Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Longfin causes cis-ectopic expression of the kcnh2a ether-a-go-go K+ channel to autonomously prolong fin outgrowth

ABSTRACT: longfin causes cis-ectopic expression of the kcnh2a ether-a-go-go K+ channel to autonomously prolong fin outgrowth

PROVIDER: PRJNA565225 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10106416.fastq.gz	Fastqsanger.gz
	SRR10106417.fastq.gz	Fastqsanger.gz
	SRR10106418.fastq.gz	Fastqsanger.gz
	SRR10106419.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

longfin causes cis-ectopic expression of the kcnh2a ether-a-go-go K+ channel to autonomously prolong fin outgrowth.

Project description:Organs stop growing to achieve a characteristic size and shape in scale with the body of an animal. Likewise, regenerating organs sense injury extents to instruct appropriate replacement growth. Fish fins exemplify both phenomena through their tremendous diversity of form and remarkably robust regeneration. The classic zebrafish mutant longfint2 develops and regenerates dramatically elongated fins and underlying ray skeleton. We show longfint2 chromosome 2 overexpresses the ether-a-go-go-related voltage-gated potassium channel kcnh2a. Genetic disruption of kcnh2a in cis rescues longfint2, indicating longfint2 is a regulatory kcnh2a allele. We find longfint2 fin overgrowth originates from prolonged outgrowth periods by showing Kcnh2a chemical inhibition during late stage regeneration fully suppresses overgrowth. Cell transplantations demonstrate longfint2-ectopic kcnh2a acts tissue autonomously within the fin intra-ray mesenchymal lineage. Temporal inhibition of the Ca2+-dependent phosphatase calcineurin indicates it likewise entirely acts late in regeneration to attenuate fin outgrowth. Epistasis experiments suggest longfint2-expressed Kcnh2a inhibits calcineurin output to supersede growth cessation signals. We conclude ion signaling within the growth-determining mesenchyme lineage controls fin size by tuning outgrowth periods rather than altering positional information or cell-level growth potency.

| S-EPMC8217709 | biostudies-literature

longfin causes cis-ectopic expression of the kcnh2a ether-a-go-go K+ channel to autonomously prolong fin outgrowth

Project description:longfin mutant zebrafish grow and regenerate abnormally long fins. We sought to determine misregulated transcripts in the distal regenerate of 96 hpa caudal fins that could contribute to fin overgrowth or be the longfin causal gene.

2020-09-12 | GSE137352 | GEO

eag

Project description:Drosophila melanogaster eag, ether a go-go, is differentially expressed in 3 experiment(s);

| FBgn0000535 | ExpressionAtlas

eag

Project description:Drosophila melanogaster eag, ether a go-go, is expressed in 3 baseline experiment(s);

| FBgn0000535 | ExpressionAtlas

Project description:Oryza sativa Japonica Group GO, Glutamate carboxypeptidase, Hormone homeostasis, Regulation of developmental processe, is differentially expressed in 20 experiment(s);

| Os03g0790600 | ExpressionAtlas

Project description:Oryza sativa Japonica Group GO, Glutamate carboxypeptidase, Hormone homeostasis, Regulation of developmental processe, is expressed in 7 baseline experiment(s);

| Os03g0790600 | ExpressionAtlas

Biosynthesis of membrane-spanning ether lipids in Thermotoga maritima

Project description:This study was conducted to identify the genes involved in the synthesis of membrane-spanning ether lipids in Thermotoga maritima MSB8.

2022-10-26 | GSE211547 | GEO

Endothelial ether lipids link blood vessels to neurodegeneration

Project description:Vascular disease contributes to neurodegeneration, which is associated with decreased blood pressure in older humans. Plasmalogens, ether phospholipids produced by peroxisomes, are decreased in Alzheimer’s disease, Parkinson’s disease and other neurodegenerative disorders. Here we show that endothelium-derived ether phospholipids affect blood pressure, behavior, and neurodegeneration in mice. In young adult mice, inducible endothelial-specific disruption of PexRAP, a peroxisomal enzyme required for ether lipid synthesis, unexpectedly decreased circulating plasmalogens. PexRAP Endothelial KnockOut (PEKO) mice responded normally to hindlimb ischemia but had lower blood pressure and increased plasma renin activity. In PEKO as compared to control mice, tyrosine hydroxylase was decreased in the locus coeruleus, which maintains blood pressure and arousal. PEKO mice moved less, slept more, and had impaired attention to and recall of environmental events as well as mild spatial memory deficits. In PEKO hippocampus, gliosis was increased and a plasmalogen associated with memory was decreased. Despite lower blood pressure, PEKO mice had generally normal homotopic functional connectivity by optical neuroimaging of the cerebral cortex. Decreased GSK3 phosphorylation, a marker of neurodegeneration, was detected in PEKO cerebral cortex. In a co-culture system, PexRAP knockdown in brain endothelial cells decreased GSK3 phosphorylation in co-cultured astrocytes that was rescued by incubation with the ether lipid alkylglycerol. Our findings suggest that the endothelium is a source of complex lipids that confer neuroprotection in mice.

2021-09-10 | PXD024116 | Pride

Go Type 2 Diabetes

Project description:Go Type 2 Diabetes

| PRJNA268369 | ENA

Prolong elevation of prolactin and sex-depnendt regulation of pain chronicity

Project description:Prolong elevation of prolactin sex-dependently regulate pain resolution via inflammatory mechanisms

2024-02-27 | GSE168563 | GEO