Ontology highlight
ABSTRACT:
PROVIDER: PRJNA824792 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18685665_1.fastq.gz | Fastqsanger.gz | |||
| SRR18685665_2.fastq.gz | Fastqsanger.gz | |||
| SRR18685666_1.fastq.gz | Fastqsanger.gz | |||
| SRR18685666_2.fastq.gz | Fastqsanger.gz | |||
| SRR18685667_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:The role of autophagy and metabolism in regulating the pluripotency of stem cells is not well understood. LAMP2A is a key gene in CMA. Here we compared transcriptomic changes in LAMP2A-overexpressed D3 versus control cells, as well as changes in LAMP2A-overexpressed cells with versus without DM-αKG treatment (4mM, 72 hrs). We found that overexpression of LAMP2A leads to decreased expression of genes related to stem cell differentiation, and this can be largely restored by DM-αKG supplement. This study provides a promising link for autophagy, metabolism, and pluripotency of stem cells.
2020-11-08 | GSE144093 | GEO
Project description:Total fertilization failure (TFF) is an important cause of infertility; however, the genetic basis of TFF caused by male factors remain to be clarified. In this study, whole-exome sequencing was firstly used to screen for genetic causes of TFF after intracytoplasmic sperm injection (ICSI), and homozygous variants in the novel gene IQ motif containing N (IQCN) were identified in two affected individuals with abnormal acrosome structure. Then, Iqcn knockout mice were generated by CRISPR-Cas9 technology and showed that the knockout male mice resembled TFF phenotype with oocyte activation failure. Additionally, we found that IQCN regulates the microtubule nucleation during manchette assembly via calmodulin and related calmodulin-binding proteins, which resulted in head deformity with aberrant oocyte activation factor PLCζ. Fortunately, ICSI with assisted oocyte activation can overcome IQCN-associate male infertility. Thus, our study firstly identifies the function of IQCN, highlights the relationship between the manchette assembly and fertilization, and provides a genetic marker and a therapeutic option for male-source TFF.
2022-11-22 | PXD036197 | Pride
Project description:Fam170a deficiency causes male infertility
| PRJNA1180445 | ENA
Project description:Spermatogenesis, an efficient and complex system in male germline development, requires a series of elaborately regulated genetic events in which diploid spermatogonia differentiate into haploid spermatozoa. N6-methyladenosine (m6A) is important for spermatogenesis. ALKBH5 is an m6A eraser, and knockout of ALKBH5 increases the level of total m6A methylation and causes male infertility.
2021-12-13 | GSE186217 | GEO
Project description:Plants do not specify their germline until late in their life cycle. Hence, the plant germline is normally specified from terminally differentiated somatic cells, though the precise mechanism(s) are unknown. We have found that male gametogenesis in maize is associated with the accumulation of distinct 21-nt phased small-interfering RNAs (phasiRNAs) generated by meiosis-associated argonaute (MAGO) proteins. MAGO1 accumulates in the epidermis of pre-meiotic anthers while MAGO2 is found in developing meiocytes. We have found that MAGO proteins are required for meiocyte development as mutants display chromosomal defects and male infertility. Furthermore, we detect the heat stress-induced activation of a distinct class of Long terminal repeat retrotransposons in the male germline of MAGO mutants. Our data suggests that MAGO proteins and the reproductive phasiRNAs play important roles protecting the germline from transposable elements during environmental stress conditions.
2022-01-04 | PXD013891 | Pride
Project description:Proteomic analysis comparing LAMP2A-TGFβtreated group versus Vector-TGFβ 3 treated group in NIH3T3 fibroblast cells to study the effect of LAMP2A overexpression on protein expression changes During Fibroblast Activation.
2024-09-02 | PXD055463 |
Project description:Chaperone-mediated autophagy (CMA) is a homeostatic process essential for the lysosomal degradation of individual proteins. CMA activity directly depends on the levels of LAMP2A, critical receptor at the lysosomal membrane, to which CMA substrate proteins are bound. In glioblastoma (GBM), the most common and aggressive brain cancer in the adulthood, high levels of LAMP2A have been linked to TMZ resistance and tumor-associated pericytes. However, the implication of LAMP2A, and hence CMA, in glioblastoma stem cells (GSCs) remains unknown. In this work, we show that LAMP2A expression is enriched in patient-derived GSC population and its knock-down diminishes GSCs tumorigenic activities. Proteomic and transcriptomic analysis of LAMP2A knocked-down GSCs revealed reduced extracellular matrix (ECM) interaction effectors in both analyses. Moreover, immune system and mitochondrial metabolism related pathways were remarkably deregulated at proteome level, whereas PI3K-AKT and p53 pathways were altered in RNAseq study. Moreover, clinical samples of GBM tissue presented overexpression of LAMP2 and its high levels correlated with advanced glioma grade and poor overall survival. In conclusion, we identified a novel role of CMA directly regulating GSCs activity via multiple pathways at proteome and transcriptome level.
