Single-oocyte mRNA sequencing reveals that AMH-overexpression alters oocyte gene expression
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1214764 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32093000.fastq.gz | Fastqsanger.gz | |||
| SRR32093001.fastq.gz | Fastqsanger.gz | |||
| SRR32093002.fastq.gz | Fastqsanger.gz | |||
| SRR32093003.fastq.gz | Fastqsanger.gz | |||
| SRR32093004.fastq.gz | Fastqsanger.gz |
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Project description:Research Question: Does over-expression of AMH lead to changes in oocyte gene expression in mice? Design: Naturally ovulated oocytes were dissected from the oviduct of wild-type, and AMH-overexpressing (Thy1.2-AMHTg/0) mice and single oocytes underwent transcriptome sequencing (n=11 and n=10, respectively). Results: Oocytes from Thy1.2-AMHTg/0 females displayed 39 significantly expressed differentially expressed genes (DEGs) compared to wild-type mouse oocytes. The most prominent gene expression changes were a 70-fold increase in Rpsa3a, a 22-fold increase in Hormad1 and a 5.6-fold increases in Fnip2 in the oocytes from Thy1.2-AMHTg/0 mice. Gene ontology analysis indicated that among the DEGs, the most enriched pathways were mitochondrial genes and DNA repair genes. Conclusions: These data show that overexpression of AMH, through its actions on granulosa cells, can lead to changes in the expression of specific genes in mouse oocytes.
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Project description:The current study was designed to investigate the actions of Anti-MM-CM-<llerian Hormone (AMH) on primordial follicle assembly. Ovarian primordial follicles develop from the breakdown of oocyte nests during fetal development for the human and immediately after birth in rodents. AMH was found to inhibit primordial follicle assembly, decrease the initial primordial follicle pool size and promote the persistence of small oocyte nests in a rat ovarian organ culture. The AMH expression was found to be primarily in the stromal tissue of the ovaries at this period of development, suggesting a stromal-epithelial cell interaction for primordial follicle assembly. AMH was found to promote alterations in the ovarian transcriptome during primordial follicle assembly with over 200 genes with altered expression. A gene network was identified suggesting a potential central role for the Fgf2/Nudt6 antisense transcript in the follicle assembly process. A number of signal transduction pathways are regulated by AMH actions on the ovarian transcriptome, in particular the transforming growth factor M-bM-^@M-^S beta (TGFM-CM-^_) signaling process. AMH is the first hormone/protein shown to have an inhibitory action on primordial follicle assembly. Due to the critical role of the primordial follicle pool size for female reproduction, elucidation of the factors, such as AMH, that regulate the assembly process will provide insights into potential therapeutics to manipulate the pool size and female reproduction. We used microarrays to determine genes expressed differentially between control and AMH (Anti-MM-CM-<llerian Hormone) treated P0 ovary RNA samples from 3 control groups are compared to 3 AMH treated ovary groups
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Project description:The current study was designed to investigate the actions of Anti-Müllerian Hormone (AMH) on primordial follicle assembly. Ovarian primordial follicles develop from the breakdown of oocyte nests during fetal development for the human and immediately after birth in rodents. AMH was found to inhibit primordial follicle assembly, decrease the initial primordial follicle pool size and promote the persistence of small oocyte nests in a rat ovarian organ culture. The AMH expression was found to be primarily in the stromal tissue of the ovaries at this period of development, suggesting a stromal-epithelial cell interaction for primordial follicle assembly. AMH was found to promote alterations in the ovarian transcriptome during primordial follicle assembly with over 200 genes with altered expression. A gene network was identified suggesting a potential central role for the Fgf2/Nudt6 antisense transcript in the follicle assembly process. A number of signal transduction pathways are regulated by AMH actions on the ovarian transcriptome, in particular the transforming growth factor – beta (TGFß) signaling process. AMH is the first hormone/protein shown to have an inhibitory action on primordial follicle assembly. Due to the critical role of the primordial follicle pool size for female reproduction, elucidation of the factors, such as AMH, that regulate the assembly process will provide insights into potential therapeutics to manipulate the pool size and female reproduction. We used microarrays to determine genes expressed differentially between control and AMH (Anti-Müllerian Hormone) treated P0 ovary
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Project description:Fsh-mediated regulation of zebrafish spermatogenesis includes modulating the expression of testicular growth factors. Here, we study if and how two Sertoli cell-derived Fsh-responsive growth factors, anti-Müllerian hormone (Amh; inhibiting steroidogenesis and germ cell differentiation) and insulin-like growth factor 3 (Igf3; stimulating germ cell differentiation), cooperate in regulating spermatogonial development. In dose response and time course experiments with primary testis tissue cultures, Fsh upregulated igf3 transcript levels and down-regulated amh transcript levels; igf3 transcript levels were more rapidly up-regulated and responded to lower Fsh concentrations than were required to decrease amh mRNA levels. Quantification of immunoreactive Amh and Igf3 on testis sections showed that Fsh increased slightly Igf3 staining but decreased clearly Amh staining. Studying the direct interaction of the two growth factors showed that Amh compromised Igf3-stimulated proliferation of type A (both undifferentiated [Aund] and differentiating [Adiff]) spermatogonia. Also the proliferation of those Sertoli cells associated with Aund spermatogonia was reduced by Amh. To gain more insight into how Amh inhibits germ cell development, we examined Amh-induced changes in testicular gene expression by RNA sequencing. The majority (69%) of the differentially expressed genes was down-regulated by Amh, including several stimulators of spermatogenesis, such as igf3 and steroidogenesis-related genes. At the same time, Amh increased the expression of inhibitory signals, such as inha and id3, or facilitated prostaglandin E2 (PGE2) signaling. Evaluating one of the potentially inhibitory signals, we indeed found in tissue culture experiments that PGE2 promoted the accumulation of Aund at the expense of Adiff and B spermatogonia. Our data suggest that an important aspect of Fsh bioactivity in stimulating spermatogenesis is implemented by restricting the different inhibitory effects of Amh and by counterbalancing them with stimulatory signals, such as Igf3
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