Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Dact1/2 modifies noncanonical Wnt signaling and calpain 8 expression to regulate convergent extension and craniofacial development

ABSTRACT: dact1/2 modifies noncanonical Wnt signaling and calpain 8 expression to regulate convergent extension and craniofacial development

PROVIDER: PRJNA1003061 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR25557904.fastq.gz	Fastqsanger.gz
	SRR25557905.fastq.gz	Fastqsanger.gz
	SRR25557906.fastq.gz	Fastqsanger.gz
	SRR25557907.fastq.gz	Fastqsanger.gz
	SRR25557908.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

dact1/2 modifies noncanonical Wnt signaling and calpain 8 expression to regulate convergent extension and craniofacial development

Project description:Wnt signaling plays a fundamental role in the initial patterning and development of the embryo, including in the regulation of convergent extension during gastrulation and the establishment of the dorsal axis. Further, Wnt signaling is a crucial regulator of craniofacial morphogenesis. The relationship between early embryo patterning and craniofacial outcomes warrants further study. The adapter proteins Dact1 and Dact2 modulate the Wnt signaling pathway through binding to Disheveled, however, the distinct roles of Dact1 and Dact2 during embryogenesis remain to be fully elucidated. In this study, we investigated the spatiotemporal gene expression patterns of dact1 and dact2 during zebrafish embryogenesis, revealing both shared and unique domains of expression. We found that both dact1 and dact2 contribute to axis extension, with compound mutants exhibiting a similar convergent extension defect and craniofacial phenotype to the wnt11f2/slb mutant. Utilizing single-cell RNAseq and gpc4-/- zebrafish, a convergent extension mutant with an opposite craniofacial phenotype, we identified dact1/2 specific roles during early development. Using this subtractive approach, we discovered a novel role for dact1/2 in regulating the mRNA expression of the classical calpain, capn8, suggesting a previously unappreciated role of calcium-dependent proteolysis during embryogenesis. Taken together, our findings highlight the distinct and overlapping roles of dact1 and dact2 in embryonic craniofacial development, providing new insights into the multifaceted regulation of Wnt signaling.

2024-09-04 | GSE240264 | GEO

<i>dact1/2</i> modifies noncanonical Wnt signaling and <i>calpain 8</i> expression to regulate convergent extension and craniofacial development.

Project description:Wnt signaling plays a crucial role in the early embryonic patterning and development, to regulate convergent extension during gastrulation and the establishment of the dorsal axis. Further, Wnt signaling is a crucial regulator of craniofacial morphogenesis. The adapter proteins Dact1 and Dact2 modulate the Wnt signaling pathway through binding to Disheveled, however, the distinct relative functions of Dact1 and Dact2 during embryogenesis remain unclear. We found that dact1 and dact2 genes have dynamic spatiotemporal expression domains that are reciprocal to one another and to wnt11f2l, that suggest distinct functions during zebrafish embryogenesis. We found that both dact1 and dact2 contribute to axis extension, with compound mutants exhibiting a similar convergent extension defect and craniofacial phenotype to the wnt11f2 mutant. Utilizing single-cell RNAseq and gpc4 mutant that disrupts noncanonical Wnt signaling, we identified dact1/2 specific roles during early development. Comparative whole transcriptome analysis between wildtype, gpc4 and dact1/2 mutants revealed a novel role for dact1/2 in regulating the mRNA expression of the classical calpain capn8. Over-expression of capn8 phenocopies dact1/2 craniofacial dysmorphology. These results identify a previously unappreciated role of capn8 and calcium-dependent proteolysis during embryogenesis. Taken together, our findings highlight the distinct and overlapping roles of dact1 and dact2 in embryonic craniofacial development, providing new insights into the multifaceted regulation of Wnt signaling.

| S-EPMC10659360 | biostudies-literature

DEK1 calpain overexpression

Project description:Aim: To understand the role of DEK1 in Arabidopsis development. Background: DEK1 has an essential role during embryogenesis and is involved in the maintenance of the epidermis. Tissues: Comparison of wild-type and ADEK1 calpain-overexpressing line. 9 samples were used in this experiment.

