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Mus musculus strain:GV oocytes wild type (C57BL/6N), GV Dnmt knockout mice (hybrid genetic background, 129SvJae?C57BL/6N)

ABSTRACT: Mouse oocyte methylome

PROVIDER: PRJDB101 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	DRR002141.fastq.gz	Fastqsanger.gz
	DRR002142.fastq.gz	Fastqsanger.gz
	DRR002143.fastq.gz	Fastqsanger.gz
	DRR002144.fastq.gz	Fastqsanger.gz
	DRR002145.fastq.gz	Fastqsanger.gz

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GluD1 knockout mice with a pure C57BL/6N background show impaired fear memory, social interaction, and enhanced depressive-like behavior.

Project description:The GluD1 gene is associated with susceptibility for schizophrenia, autism, depression, and bipolar disorder. However, the function of GluD1 and how it is involved in these conditions remain elusive. In this study, we generated a Grid1 gene-knockout (GluD1-KO) mouse line with a pure C57BL/6N genetic background and performed several behavioral analyses. Compared to a control group, GluD1-KO mice showed no significant anxiety-related behavioral differences, evaluated using behavior in an open field, elevated plus maze, a light-dark transition test, the resident-intruder test of aggression and sensorimotor gating evaluated by the prepulse inhibition test. However, GluD1-KO mice showed (1) higher locomotor activity in the open field, (2) decreased sociability and social novelty preference in the three-chambered social interaction test, (3) impaired memory in contextual, but not cued fear conditioning tests, and (4) enhanced depressive-like behavior in a forced swim test. Pharmacological studies revealed that enhanced depressive-like behavior in GluD1-KO mice was restored by the serotonin reuptake inhibitors imipramine and fluoxetine, but not the norepinephrine transporter inhibitor desipramine. In addition, biochemical analysis revealed no significant difference in protein expression levels, such as other glutamate receptors in the synaptosome and postsynaptic densities prepared from the frontal cortex and the hippocampus. These results suggest that GluD1 plays critical roles in fear memory, sociability, and depressive-like behavior.

| S-EPMC7032715 | biostudies-literature

Single-cell proteomics in EIF5 knockout mouse GV oocytes at PD21

Project description:Changes in GV phase oocyte proteome after specific knockout of mouse oocytes with ZP3-cre

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Impact of High Salt Diet on Cerebral Vascular Function and Stroke in Tff3-/-/C57BL/6N Knockout and WT (C57BL/6N) Control Mice.

Project description:High salt (HS) dietary intake leads to impaired vascular endothelium-dependent responses to various physiological stimuli, some of which are mediated by arachidonic acid (AA) metabolites. Transgenic Tff3-/- gene knockout mice (Tff3-/-/C57BL/6N) have changes in lipid metabolism which may affect vascular function and outcomes of stroke. We aimed to study the effects of one week of HS diet (4% NaCl) on vascular function and stroke induced by transient occlusion of middle cerebral artery in Tff3-/- and wild type (WT/C57BL/6N) mice. Flow-induced dilation (FID) of carotid artery was reduced in WT-HS mice, but not affected in Tff3-/--HS mice. Nitric oxide (NO) mediated FID. NO production was decreased with HS diet. On the contrary, acetylcholine-induced dilation was significantly decreased in Tff3-/- mice on both diets and WT-HS mice. HS intake and Tff3 gene depletion affected the structural components of the vessels. Proteomic analysis revealed a significant effect of Tff3 gene deficiency on HS diet-induced changes in neuronal structural proteins and acute innate immune response proteins' expression and Tff3 depletion, but HS diet did not increase the stroke volume, which is related to proteome modification and upregulation of genes involved mainly in cellular antioxidative defense. In conclusion, Tff3 depletion seems to partially impair vascular function and worsen the outcomes of stroke, which is moderately affected by HS diet.

