Consortia.

Project description:Purpose: Deconstructing the soil microbiome into reduced-complexity functional modules represents a novel method of microbiome analysis. The goals of this study are to confirm differences in transcriptomic patterns among five functional module consortia. Methods: mRNA profiles of 3 replicates each of functional module enrichments of soil inoculum in M9 media with either 1) xylose, 2) n-acetylglucosamine, 3) glucose and gentamycin, 4) xylan, or 5) pectin were generated by sequencing using an Illumina platform (GENEWIZ performed sequencing). Sequence reads that passed quality filters were aligned to a soil metagenome using Burrows Wheeler Aligner. Resulting SAM files were converted to raw reads using HTSeq, and annotated using Uniref90 or EGGNOG databases. Results: To reduce the size of the RNA-Seq counts table and increase its computational tractability, transcripts containing a minimum of 75 total counts, but no more than 3 zero counts, across the 15 samples were removed. The subsequent dataset was normalized using DESeq2, resulting in a dataset consisting of 6947 unique transcripts across the 15 samples, and 185,920,068 reads. We identified gene categories that were enriched in a sample type relative to the overall dataset using Fisher’s exact test. Conclusions: our dataset confirms that the functional module consortia generated from targeted enrichments of a starting soil inoculum had distinct functional trends by enrichment type.

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Analysis of MOF under stress conditions

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MOF acetyl transferase regulates transcription and respiration in mitochondria

Project description:Histone acetylation is sensitive to metabolic cues, however interplay between histone acetyl transferases and cellular metabolism remains poorly understood. Here we report the localization of a classical nuclear HAT- MOF and members of Non-Specific Lethal complex in mitochondria. MOF regulates expression of oxidative phosphorylation (OXPHOS) genes, residing in both nuclear and mitochondrial genomes, selectively in aerobically respiring cells. Furthermore, MOF/KANSL1 depletion causes impaired mitochondrial translation and reduced respiration. MOF loss is catastrophic for tissues with high-energy consumption. In mouse hearts, Mof knockout causes hypertrophic cardiomyopathy, compromised ventricular contractility/ stroke volume and ultimately leads to cardiac failure within three weeks of birth. RNA-seq analysis of the cardiomyocytes revealed deregulation of mitochondrial nutrient metabolism and OXPHOS pathways. Consistently, electron microscopy on affected tissues revealed mitochondrial deterioration with high tissue heterogeneity, commonly observed in mitochondrial diseases. Thus, we reveal a novel function of MOF in mitochondrial homeostasis and propose MOF as a sensor connecting epigenetic regulation to metabolism.

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