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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

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			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

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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

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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

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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

Revealing RNA poly(A) tail dynamics during spermiogenesis and its function to support male fertility [dRNA-seq_mutants]

Project description:TENT5C is a terminal nucleotidyltransferase with mRNA polyadenylation activity, required for the fastening of the flagella and the head of the sperm. However, TENT5C’s role in shaping the poly(A) tail of the elongating spermatid transcriptome remains limited. Here we show that the poly(A) polymerase activity of TENT5C is required for fertility and spermiogenesis: male mice expressing catalytically inactive TENT5C (Tent5cdCat/dCat) are sterile and produce headless spermatozoa phenocopying TENT5C-deficient animals. We found that the transcript encoding for the structural proteins SMCP and ODF1 are directly targeted by TENT5C. We propose a model in which TENT5C secures the fastening of the flagella to the head of the sperm by targeting ODF1 in elongating spermatids.

2025-03-20 | GSE290699 | GEO

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

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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

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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

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RBM5 is a male germ cell splicing factor and is required for spermatid differentiation and male fertility.

Project description:Alternative splicing of precursor messenger RNA (pre-mRNA) is common in mammalian cells and enables the production of multiple gene products from a single gene, thus increasing transcriptome and proteome diversity. Disturbance of splicing regulation is associated with many human diseases; however, key splicing factors that control tissue-specific alternative splicing remain largely undefined. In an unbiased genetic screen for essential male fertility genes in the mouse, we identified the RNA binding protein RBM5 (RNA binding motif 5) as an essential regulator of haploid male germ cell pre-mRNA splicing and fertility. Mice carrying a missense mutation (R263P) in the second RNA recognition motif (RRM) of RBM5 exhibited spermatid differentiation arrest, germ cell sloughing and apoptosis, which ultimately led to azoospermia (no sperm in the ejaculate) and male sterility. Molecular modelling suggested that the R263P mutation resulted in compromised mRNA binding. Within the adult mouse testis, RBM5 localises to somatic and germ cells including spermatogonia, spermatocytes and round spermatids. Through the use of RNA pull down coupled with microarrays, we identified 11 round spermatid-expressed mRNAs as putative RBM5 targets. Importantly, the R263P mutation affected pre-mRNA splicing and resulted in a shift in the isoform ratios, or the production of novel spliced transcripts, of most targets. Microarray analysis of isolated round spermatids suggests that altered splicing of RBM5 target pre-mRNAs affected expression of genes in several pathways, including those implicated in germ cell adhesion, spermatid head shaping, and acrosome and tail formation. In summary, our findings reveal a critical role for RBM5 as a pre-mRNA splicing regulator in round spermatids and male fertility. Our findings also suggest that the second RRM of RBM5 is pivotal for appropriate pre-mRNA splicing.

| S-EPMC3723494 | biostudies-literature

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