Ontology highlight
ABSTRACT:
PROVIDER: PRJNA379479 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5351560.fastq.gz | Fastqsanger.gz | |||
| SRR5351561.fastq.gz | Fastqsanger.gz | |||
| SRR5351562.fastq.gz | Fastqsanger.gz | |||
| SRR5351563.fastq.gz | Fastqsanger.gz | |||
| SRR5351564.fastq.gz | Fastqsanger.gz |
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Project description:The Chinese forest musk deer (FMD; Moschus berezovskii) is an endangered artiodactyl mammal. Musk secreted by the musk gland of male FMD has extremely high economic and medicinal value. At present, little is known about the development of musk glands and the molecular mechanism of musk secretion. In the present research, using snRNA-seq and snATAC-seq association analysis performed on musk glands of forest musk deer, coupled with several bioinformatics analyses, the dynamic transcriptional cell atlas of musk gland development was revealed and the genes and transcription factors affecting musk secretion were determined. Based on uniform manifold approximation and projection (UMAP) analysis, we identified 12 cell types from musk glands, including two different acinar cells (clusters 0 and 10). In addition, the expression of core target genes and core transcription factors was verified by fluorescence in situ hybridization and immunohistochemistry. Combined with weighted gene co-expression network analysis (WGCNA), we obtained a deeper biological understanding of the relationship between core transcription factors, differentially expressed genes and musk secretion related pathways. This study lays a foundation for improving musk yield and meeting market demand. In the meantime, it also contributes to reducing the hunting and poaching of wild forest musk deer, protecting forest musk deer resources and maintaining ecological balance.
2023-08-31 | GSE182087 | GEO
Project description:Atherosclerosis (AS) is one of the most common diseases in middle-age and elderly population. Lipid metabolism disorder induced foaming of vascular smooth muscle cell (VSMC) is an important pathological process of AS. Mitochondria plays an important role in lipids metabolism. While it is not known whether regulating mitochondrial function can protect ox-LDL induced VSMC foaming via metabolic reprogramming. With ox-LDL induced mouse model of VSMC injury, the injury effect of ox-LDL and the protective effect of mdivi-1, the mitochondrial fission inhibitor on mitochondrial morphology and function of VSMC, and the formation of lipid droplet were observed. With metabonomics and proteomics techniques, the main lipid metabolites and regulation proteins were identified. The results showed that Ox-LDL induced a significant mitochondrial fission and fragmentation of VSMC, and mitochondrial function disorder along with lipid deposition and foaming. Mdivi-1 significantly antagonized the damage effect of ox-LDL on mitochondrial morphology and function of VSMC, and blocked the lipid deposition. Metabonomics analysis found 848 different metabolites between ox-LDL and mdivi-1 treatment group, in which the lipid metabolites were the main, and heptadecanoic acid, palmitoleic acid and myristic acid were the critical metabolites changed most. Proteomics results showed that there were 125 differential expressed proteins between ox-LDL and mdivi-1 treatment, acetyl -CoA carboxylase1 and fatty acid synthase were the main differential expressed proteins. This study suggest that Mitochondrial fission plays an important role in VSMC lipid deposition and foaming. Inhibition of mitochondrial fission may effectively fight against ox-LDL induced lipid deposition and foaming of VSMC via improving mitochondrial function and metabolic reprogramming. This finding provides a new insight for prevention and treatment of AS.
2022-10-14 | PXD035671 | Pride
Project description:Bone morphogenic proteins (BMPs) function in virtually all tissues with cell-type specific outcomes. Since there are a relatively small number of BMP receptors this exquisite signaling specificity requires additional molecules to regulate the output of this pathway. We demonstrated that the receptor tyrosine kinase MuSK that is selectively expressed in muscle and plays a critical role in synapse formation and maintenance binds to BMP4 and related BMPs. Since BMPs regulate the transcription of a set of genes, we performed microarrays for wild-type and MuSK null muscle cells to test if MuSK regulates BMP responses in muscle cells. We shought to determine if MuSK regulates BMP responses in muscle cells and if the cell context made any difference in MuSK regulation of BMP pathway. To test this, expression profiles of untreated vs. BMP4-treated undifferentiated myoblast and differentiated myotube cultures were generated for both wild-type and MuSK-null genotypes. All conditions were done in triplicates. In total 24 arrays were analyzed.
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Project description:Myasthenia gravis (MG) is an autoantibody-mediated autoimmune disorder of the neuromuscular junction. Some patients with MG have pathogenic mAbs that recognize muscle-specific tyrosine kinase (MuSK). Patients respond well to CD20-mediated B-cell depletion therapy (BCDT); most achieve complete stable remission. However, relapse often occurs. To further understand the immunomechanisms underlying relapse we sought to study autoantibody-producing B-cells over the course of BCDT. We developed a monomeric fluorescently labelled antigen to enrich for MuSK-specific B-cells, which was validated with a novel Nalm6 cell line engineered to express a human MuSK autoantibody as B-cell receptor. We found that MuSK-specific B-cells are rare within the circulation (<3 per 10 million cells). From two MuSK-specific B-cells isolated from two distinct patients, we generated human recombinant MuSK mAbs. The autoantibodies originated from plasmablasts, used the IgG4 subclass, recognized the Ig1-like domain of MuSK and showed pathogenic capacity using an in vitro AChR clustering assay. Persistent clones of the mAbs were identified through B-cell repertoire tracing. Clonal variants of 2E6 were detected at several timepoints spanning more than five years months and reemerged after BCDT-mediated remission, appearing several months prior to relapse. These results indicate that a reservoir of rare pathogenic MuSK autoantibody-expressing B cell clones survive BCDT, then reemerge prior to manifestation of clinical relapse. This study provides both a mechanistic understanding of MuSK MG relapse and a valuable candidate biomarker for relapse prediction.
