Ontology highlight
ABSTRACT:
PROVIDER: PRJNA600399 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10870449_1.fastq.gz | Fastqsanger.gz | |||
| SRR10870449_2.fastq.gz | Fastqsanger.gz | |||
| SRR10870450_1.fastq.gz | Fastqsanger.gz | |||
| SRR10870450_2.fastq.gz | Fastqsanger.gz | |||
| SRR10870451_1.fastq.gz | Fastqsanger.gz |
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Project description:Sperm motility is one of the most important indicator for evaluating roosters’ fecundity. However, the molecular regulation underlying chicken sperm motility is not yet clear. MicroRNA (miRNA) plays epigenetic roles in reproduction. In this study, we compared the testicular miRNAs of Beijing-you roosters with high (HS) and low (LS) sperm motility using Solexa sequencing. Length distribution analysis showed that the dominant size of the small RNAs detected in the testis was 24~28 nt. In total, 518 known and 106 novel miRNAs were identified. A number of 23 miRNAs were found differentially expressed (P < 0.05, |log2fold change| ≥ 1) between the HS and LS, including 18 known and five novel miRNAs. Function enrichment of predicted target genes of the differential miRNAs indicated that the differentially expressed miRNAs were involved in the pathways of GnRH signaling, MAPK signaling, and Wnt signaling. The miRNA-gene interaction network revealed two key candidate miRNA-gene pairs that may affect chicken sperm motility viz gga-miR-155/KCNA1 and gga-miR-7480-5p/AHI1. qRCR was also used to further validate their expression. The results here provide deep insight into the expression of miRNA in the testis of chicken and suggest their roles in sperm motility regulation.
2018-01-13 | GSE109141 | GEO
Project description:The male reproductive tract tissue samples were obtained from six 38-wk-old turkeys. The gene expression pattern in turkey testis, epididymis and ductus deferens were determined by high-throughput transcriptome sequencing. The obtained sequence reads were mapped to the turkey genome, and relative expression values were calculated for the analysis of differential expressed genes. Bioinformatics analysis revealed several candidate genes potentially involved in spermatogenesis, spermiogenesis and flagella formation in testis and post-testicular sperm maturation in epididymis and ductus deferens. The achievement of spermatozoa motility during post-testicular maturation were found to be linked with development of flagellum actin filaments and biochemical processes including Ca2+ influx and protein phosphorylation/dephosphorylation. Finally, genes involved in reproductive system development and morphogenesis were identified.
2019-12-21 | GSE142428 | GEO
Project description:The adverse effects of sleep disorders on male fertility are increasingly concerning. In this study, a rat model of chronic sleep restriction (CSR) was established using the modified multiplatform method. The effects of CSR on the fertility of male rats were evaluated first based on sexual behavior. Serum hormones, including testosterone (T), prolactin (PRL), luteinizing hormone (LH) and follicle-stimulating hormone (FSH), and sperm parameters (concentration, viability, motility, deformation rate) were measured, and testicular histology was analysed by hematoxylin and eosin staining. The transcriptional differences between CSR rats and control rats were detected by RNA sequencing (RNA-Seq), and DNA methylation was then detected by bisulfite sequencing. After the differently expressed genes of CSR rats were sequenced and screened, some representative up- and down-regulated genes were randomly sampled to verify the sequencing results by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). Finally, functional annotations were completed, including gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomic (KEGG) pathway analyses. The results showed that the sexual behavior of CSR rats did not change when compared with control group rats. The sperm concentration, viability and motility of the CSR rats decreased significantly, while the sperm malformation rate increased significantly. In the KEGG pathway analysis database, some specific differentially expressed genes were screened, which are involved in metabolic pathways, inflammation-related pathways, the renin-angiotensin system, etc. However, the aforesaid differentially expressed genes in the testes were not related to their DNA methylation status. CSR could significantly reduce the fertility of male rats, and one of its mechanisms occurs by altering gene expression in the testes, which has nothing to do with their DNA methylation. It was suggested that CSR could cause male infertility by significantly altering the testicular transcriptome.
2019-12-16 | GSE141699 | GEO
Project description:Phosphoprotein phosphatase 1 catalytic subunit gamma 2 (PPP1CC2), a PPP1 isoform restricted to testicular germ cells and spermatozoa, is essential for completion of spermatogenesis and highly similar PPP1C isoforms are capable of compensating for the loss of Ppp1cc in every tissue except in testis. In addition, inhibition of the enzymatic activity of PPP1C in spermatozoa stimulates motility. The key to understand the regulation of PPP1CC2 lies in the identification and characterization of its interacting partners. By integrating tissue-specific protein expression and protein-protein interaction data, we identified testis/sperm-enriched/specific PPP1CC complexes and potential key PPP1 interacting proteins (PIPs) for male reproduction. We constructed a testis/sperm-enriched network, analyzed several topological properties and specified the biological/physiological properties of the proteins in the network. Proteins were classified into modules according to their topological features and functional annotations, which clarified the mechanisms underlying testis and sperm function and, more specifically, the role of PPP1CC in spermatogenesis and sperm motility. Previously uncharacterized PIPs, such as AKAP4, were identified based on analyses of the interaction network. The PPP1CC2 interaction with AKAP4 in human sperm was also validated by different methods and the complex was proposed as potential targets for male contraception due to its significance in spermatozoa motility.
