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β cell specific Crif1 haploinsufficiency effect.

ABSTRACT: β cell specific Crif1 haploinsufficiency effect.

PROVIDER: PRJNA637028 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11916727_1.fastq.gz	Fastqsanger.gz
	SRR11916727_2.fastq.gz	Fastqsanger.gz
	SRR11916728_1.fastq.gz	Fastqsanger.gz
	SRR11916728_2.fastq.gz	Fastqsanger.gz
	SRR11916729_1.fastq.gz	Fastqsanger.gz

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β cell specific Crif1 haploinsufficiency effect.

Project description:CRIF1 is a mitochondrial protein essential for the synthesis and formation of the OxPhos complex in the inner mitochondrial membrane. Beta cell specific Crif1 haploinsufficiency resulted in defect of first phase insulin secretion, and caused islet cell composition change as well as proliferation of beta cell for a compensation to maintain metabolic homeostasis. These results suggest that mitochondrial OxPhos function of beta cell has roles for beta cell compensation as well as insulin secretion.

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Transcriptomic analysis in cerebral microvessels from the brain of endothelial-specific Crif1 deficiency mouse

Project description:Endothelial cells (ECs) in cerebral vessels are considered the primary targets in acute hemorrhagic brain injuries. EC dysfunction can aggravate neuronal injuries by causing secondary inflammatory responses and blood-brain barrier (BBB) disruption. ECs comprising the BBB are known to have a higher mitochondrial volume compared with peripheral ECs. In previous study, we reported Tek-CRIF1-knockout (KO) mice, with EC-specific deletion of the mitochondrial OxPhos-related gene, Crif1, also known as Gadd45gip1 (encoding GADD45G-interacting protein 1), display profound BBB defects accompanied by reduced expression of junctional proteins in ECs. To identify signaling pathways involved in linking EC-specific mitochondrial dysfunction and BBB disruption, we first performed RNA sequencing using isolated cerebral vessels from Tek-CRIF1 mice. This transcriptome analyses of the Tek-CRIF1-KO mouse revealed significant changes in some signaling, a pathway intimately involved in BBB maintenance.

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Differential gene expression analysis in liver, inguinal white adipose tissue (iWAT), skeletal muscle, and hypothalamus of mice with liver-specific Crif1 deficiency

Project description:CR6-interacting factor-1 (CRIF1) interacting with large mitoribosome subunits is essential for the maturation and insertion of oxidative phosphorylation (OxPhos) polypeptides into the mitochondrial inner membrane. Recently, it has reported that the genetic ablation of Crif1 in a tissue-specific manner results in mitochondrial stress response (MSR) including mitochondrial unfolded protein response (UPRmt). In this study, we aim to obtain a comprehensive understanding of systemic energy metabolism in response to hepatic mitochondrial dysfunction. Through the liver-specific Crif1 deficient mice (LKO), we explore the adaptive response not only in the liver but also in inguinal white adipose tissue (iWAT). Moreover, RNA sequencing in liver, iWAT, skeletal muscle, and hypothalamus suggest that hepatic mitochondrial dysfunction enhance metabolic pathways, including glycolysis, fatty acid elongation and degradation, and 1C metabolism in liver and insulin signaling in iWAT. RNA sequencing also suggests that hepato-mitokines, GDF15 and FGF21 are highly increased in liver of LKO mice. To identify the role of hepato-mitokines, we generate double knockout mice (LKO/Gdf15-/- and LKO/Fgf21-/-), suggesting that GDF15 is responsible for the regulation of the body and fat mass and FGF21 has a critical role for the insulin sensitivity and energy expenditure in this mice.

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