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Mus musculus strain:C57BL/6N, 129SvJae x C57BL/6N

Project description:Mouse DNA methylome (WBA-seq)

| PRJDB19 | ENA

The landscape of H3K9me2 and CTCF in mice GV oocytes

Project description:During oocyte growth, various epigenetic modifications are gradually established, accompanied by accumulation of large amounts of mRNAs and proteins. However, little is known about the relationship between epigenetic modifications and meiotic progression. Here, by using Gdf9-Cre to achieve oocyte-specific ablation of Ehmt2 (Euchromatic-Histone-Lysine-Methyltransferase 2) from the primordial follicle stage, we found that female mutant mice were infertile. Oocyte-specific knockout of Ehmt2 caused failure of homologous chromosome separation independent of persistently activated SAC during the first meiosis. Further studies revealed that lacking maternal Ehmt2 affected the transcriptional level of Ccnb3, while microinjection of exogenous Ccnb3 mRNA could partly rescue the failure of homologous chromosome segregation. Of particular importance was that EHMT2 regulated ccnb3 transcriptions by regulating CTCF binding near ccnb3 gene body in genome in oocytes. In addition, the mRNA level of Ccnb3 significantly decreased in the follicles microinjected with Ctcf siRNA. Therefore, our findings highlight the novel function of maternal EHMT2 on the metaphase I-to-anaphase I transition in mouse oocytes: regulating the transcription of Ccnb3.

2024-08-22 | GSE182557 | GEO

Single-cell RNA sequencing of Zfp36l2 knock-out and floxed GV mouse oocytes.

Project description:Global transcriptional silencing is a highly conserved evolutionary event central to the transition from the fully differentiated oocyte to the totipotent embryo. Despite its importance in the development of all animals, this pivotal genome-wide event remains poorly understood. Here, we report the unexpected finding that oocyte global transcriptional silencing depends on an mRNA decay activator. Oocyte-specific loss of ZFP36L2—an RNA-binding protein critical for AU-rich element-mediated mRNA decay—prevents oocytes from undergoing global transcriptional silencing. ZFP36L2- deficient oocytes are developmentally incompetent, with defects in maturation and fertilization leading to complete female infertility. Single cell RNA-seq analysis revealed that ZFP36L2 regulates scores of transcription regulators with central roles in chromatin modification and transcription initiation and elongation. This dysregulation resulted in failure to accumulate histone methylation marks associated with the silent, competent state. Our results define a critical role for an oocyte mRNA decay activator in the downregulation of transcription activators, leading to histone methylation, global transcriptional silencing and competence to transition from oocyte to embryo.

2017-09-25 | GSE96638 | GEO

Mus musculus strain:C57BL/6N, C57BL/6J

Project description:Mouse DNA methylome (PBAT)

| PRJDB20 | ENA

Mus musculus strain:C57BL/6N, C57BL/6J

Project description:Mouse DNA methylome (MethylC-seq)

| PRJDB18 | ENA

Microarray data of prepubertal, peripubertal, and adult oocytes, and from GV and MII oocytes matured in vivo or in vitro

Project description:Expression data from prepubertal, peripubertal, and adult derived mouse oocytes, and from germinal vesicle (GV), in vivo matured, and in vitro matured mouse oocytes. Oocytes derived from prepubertal females, or oocytes matured in vitro, are less developmentally competent compared to adult derived, or in vivo matured, oocytes, indicated by decreased embryonic development. One potential mechanism for decreased developmental potetential in prepubertal or in vitro matured oocytes is inadequate or inappropriate RNA degradation during oocyte maturation (progression from GV to MII). To investigate mechanisms involved in establishing oocyte cytoplasmic maturation and developmental competence, Affymetrix GeneChip microarrays were used. Keywords: Oocyte developmental competence

2010-07-12 | GSE12432 | GEO

Mus musculus strain:C57BL/6N

Project description:Mouse PGC DNA methylome (PBAT)

| PRJDB145 | ENA