2022-08-02 | PXD029393 | Pride
Project description:Chaperone-mediated autophagy (CMA) is a homeostatic process essential for the lysosomal degradation of individual proteins. CMA activity directly depends on the levels of LAMP2A, critical receptor at the lysosomal membrane, to which CMA substrate proteins are bound. In glioblastoma (GBM), the most common and aggressive brain cancer in the adulthood, high levels of LAMP2A have been linked to TMZ resistance and tumor-associated pericytes. However, the implication of LAMP2A, and hence CMA, in glioblastoma stem cells (GSCs) remains unknown. In this work, we show that LAMP2A expression is enriched in patient-derived GSC population and its knock-down diminishes GSCs tumorigenic activities. Proteomic and transcriptomic analysis of LAMP2A knocked-down GSCs revealed reduced extracellular matrix (ECM) interaction effectors in both analyses. Moreover, immune system and mitochondrial metabolism related pathways were remarkably deregulated at proteome level, whereas PI3K-AKT and p53 pathways were altered in RNAseq study. Moreover, clinical samples of GBM tissue presented overexpression of LAMP2 and its high levels correlated with advanced glioma grade and poor overall survival. In conclusion, we identified a novel role of CMA directly regulating GSCs activity via multiple pathways at proteome and transcriptome level.
2023-03-11 | PXD027069 | Pride
Project description:Autophagy has been implicated to be involved in spermatogenesis and dysfunction of autophagy can lead to male infertility. However, sophisticated transcriptional signatures of autophagic genes in spermatogenesis and its significance remain uncharacterized. Here, we explore the transcriptional profiling of autophagy-related genes across human spermatogenesis in donors with normal fertility and nonobstructive azoospermia (NOA) patient using single-cell RNA sequencing (scRNA-seq) analysis. Core component gene sets in each step of autophagy exhibit stage-specific expression pattern in human spermatogenesis, which is further confirmed by immunostaining; in this context, we further uncover a unique stage-specific enrichment of a cohort autophagy-related genes. Human-to-mouse comparison analysis reveals that this stage-specific expression pattern of autophagy-related genes is highly conserved in mammals and dysregulation of this pattern is associated with human male infertility. Moreover, we discover several stage-specific autophagic genes, which have not been identified to regulate spermatogenesis before. Among these candidate genes, Cst3, an actively expressed autophagic gene in spermatogonia and early spermatocytes, is involved in the regulation of SSC maintenance and subsequent male germ cell development. Downregulation of Cst3 increases the autophagy activity in mouse SSCs, which exerts its roles by regulating the expression of SSC core factors such as Oct4, Id1 and Nanos3. Collectively, our study provides novel insights into the global transcriptional signatures of autophagy-related genes and confirms the role of proper autophagy activity in SSC maintenance and normal spermatogenesis, opening new avenues for further investigation of the correlation between autophagy and spermatogenesis as well as male infertility.
2021-03-24 | GSE157421 | GEO
Project description:Germline development provides the founding cells for spermatogenesis and oogenesis in males and females, respectively. Disrupted germline differentiation or compromised testis development can lead to subfertility or infertility and are strongly associated with testis cancer in humans. In mice, SRY and SOX9 induce expression of a range of genes, including Fgf9, that promote Sertoli cell differentiation and testis development. FGF9 is also thought to promote male germline differentiation but the pathway through which it signals is unknown. As FGFs signal through Mitogen-Activated Protein Kinases (MAPKs) in other tissues, we explored whether FGF9 regulates male germline development through MAPK by inhibiting either FGF or MEK1/2 signalling in fetal testis cultures from embryonic day (E)12.5, immediately after gonadal sex determination and testis cord formation, but prior to male germline commitment. Inhibition of MEK1/2 disrupted mitotic arrest, dysregulated a broad range of male germline development genes and prevented the upregulation of key male germline markers DPPA4 and DNMT3L. In contrast, when FGF signalling was inhibited, the male germline specific transcriptional program and the expression of male germline markers DPPA4 and DNMT3L were unaffected, and the germ cells entered mitotic arrest normally. While male germline development was not disrupted by FGF inhibition, a significant number of genes were commonly altered after 24h of FGF or MEK1/2 inhibition including genes involved in maintenance germline stem cells, Nodal signalling, proliferation, and germline cancer. Together, these data demonstrate a novel and essential role for MEK1/2 signalling in male germline differentiation, but a surprisingly limited role for FGF signalling. Our data strongly indicate that additional ligands act through MEK1/2 to promote male germline differentiation and highlight a need for further mechanistic understanding of male germline development.
2023-11-21 | GSE221458 | GEO