2009-12-09 | E-GEOD-19268 | biostudies-arrayexpress

DEK1 calpain overexpression

2009-12-10 | GSE19268 | GEO

The proteasome subunit psmb1 is essential for craniofacial cartilage maturation and morphogenesis

Project description:Craniofacial dysmorphisms are among the most common birth defects. Proteasome mutations frequently result in craniofacial dysmorphisms including lower jaw malformations; however, the underlying mechanisms are unknown. Here we use a zebrafish proteasome subunit beta 1 (psmb1) mutant to define the cellular mechanisms underlying proteasome mutation-induced craniofacial dysmorphisms. psmb1 mutants exhibit a flattened ceratohyal and smaller Meckel’s and palatoquadrate cartilages. Ceratohyal flattening is a result of failed chondrocyte convergent extension, accompanied by reduced numbers of chondrocytes in the lower jaw due to defects in chondrocyte differentiation. Morphogenesis of craniofacial muscles and tendons is similarly perturbed. psmb1 mutants lack the hyohyal muscles and craniofacial tendons are shortened and disorganized. We additionally identify a critical period for proteasome function in craniofacial development, specifically during chondrocyte and muscle differentiation. psmb1 overexpression in sox10+ cells of mutant embryos rescued both cartilage and tendon phenotypes but induced only a partial rescue of the muscle phenotype, indicating that psmb1 is required in both tissue-autonomous and non-autonomous fashions during craniofacial development. Overall, our work demonstrates that psmb1 is required for craniofacial cartilage, tendon, and muscle differentiation and morphogenesis.

2024-07-12 | GSE243072 | GEO

Mitochondrial dysfunction and consequences in calpain-3-deficient muscle

Project description:Microarray profiling to determine muscle cell-specific consequences of calpain-3 deficiency

2022-03-28 | GSE199621 | GEO

Mitochondrial dysfunction and consequences in calpain-3-deficient muscle myoblasts

Project description:Microarray profiling to determine muscle cell-specific consequences of calpain-3 deficiency

2022-03-28 | GSE199620 | GEO

Altered Ca+2 homeostasis induces Calpain-Cathepsin axis activation in sCJD.

Project description:Sporadic Creutzfeldt-Jakob disease (sCJD) is the most prevalent form of human prion disease and it is characterized by the presence of neuronal loss, spongiform degeneration, chronic inflammation and the accumulation of misfolded and pathogenic prion protein (PrPSc). The molecular mechanisms underlying these alterations are largely unknown, but the presence of intracellular neuronal calcium (Ca+2) overload, a general feature in models of prion diseases, is suggested to play a key role in prion pathogenesis. Here we describe the presence of massive regulation of Ca+2 responsive genes in sCJD brain tissue, accompanied by two Ca+2-dependent processes: endoplasmic reticulum stress and the activation of the cysteine proteases Calpains 1/2. Pathogenic Calpain activation in sCJD is linked to the cleavage of their cellular substrates, impaired autophagy and lysosomal damage, which is partially reversed by Calpain inhibition in a cellular prion model. Calpain 1 treatment enhances seeding activity of PrPSc in a prion conversion assay. Neuronal lysosomal impairment caused by Calpain over activation leads to the release of the lysosomal protease Cathepsin S that in sCJD mainly localises in axons. Additionally, massive Cathepsin S overexpression is detected in microglial cells. Alterations in Ca+2 homeostasis and activation of Calpain-Cathepsin axis already occur at pre-clinical stages of the disease as detected in a humanized sCJD mouse model. Altogether our work indicates that unbalanced Calpain-Cathepsin activation is a relevant contributor to the pathogenesis of sCJD at multiple molecular levels and a potential target for therapeutic intervention.

2017-05-15 | GSE90977 | GEO

mRNA expression profile in murine bone marrow-derived macrophages that were isolated from calpain-6 wild-type and deficient mice

Project description:Transcriptional profiling of calpain-6-deficient murine bone marrow-derived macrophages comparing with calpain-6 wild-type macrophages. Total RNA was extracted from the pooled cells. Two-condition experiment, wild-type macrophages vs. calpain-6-deficiennt macrophages. The cells were derived from four mice, and were pooled for analysis.

2016-06-29 | E-GEOD-83815 | biostudies-arrayexpress

FLNc Calpain GluC SRM Analysis

Project description:Human filamin C (FLNc) is a target of the protease calpain at Y2625. To confirm the dependency of calpain cleavage from FLNc phosphorylation at position S2623/S2624 by PKCa, FLNc was overexpressed in HEK293 cells and cells were treated with PMA to stimulated kinase activity, with Gö6976 to inhibit kinase activity or mock-treated with DMSO. Subsequently, recombinant calpain-1 and GluC were used and the resulting peptide TVTSSSSRGSSY was monitored by SRM analyses.

2017-01-02 | PXD005097 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data