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Primate-specific ZNF808 is essential for pancreatic development in humans [ChIP-seq]

ABSTRACT: Primate-specific ZNF808 is essential for pancreatic development in humans [ChIP-seq]

PROVIDER: PRJNA844007 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19451558_1.fastq.gz	Fastqsanger.gz
	SRR19451558_2.fastq.gz	Fastqsanger.gz
	SRR19451559_1.fastq.gz	Fastqsanger.gz
	SRR19451559_2.fastq.gz	Fastqsanger.gz
	SRR19451560_1.fastq.gz	Fastqsanger.gz

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Primate-specific ZNF808 is essential for pancreatic development in humans

Project description:Primate-specific ZNF808 is essential for pancreatic development in humans

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Primate-specific ZNF808 is essential for pancreatic development in humans [RNA-seq]

Project description:Primate-specific ZNF808 is essential for pancreatic development in humans [RNA-seq]

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Primate-specific ZNF808 is essential for pancreatic development in humans [RNA-seq]

Project description:Functional investigation of the role primate-specific gene ZNF808 over pancreas differentiation. Loss of function of ZNF808 is a cause of pancreatic agenesis, which is a failure of pancreas development.

2023-09-04 | GSE205163 | GEO

Primate-specific ZNF808 is essential for pancreatic development in humans [ChIP-seq]

2023-09-04 | GSE205152 | GEO

Primate-specific ZNF808 is essential for pancreatic development in humans.

Project description:Identifying genes linked to extreme phenotypes in humans has the potential to highlight biological processes not shared with all other mammals. Here, we report the identification of homozygous loss-of-function variants in the primate-specific gene ZNF808 as a cause of pancreatic agenesis. ZNF808 is a member of the KRAB zinc finger protein family, a large and rapidly evolving group of epigenetic silencers which target transposable elements. We show that loss of ZNF808 in vitro results in aberrant activation of regulatory potential contained in the primate-specific transposable elements it represses during early pancreas development. This leads to inappropriate specification of cell fate with induction of genes associated with liver identity. Our results highlight the essential role of ZNF808 in pancreatic development in humans and the contribution of primate-specific regions of the human genome to congenital developmental disease.

| S-EPMC10703691 | biostudies-literature

Primate-specific ZNF808 is essential for pancreatic development in humans

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

2023-09-04 | GSE205164 | GEO

A Single-cell Transcriptomic Atlas of Primate Pancreatic Islet Aging

Project description:A Single-cell Transcriptomic Atlas of Primate Pancreatic Islet Aging

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A postnatal network of co-hepato/pancreatic stem/progenitors in the biliary trees of pigs versus humans

Project description:A network of co-hepato/pancreatic stem/progenitors exists in pigs and humans in Brunner’s Glands (BGs) in the submucosa of the duodenum, in peribiliary glands (PBGs) of intrahepatic and extrahepatic biliary trees, and in pancreatic duct glands (PDGs) of intrapancreatic biliary trees, collectively supporting hepatic and pancreatic regeneration postnatally. The network is found in humans postnatally throughout life and, so far, has been demonstrated in pigs postnatally at least through to young adults. These stem/progenitors in vivo in pigs are in highest numbers in BGs and in PDGS nearest the duodenum, and in humans are in BGs and in PBGs in the hepato/pancreatic common duct, a duct missing postnatally in pigs. Elsewhere in PDGs in pigs and in all PDGs in humans are only committed unipotent or bipotent progenitors.

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Heterogeneous effects of calorie content and nutritional components underlie dietary influence over pancreatic cancer susceptibility in mice and humans

Project description:Pancreatic cancer is a rare but fatal form of cancer, the fourth highest in absolute mortality. The main reason for the high mortality is late detection, caused in part by an incomplete understanding of the initiating factors. Known risk factors include obesity, diet and type 2 diabetes, however the low incidence rate and interconnection of these factors confound the isolation of individual effects from patient data. Here we use epidemiological analysis of prospective human cohorts and parallel tracking of pancreatic cancer in mice to dissect the impacts of obesity, diet and diabetes on pancreatic cancer development, growth and lethality. Through longitudinal magnetic resonance imaging and multi-omics analysis in mice we found distinct effects of obesity and the protein, sugar and fat composition of diet, and no added impact of diabetes. Using epidemiological approaches in humans, we found that dietary plant fats reduced the risk of future pancreatic cancer development, while dietary sugars gave a genotype-dependent increased susceptibility to pancreatic cancer. An interaction between MAD2L1 and dietary glucose in pancreatic cancer pathogenesis was supported through both genetic epidemiology in human patients and molecular analysis of mouse models. These results demonstrate that both quantitative and qualitative dietary effects are at play in pancreatic cancer kinetics, in both mice and humans. Translation of these results to a clinical setting could aid identification of theat-risk population for screening and potential harness dietary modification as a therapeutic measure.

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Project description:While genome sequencing has identified numerous non-coding alterations between primate species, which of these are regulatory and potentially relevant to the evolution of the human brain is unclear. Here, we annotate cis-regulatory elements (CREs) in the human, rhesus macaque and chimpanzee genome using ChIP-sequencing in different anatomical parts of the adult brain. We find high similarity in the genomic positioning of CREs between rhesus macaque and humans, suggesting that the majority of these elements were already present in a common ancestor 25 million years ago. Most of the observed regulatory changes between humans and rhesus macaque occurred prior to the ancestral separation of humans and chimpanzee, leaving a modest set of regulatory elements with predicted human-specificity. Our data refine previous predictions and hypotheses on the consequences of genomic changes between primate species, and allow the identification of regulatory alterations relevant to the evolution of the brain. ChIP-Sequencing for H3K27ac on 8 distinct brain regions from human (three biological replicates per brain region), chimpanzee (two biological replicates per brain region) and rhesus macaque (three biological replicates per brain region).

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