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Project description:ARDS-mediated lung transcriptome alterations were identified in forest musk deer. Moreover, multiple transcripts/genes involved in lung development and lung defense responses to bacteria/viruses/fungi in ARDS were filtered out in forest musk deer.
2022-10-19 | GSE191259 | GEO
Project description:Myofiber size regulation is critical in health, disease, and aging. MuSK (muscle-specific kinase) is a BMP (bone morphogenetic protein) co-receptor that promotes and shapes BMP signaling that is expressed at all neuromuscular junctions and is also present extrasynaptically in the slow soleus muscle. To investigate the role of the MuSK-BMP pathway in vivo we generated mice lacking the BMP-binding MuSK Ig3 domain. These ∆Ig3-MuSK mice are viable and fertile with innervation levels comparable to wild type. In 3-month-old mice myofibers are smaller in the slow soleus, but not in the fast TA. Here we use bulk RNA-seq to perform transcriptomic analysis of slow and fast mouse muscle. RNAseq analysis revealed soleus-selective decreases in RNA metabolism and protein synthesis pathways as well as dysregulation of IGF1 pathway components. Moreover, Akt-mTOR signaling is reduced in soleus but not TA. We propose that the MuSK-BMP pathway acts extrasynaptically to maintain myofiber size in slow muscle by promoting protein synthetic pathways including the IGF1-Akt-mTOR signaling. These results reveal a novel mechanism for regulating myofiber size in slow muscle and introduce the MuSK-BMP pathway as a target for promoting muscle growth and combatting atrophy.
2024-01-10 | GSE212352 | GEO
Project description:Humans co-existed and interbred with other hominins which later became extinct. These archaic hominins are known to us only through fossil records and for two cases, genome sequences. Here we engineer Neanderthal and Denisovan sequences into thousands of artificial genes to reconstruct the pre-mRNA processing patterns of these extinct populations. Of the 5,224 alleles tested in this massively parallel splicing reporter assay (MaPSy), we report 969 exonic splicing mutations (ESMs) that correspond to differences in exon recognition between extant and extinct hominins. Using MaPSy splicing variants, predicted splicing variants, and splicing quantitative trait loci, we show that splice-disrupting variants experienced greater purifying selection in anatomically modern humans than in Neanderthals. Adaptively introgressed variants were enriched for moderate effect splicing variants, consistent with positive selection for alternative spliced alleles following introgression. As particularly compelling examples, we characterized a novel tissue-specific alternative splicing variant at the adaptively introgressed innate immunity gene TLR1, as well as a novel Neanderthal introgressed alternative splicing variant in the gene HSPG2 that encodes perlecan. We further identified potentially pathogenic splicing variants found only in Neanderthals and Denisovans in genes related to sperm maturation and immunity. Finally, we found splicing variants that may contribute to variation among modern humans in total bilirubin, balding, hemoglobin levels, and lung capacity. Our findings provide novel insights into natural selection acting on splicing in human evolution and demonstrate how functional assays can be used to identify candidate causal variants underlying differences in gene regulation and phenotype.
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Project description:Bone morphogenic proteins (BMPs) function in virtually all tissues with cell-type specific outcomes. Since there are a relatively small number of BMP receptors this exquisite signaling specificity requires additional molecules to regulate the output of this pathway. We demonstrated that the receptor tyrosine kinase MuSK that is selectively expressed in muscle and plays a critical role in synapse formation and maintenance binds to BMP4 and related BMPs. Since BMPs regulate the transcription of a set of genes, we performed microarrays for wild-type and MuSK null muscle cells to test if MuSK regulates BMP responses in muscle cells.
2015-08-03 | GSE59567 | GEO
Project description:The development of the neuromuscular synapse depends on signaling processes which involve protein phosphorylation as a crucial regulatory event. The receptor tyrosine kinase MuSK is the key signaling molecule at the neuromuscular synapse whose activity is required for the formation of a mature and functional neuromuscular synapse. However, the signaling cascade downstream of MuSK and the regulation of the different components is still poorly understood. Here we present data from a quantitative phosphoproteomics approach to study MuSK-dependent processes. Muscle cells were stimulated with the heparansulfate proteoglycan agrin, which activates MuSK and downstream signaling events. To get an insight into the signaling dynamics we used three different time points (unstimulated, 15 min, 60 min and 4 hrs).
2014-06-05 | PXD000878 | Pride