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MTORC1 couples SREBP-dependent transcription and splicing of de novo lipid synthesis enzymes via FAM120A de novo lipid synthesis enzymes via FAM120A

ABSTRACT: mTORC1 couples SREBP-dependent transcription and splicing of de novo lipid synthesis enzymes via FAM120A de novo lipid synthesis enzymes via FAM120A

PROVIDER: PRJNA854056 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19896716_1.fastq.gz	Fastqsanger.gz
	SRR19896716_2.fastq.gz	Fastqsanger.gz
	SRR19896717_1.fastq.gz	Fastqsanger.gz
	SRR19896717_2.fastq.gz	Fastqsanger.gz
	SRR19896718_1.fastq.gz	Fastqsanger.gz

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mTORC1 couples SREBP-dependent transcription and splicing of de novo lipid synthesis enzymes via FAM120A de novo lipid synthesis enzymes via FAM120A

Project description:mTORC1 couples SREBP-dependent transcription and splicing of de novo lipid synthesis enzymes via FAM120A de novo lipid synthesis enzymes via FAM120A

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mTORC1 couples SREBP-dependent transcription and splicing of de novo lipid synthesis enzymes via FAM120A de novo lipid synthesis enzymes via FAM120A

Project description:FAM120A as a transcriptional co-activator that couples transcription and splicing of lipid synthesis enzymes downstream of mTORC1-SRPK2 signaling. Mechanistically, the mTORC1-activated SRPK2 phosphorylates a splicing factor SRSF1, enhancing its binding to FAM120A. FAM120A directly interacts with a lipogenic transcription factor SREBP1 at active promoters, thereby bridging newly transcribed lipogenic genes to the RNA splicing machinery.

2022-07-02 | GSE207172 | GEO

Systematic mapping of genetic interactions for de novo fatty acid synthesis identifies C12orf49 as a regulator of lipid metabolism [CRISPR]

Project description:The de novo synthesis of fatty acids has emerged as a therapeutic target for various diseases including cancer. Since cancer cells are intrinsically buffered to combat metabolic stress, it is important to understand how cells may adapt to loss of de novo fatty acid biosynthesis. Here we use pooled genome-wide CRISPR screens to systematically map genetic interactions (GIs) in human HAP1 cells carrying a loss-of-function mutation in FASN, which catalyzes the formation of long-chain fatty acids. FASN mutant cells show a strong dependence on lipid uptake that is reflected by negative GIs with genes involved in the LDL receptor pathway, vesicle trafficking, and protein glycosylation. Further support for these functional relationships is derived from additional GI screens in query cell lines deficient for other genes involved in lipid metabolism, including LDLR, SREBF1, SREBF2, ACACA. Our GI profiles also identify a potential role for the previously uncharacterized gene LUR1/C12orf49 in exogenous lipid uptake regulation through modulation of SREBF2 signalling in response to lipid starvation. Overall, our data highlight the genetic determinants underlying the cellular adaptation associated with loss of de novo fatty acid synthesis and demonstrate the power of systematic GI mapping for uncovering metabolic buffering mechanisms in human cells.

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De Novo Purine Synthesis Mediates Circadian Control of Cell Cycle in Zebrafish (array)

Project description:Cell cycle and metabolism are two major outputs controlled by circadian rhythm in many organisms. Here we show that the three processes were linked through inosine 5'-phosphate dehydrogenase (impdh), a rate-limiting enzyme in de novo purine synthesis. We using adult zebrafish as a model system,we applied a genome-wide transcriptome approach that allowed us to investigate circadian gene expression. The whole-genome transcriptome profiles of adult brain in time-series were assayed on Agilent zebrafish microarrays. We used a similar statistical method to identify zebrafish circadian genes (ZCOG) as our previous study in larval zebrafish. Three isoforms of impdh show strong circadian oscillations in different tissues of zebrafish. impdh1a contributes to the ocular development and pigment synthesis, impdh2 promotes and impdh1b delays the development. By limiting the GTP required by DNA synthesis, impdh2 contributes to the daily rhythm of S phase in cell cycle. Multiple enzymes in the de novo purine synthesis pathway show the same circadian oscillations with peaks similar to impdh2. The circadian expression of this pathway is conserved in mouse liver. In summary, we show that the circadian regulation of de novo purine synthesis that supplies crucial building blocks for DNA replication is critical for gating cell cycle in circadian rhythm. Adult zebrafish were sacrificed and dissected at 4h intervals starting at CT0 in both LD and DD conditions for 12 time points. Total RNA of individual zebrafish brain was extracted using Trizol (Invitrogen, Carlsbad, CA) according to the manufacturerM-bM-^@M-^Ys instruction. Microarrays were manufactured by Agilent Technologies (Agilent Technologies, Palo Alto, CA), containing 43,603 probes for zebrafish whole-genome transcriptional profiling.

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De Novo Purine Synthesis Mediates Circadian Control of Cell Cycle in Zebrafish (array)

2013-10-01 | GSE51277 | GEO

De novo gene synthesis by an antiviral reverse transcriptase

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Changes in tryptophan de novo NAD synthesis associated with chronic intestinal inflammation

Project description:Tryptophan metabolism and de novo NAD biosynthesis is associated with behavioural changes in IBD patients. The microbiota and tryptophan de novo syntheses of the distal colon, distal colon and brain of C57BL/6 control mice and Winnie mice littermates with chronic intestinal inflammation were compared using RNA-Seq. Differentially expressed genes were analysed using Micromon software. Changes in tryptophan and nicotinamide metabolism-associated gene expressions, metabolites, and abundance of gut microbiota associated with chronic intestinal inflammation and dysregulated tryptophan metabolism in the Winnie mouse distal colon and brain were apparent. Our findings shed light on the physiological alterations in tryptophan metabolism, specifically its diversion from the serotonergic pathway towards the kynurenine pathway and the consequential effects on de novo NAD+ synthesis, in the context of chronic intestinal inflammation

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