Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of the circadian clock genes as components of the compensatory mechanism in nphp8 mutant zebrafish

ABSTRACT: The nphp8sa24730 mutant zebrafish displayed a marked decrease in glomerular cysts and cloaca malformation over subsequent generations, implying the existence and activation of compensatory mechanisms that could rescue the ciliopathy-associated phenotypes. To uncover these mechanisms, we compared the transcriptional profiles of two-day-old maternal zygotic homozygous nphp8sa24730 mutant larvae and control siblings by RNA sequencing (RNA-seq).

ORGANISM(S): Danio rerio

PROVIDER: GSE206983 | GEO | 2022/07/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Comparative proteomic analysis of microvescicoles and exosomes isolated from urine of medullary sponge kidney disease (MSK) versus Autosomal dominant polycystic kidney disease (ADPKD) patients.

Project description:Microvescicles (MV) and exosomes (EX) seem to be involved in the pathogenetic machinery of the autosomal dominant polycystic kidney disease (ADPKD), but, at the moment, no studies have assessed their role in medullary sponge kidney disease (MSK), a sporadic kidney malformation featuring cysts, nephrocalcinosis and recurrent renal stones. To discover their role in this disease we employed a proteomic-based research strategy.

2019-11-25 | PXD011283 | Pride

Identification of the circadian clock genes as components of the compensatory mechanism in nphp8 mutant zebrafish

Project description:Identification of the circadian clock genes as components of the compensatory mechanism in nphp8 mutant zebrafish

| PRJNA853203 | ENA

Disruption of the clock components CLOCK and BMAL1 leads to hypoinsulinaemia and diabetes.

Project description:The molecular clock maintains energy constancy by producing circadian oscillations of rate-limiting enzymes involved in tissue metabolism across the day and night. During periods of feeding, pancreatic islets secrete insulin to maintain glucose homeostasis, and although rhythmic control of insulin release is recognized to be dysregulated in humans with diabetes, it is not known how the circadian clock may affect this process. Here we show that pancreatic islets possess self-sustained circadian gene and protein oscillations of the transcription factors CLOCK and BMAL1. The phase of oscillation of islet genes involved in growth, glucose metabolism and insulin signalling is delayed in circadian mutant mice, and both Clock and Bmal1 (also called Arntl) mutants show impaired glucose tolerance, reduced insulin secretion and defects in size and proliferation of pancreatic islets that worsen with age. Clock disruption leads to transcriptome-wide alterations in the expression of islet genes involved in growth, survival and synaptic vesicle assembly. Notably, conditional ablation of the pancreatic clock causes diabetes mellitus due to defective beta-cell function at the very latest stage of stimulus-secretion coupling. These results demonstrate a role for the beta-cell clock in coordinating insulin secretion with the sleep-wake cycle, and reveal that ablation of the pancreatic clock can trigger the onset of diabetes mellitus.

| S-EPMC2920067 | biostudies-literature

RNA sequencing of the urethral epithelial progenitor cells

Project description:We will use micro-dissection to isolate cells from the embryonic mouse cloaca, and perform RNA-Seq analysis to identify molecular markers of the region of the cloaca that will give rise to the urethral epithelium.

2017-10-14 | GSE88764 | GEO

Proteomic-based research strategy identified laminin subunit alpha 2 as a potential urinary-specific biomarker for the medullary sponge kidney disease

Project description:Medullary sponge kidney (MSK) disease, a rare kidney malformation featuring recurrent renal stones and nephrocalcinosis, continues to be diagnosed using expensive and time-consuming clinical/instrumental tests (mainly urography). Currently, no molecular diagnostic biomarkers are available. To identify such we employed a proteomic-based research strategy utilizing urine from 22 patients with MSK and 22 patients affected by idiopathic calcium nephrolithiasis (ICN) as controls. Notably, two patients with ICN presented cysts. In the discovery phase, the urine of 11 MSK and 10 controls, were randomly selected, processed, and analyzed by mass spectrometry. Subsequently, several statistical algorithms were undertaken to select the most discriminative proteins between the two study groups. ELISA, performed on the entire patients’ cohort, was used to validate the proteomic results. After an initial statistical analysis, 249 and 396 proteins were identified exclusive for ICN and MSK, respectively. A Volcano plot and ROC analysis, performed to restrict the number of MSK-associated proteins, indicated that 328 and 44 proteins, respectively, were specific for MSK. Interestingly, 119 proteins were found to differentiate patients with cysts (all patients with MSK and the two ICN with renal cysts) from ICN without cysts. Eventually, 16 proteins were found to be common to three statistical methods with laminin subunit alpha 2 (LAMA-2) reaching the higher rank by a Support Vector Machine, a binary classification/prediction scheme. ELISA for LAMA-2 validated proteomic results. Thus, using high-throughput technology, our study identified a candidate MSK biomarker possibly employable in future for the early diagnosis of this disease.

2021-05-24 | PXD025744 | Pride

Recruitment of ETS1 to activated accessible regions promotes cilia genes transcriptional program in ciliopathy [RNA-seq]

Project description:Defects in cilia genes that is critical in cilia formation and function can cause complicated ciliopathy syndromes involving multiple organs and tissues; however, the underlying regulatory mechanisms of cilia gene networks in ciliopathy are largely unknown. Here, we define the genome-wide redistribution of chromatin accessibilities and extensive divergence of cilia genes expression programs happened in ciliopathy. Mechanistically, the distinct ciliopathy-activated accessible regions (CAAs) are characterized to positively regulate robust changes of flanking cilia genes, which are a key transcriptional feature of cilia required for the response to developmental signals. Moreover, the single transcriptional factors, ETS1, can be recruited to CAAs thus prominently reconstructing chromatin accessibility in ciliopathy. CAAs collapse driven by ETS1 suppression subsequently cause defective cilia formation and impaired developmental signal transduction, which eventually develops ciliopathy phenotypes of short fins and pericardium edema in larval fishes. Therefore, our results depicted a dynamic landscape of chromatin accessibility in ciliopathy, and uncover an insightful role of ETS1 in controlling global cilia genes transcriptional program by reprogramming widespread chromatin state.

2022-07-28 | GSE209661 | GEO

Recruitment of ETS1 to activated accessible regions promotes cilia genes transcriptional program in ciliopathy [CUT&Tag]

2022-07-28 | GSE209660 | GEO

Recruitment of ETS1 to activated accessible regions promotes cilia genes transcriptional program in ciliopathy [ATAC-seq]

2022-07-28 | GSE209659 | GEO

Recruitment of ETS1 to activated accessible regions promotes cilia genes transcriptional program in ciliopathy [WES]

2023-04-26 | GSE230552 | GEO

maize mms21 seedling total proteome

Project description:Three maize mms21 mutant alleles and their normal siblings were harvested 10 days after planting for total proteome analysis.

2021-10-07 | PXD026853 | Pride