Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Tsga8 is required for spermatid morphogenesis and male fertility in mice

ABSTRACT: Tsga8 is required for spermatid morphogenesis and male fertility in mice

PROVIDER: PRJNA619065 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11458773.fastq.gz	Fastqsanger.gz
	SRR11458774.fastq.gz	Fastqsanger.gz
	SRR11458775.fastq.gz	Fastqsanger.gz
	SRR11458776.fastq.gz	Fastqsanger.gz
	SRR11458777.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 14

Similar Datasets

Tsga8 is required for spermatid morphogenesis and male fertility in mice

Project description:During spermatogenesis, intricate gene expression is coordinately regulated by epigenetic modifiers, which are required for differentiation of spermatogonial stem cells (SSCs) contained among undifferentiated spermatogonia. We previously found that KMT2B conveys H3K4me3 at bivalent and monovalent promoters in undifferentiated spermatogonia. Because these genes are expressed late in spermatogenesis or during embryogenesis, we expect that many of them are potentially programmed by KMT2B for future expression. Here, we show that one of the genes targeted by KMT2B, Tsga8, plays an essential role in spermatid morphogenesis. Loss of Tsga8 in mice leads to male infertility associated with abnormal chromosomal distribution in round spermatids, malformation of elongating spermatid heads and spermiation failure. Tsga8 depletion leads to dysregulation of thousands of genes, including the X chromosome genes that are reactivated in spermatids, and insufficient nuclear condensation accompanied by reductions of TNP1 and PRM1, key factors for histone-to-protamine transition. Intracytoplasmic sperm injection (ICSI) of spermatids rescued the infertility phenotype, suggesting competency of the spermatid genome for fertilization. Thus, Tsga8 is a KMT2B target that is vitally necessary for spermiogenesis and fertility.

2021-04-16 | GSE147805 | GEO

NAT10-mediated N4-Acetylcytidine is Required for Spermatogenesis and Male Fertility

Project description:NAT10-mediated N4-Acetylcytidine is Required for Spermatogenesis and Male Fertility

| PRJNA789775 | ENA

RNF20 is required for male fertility through H2B ubiquitination in Sertoli cells

Project description:RNF20 is required for male fertility through H2B ubiquitination in Sertoli cells

| PRJNA934381 | ENA

The evolutionarily conserved gene Arrdc5 is required for male fertility in mice

Project description:The evolutionarily conserved gene Arrdc5 is required for male fertility in mice

| PRJNA849507 | ENA

DOT1L promotes spermatid differentiation by regulating expression of genes required for histone-to-protamine replacement

Project description:Unique chromatin remodeling factors orchestrate dramatic changes in nuclear morphology during differentiation of the mature sperm head. A critical step in this process is histone-to-protamine exchange, which must be executed correctly to avoid sperm DNA damage, embryonic lethality, and male sterility. Here, we define an essential role for the histone methyltransferase DOT1L in the histone-to-protamine transition. We show that DOT1L is abundantly expressed in meiotic and postmeiotic germ cells and that methylation of histone H3 lysine 79 (H3K79), the modification catalyzed by DOT1L, is enriched in developing spermatids in the initial stages of histone replacement. Elongating spermatids lacking DOT1L fail to fully replace histones and exhibit aberrant protamine recruitment, resulting in deformed sperm heads and male sterility. Loss of DOT1L results in transcriptional dysregulation coinciding with the onset of histone replacement and affecting genes required for histone-to-protamine exchange. DOT1L also deposits H3K79me2 and promotes accumulation of elongating RNA Polymerase II at the testis-specific bromodomain gene Brdt. Together, our results indicate that DOT1L is an important mediator of transcription during spermatid differentiation and an indispensable regulator of male fertility.

2023-03-22 | GSE217931 | GEO

Impact of anti-tumor necrosis factors antibodies treatment on fertility of inflammatory bowel diseases male patients

Project description:Primary objectives: To assess the impact of antiTNF agents on the male inflammatory bowel diseases patients` fertility Primary outcomes:- semen quality and quantity, inclusive sperm chromatine structure analysis prior and during anti-TNF therapy- time to conception

| 2525194 | ecrin-mdr-crc

GIV/Girdin Regulates Spatiotemporal Signaling during Sperm Capacitation and is Required for Male Fertility

Project description:GIV/Girdin Regulates Spatiotemporal Signaling during Sperm Capacitation and is Required for Male Fertility

| PRJNA720623 | ENA

TMEM232 is required for the formation of sperm flagellum and male fertility in mice

Project description:TMEM232 is required for the formation of sperm flagellum and male fertility in mice

| PRJNA1119455 | ENA

Deficiency in the multicopy Sycp3-like X-linked genes Slx and Slxl1 causes major defects in spermatid differentiation

Project description:The gene Sly is present in multiple copies on the mouse Y chromosome and encodes a protein that is required for the epigenetic regulation of postmeiotic sex chromosome expression. The X chromosome carries two multicopy genes related to Sly: Slx and Slxl1. Here we investigate the role of Slx/Slxl1 using transgenically-delivered small interfering RNAs to disrupt their function. We show that Slx and Slxl1 are important for normal sperm differentiation and male fertility. Slx/Slxl1 deficiency leads to delay in spermatid elongation and sperm release. A high proportion of delayed spermatids are eliminated via apoptosis, with a consequent reduced sperm count. The remaining spermatozoa are abnormal with impaired motility and fertilizing abilities. Microarray analyses reveal that Slx/Slxl1 deficiency affects the metabolic processes occurring in the spermatid cytoplasm but does not lead to a global perturbation of sex chromosome expression; this is in contrast with the effect of Sly deficiency which leads to an up-regulation of X and Y chromosome genes. Total RNA isolated from separated round spermatids of young adult males (8 weeks postpartum) with shSLX or shSLY targeted knockdown, compared to age- and strain-matched controls.

2011-05-11 | E-GEOD-29197 | biostudies-arrayexpress

Drosophila Testis Proteome - Stage-specific testes proteomics of Drosophila melanogaster identifies essential proteins for male fertility

Project description:Spermiogenesis in Drosophila melanogaster is a highly conserved process and essential for male fertility. In this haploid phase of spermatogenesis, motile sperm are assembled from round cells, flagella are assembled, and needle-shaped nuclei with highly compacted genomes are formed. We aimed at identifying proteins relevant for the maturation phase from spermatids to sperm. As transcription takes place mainly in spermatocytes, and transcripts with relevance for post-meiotic sperm development are translationally repressed for days, we comparatively analysed the prote-ome of larval testes (stages before meiotic divisions), of testes of 1–2-day-old pupae (meiotic and early spermatid stages) and adult flies (late spermatids and sperm). We identified 6677 pro-teins, with 422 solely detected in larval testes, 623 in pupal testes and 634 in adult testes. We analysed a few so far uncharacterized proteins with repect to stage specific expression and im-portance for male fertility. For example, Mst84B (gene CG1988), a very basic cysteine- and lysine-rich nuclear protein, was present in the phase of transition from a histone-based to a pro-tamine-based chromatin structure. CG6332 encodes d-Theg, which is related to the mouse tHEG and human THEG proteins. Mutants of d-Theg lacked sperm in the seminal vesicles and were sterile. The identification of numerous predicted proteins underscores the high potential of pro-teome analysis for future analyses of spermatogenesis.

2019-02-01 | PXD010627 | 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