2022-02-28 | PXD002888 | Pride
Project description:We characterized the seminal plasma proteome of eight Beijing-you (BJY) chickens, an indigenous chicken breed in China, differ in sperm motility.
2020-04-24 | PXD016220 | Pride
Project description:STUDY QUESTION: What are the causative genetic variants in patients with male infertility due to severe sperm motility disorders?
SUMMARY ANSWER: We identified high confidence disease-causing variants in multiple genes previously associated with severe sperm motility disorders in 9 out of 21 patients (43%). We also identified variants in novel candidate genes in 8 additional patients (38%).
WHAT IS KNOWN ALREADY: Severe sperm motility disorders are a form of male infertility characterised by vital, but immotile sperm often in combination with a spectrum of structural abnormalities of the sperm flagellum. Examples of this spectrum of disorders include dysplasia of the fibrous sheath / multiple morphological abnormalities of the sperm flagella (DFS-MMAF) and severe forms of asthenozoospermia associated to non-specific structural defects. These disorders frequently recur in families and may include chronic respiratory disease. As such, genetic causes are suspected and many genes have recently been reported. Currently, depending on the clinical sub-categorisation, up to 50% of causality in patients with severe sperm motility disorders can be explained by pathogenic variants in at least 21 known genes.
STUDY DESIGN, SIZE, DURATION: We performed exome sequencing in patients with severe sperm motility disorders from two different clinics, aiming to identify the underlying genetic defects and establishing a diagnostic yield in both.
PARTICIPANTS/MATERIALS, SETTING, METHOD: Two groups of infertile men, one from Argentina (n= 9) and one from Australia (n=12), with clinically defined sperm motility disorders were included. All patients in the Argentine cohort were diagnosed with DFS-MMAF, based on transmission electron microscopy. Exome sequencing was performed in all 21 patients and variants with an allele frequency of <1% in the gnomAD population were prioritised and interpreted.
MAIN RESULTS AND ROLE OF CHANCE: In 9/21 patients (43%), we identified pathogenic variants in known sperm motility disorder genes: CFAP43 (3 patients); CFAP44 (2 patients), QRICH2 (2 patients), DNAH1 (1 patient) and DNAH6 (1 patient). The diagnostic rate did not differ markedly between the Argentinian and the Australian cohort (44% and 42%, respectively). Furthermore, we identified patients with variants in the novel candidate sperm motility genes CFAP58, DNAH12, DRC1, MDC1, PACRG, SSPL2C and TPTE2. One patient presented with two possibly damaging variants in four candidate genes and it remains unclear which variants were responsible for the severe sperm motility defect in this patient.
LIMITATIONS, REASONS FOR CAUTION: In this study, we described patients with potential bi-allelic variants in known and novel candidate genes for severe sperm motility disorders. Due to unavailability of parental DNA, we have not assessed de novo or maternally inherited dominant variants and could not phase the mutations to establish in all cases that the mutations occur on both alleles.
WIDER IMPLICATIONS OF THE FINDINGS: Our results confirm an important role for five known genes for sperm motility and we demonstrate that exome sequencing is an effective method to diagnose patients with severe sperm motility defects (9/21 diagnosed; 43%). Furthermore, our analysis revealed seven novel candidate genes for severe sperm motility disorders. Genome-wide sequencing of additional patient cohorts and re-analysis of exome data of currently unsolved cases may reveal additional variants in these novel candidate genes.
| EGAS00001005018 | EGA
Project description:BACKGROUND: In previous studies using candidate gene approaches, low sperm count (oligospermia) has been associated with altered sperm mRNA content and DNA methylation in both imprinted and non-imprinted genes. We performed a genome-wide analysis of sperm DNA methylation and mRNA content to test for associations with sperm function. METHODS AND RESULTS: Sperm DNA and mRNA were isolated from 21 men with a range of semen parameters presenting to a tertiary male reproductive health clinic. DNA methylation was measured with the Illumina Infinium array at 27,000 CpG loci. Unsupervised clustering of methylation data differentiated the 21 sperm samples by their motility values. Recursively partitioned mixture modeling (RPMM) of methylation data resulted in four distinct methylation profiles that were significantly associated with sperm motility (P=0.01). Linear models of microarray analysis (LIMMA) was performed based on motility and identified 9,189 CpG loci with significantly altered methylation (Q<0.05) in the low motility samples, with many loci located in genes associated with subfertility and epigenetic regulation. In the low motility samples, the majority of disrupted CpG loci (80%) were hypomethylated. Of the aberrantly methylated CpGs, 194 were associated with imprinted genes almost equally distributed into hypermethylated (predominantly paternally expressed) and hypomethylated (predominantly maternally expressed) groups. Sperm mRNA was measured with the Human Gene 1.0 ST Affymetrix GeneChip Array. LIMMA analysis based on motility identified 20 candidate transcripts as differentially expressed in low motility sperm, including HDAC1 (NCBI 3065), SIRT3 (NCBI 23410), and DNMT3A (NCBI 1788). Altered expression of these epigenetic regulatory genes was associated with RPMM DNA methylation class. CONCLUSIONS: Using integrative genome-wide approaches to study epigenetic and gene expression patterns in human sperm we identified CpG methylation profiles and mRNA alterations associated with low sperm motility, and that low motility sperm may have aberrant genome-wide hypomethylation due to excess HDAC1 activity. See "summary" above
2011-06-02 | E-GEOD-26881 | biostudies-arrayexpress