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Danio rerio

ABSTRACT: Yap reprograms glutamine metabolism to increase nucleotide biosynthesis and enable liver growth

PROVIDER: PRJNA324425 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3624460_1.fastq.gz	Fastqsanger.gz
	SRR3624460_2.fastq.gz	Fastqsanger.gz
	SRR3624461_1.fastq.gz	Fastqsanger.gz
	SRR3624461_2.fastq.gz	Fastqsanger.gz
	SRR3624462_1.fastq.gz	Fastqsanger.gz

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Yap reprograms glutamine metabolism to increase nucleotide biosynthesis and enable liver growth

Project description:The Hippo pathway is an important regulator of organ size and tumorigenesis. It is unclear, however, how Hippo signaling provides the cellular building blocks required for rapid growth. Here, we report that transgenic zebrafish expressing an activated form of the Hippo pathway effector Yap1 develop enlarged livers and are prone to liver tumor formation. Transcriptomic profiling reveals that Yap1 reprograms genes involved in glutamine metabolism. Analysis of gene expression in WT and lf:Yap transgenic zebrafish livers.

2016-08-02 | E-GEOD-82246 | biostudies-arrayexpress

Disruption of nucleotide biosynthesis reprograms mitochondrial metabolism to inhibit adipogenesis

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Yap regulates glucose utilization and sustains nucleotide synthesis to enable organ growth

Project description:The Hippo pathway and its nuclear effector Yap regulate organ size and cancer formation. While many modulators of Hippo activity have been identified, little is known about how Yap target genes mediate these growth effects. Here, we show that defects in hepatic progenitor potential and liver growth in yap-/- mutant zebrafish are caused by impaired glucose transport and nucleotide biosynthesis: transcriptomic and metabolomic analyses reveal that Yap directly regulates expression of glucose transporter glut1, causing decreased glycolytic flux into anabolic nucleotide biosynthesis in yap-/- mutants and impaired glucose tolerance in adults. Nucleotide supplementation improved Yap-deficient phenotypes, indicating functional importance of glucose-fuelled nucleotide biosynthesis. Yap-regulated Glut1 expression and glucose uptake are conserved in mammals. Our results identify Glut1 as a direct Yap target enhancing glucose uptake and utilization for anabolic nucleotide biosynthesis, which are required for organ growth. Our findings demonstrate the central role of Hippo signalling in metabolic homeostasis

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Project description:Yap and Taz regulate retinal pigment epithelial cell fate

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Oncogenic KRAS mediates amino acid metabolism during nutrient stress via regulation of NRF2 and ATF4 in NSCLC [shKRAS low Q]

Project description:Glutamine is a key nutrient for tumor cells that supports nucleotide and amino acid biosynthesis, replenishes the TCA cycle intermediates and contributes to redox metabolism. We identified oncogenic KRAS as a critical regulator of the response to glutamine deprivation in NSCLC. Full activation of the ATF4 stress response pathway is dependent on expression of NRF2 downstream of oncogenic KRAS in NSCLC. Through this mechanism, KRAS alters amino acid uptake and metabolism and sustains mTORC1 signaling during nutrient stress. Furthermore, we identified regulation of asparagine synthetase (ASNS) as a key effect of oncogenic KRAS signaling via ATF4 during glutamine deprivation, and a potential therapeutic target in KRAS mutant NSCLC.

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Oncogenic KRAS mediates amino acid metabolism during nutrient stress via regulation of NRF2 and ATF4 in NSCLC [shKRAS high Q]

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Oncogenic KRAS mediates amino acid metabolism during nutrient stress via regulation of NRF2 and ATF4 in NSCLC [low versus high Q]

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