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Mus musculus

ABSTRACT: Retinoic acid signaling is dispensable for somatic development and function of the developing ovary

PROVIDER: PRJNA374406 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5247410_1.fastq.gz	Fastqsanger.gz
	SRR5247410_2.fastq.gz	Fastqsanger.gz
	SRR5247411_1.fastq.gz	Fastqsanger.gz
	SRR5247411_2.fastq.gz	Fastqsanger.gz
	SRR5247402_1.fastq.gz	Fastqsanger.gz

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Project description:Retinoic acid signaling is essential for HSC development

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Retinoic acid signaling is dispensable for somatic development and function of the developing ovary

Project description:Retinoic acid (RA) is a potent inducer of cell differentiation and plays an essential role in sex-specific germ cell development in the mammalian gonad. RA is essential for male gametogenesis and hence fertility. However, RA can also disrupt sexual cell fate in somatic cells of the testis, promoting transdifferentiation of male Sertoli cells to female granulosa-like cells when the male sexual regulator Dmrt1 is absent. The feminizing ability of RA in the somatic testis suggests that RA might normally play a role in somatic cell differentiation or cell fate maintenance in the ovary. To test for this possibility we disrupted RA signaling in somatic cells of the early fetal ovary using three genetic strategies and one pharmaceutical approach. We found that deleting all three RA receptors (RARs) in the XX somatic gonad at the time of sex determination did not significantly affect ovarian differentiation, follicle development, or female fertility. Transcriptome analysis of adult triple mutant ovaries revealed remarkably little effect on gene expression in the absence of somatic RAR function. Likewise, deletion of three RA synthesis enzymes (Aldha1-3) at the time of sex determination did not masculinize the ovary. A dominant-negative RAR transgene altered granulosa cell proliferation, likely due to interference with a non-RA signaling pathway, but did not affect granulosa cell specification or fertility. Finally, culture of fetal XX gonads with an RAR antagonist blocked germ cell meiotic initiation but did not disrupt sex-biased gene expression. We conclude that RA signaling, although crucial in the ovary for meiotic initiation, is not required for granulosa cell specification, differentiation, or reproductive function.

2017-03-16 | GSE94802 | GEO

Short-term in vitro culture of rat fetal testes with all-trans retinoic acid

Project description:Analysis of gene expression and alternate splicing effects of retinoic acid treatment on gestational day 15 rat fetal testes in whole testis culture Retinoic acid exposure in cultured fetal testis has previously been demonstrated to have significant effects on the histology of the fetal testis in multiple species, as well as to alter the meiotic states of germ cells. However, previous experiments have not analyzed the mechanisms by which retinoic acid exposure leads to altered tubulogenesis and loss of seminiferous cord structure. This experiment demonstrated that retinoic acid exposure activated signaling pathways that promote the ovary development program and oppose normal testis development in mid-gestational rat fetal testes.

2017-09-26 | GSE101634 | GEO

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Project description:Transcription Factor TLX1 Controls Retinoic Acid Signaling to Ensure Spleen Development [ChIP-Seq]

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Project description:Transcription Factor TLX1 Controls Retinoic Acid Signaling to Ensure Spleen Development [Microarray Expression]

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PROP1-Dependent Retinoic Acid Signaling Regulates Developmental Pituitary Morphogenesis and Hormone Expression

Project description:Dietary vitamin A is metabolized into bioactive retinoic acid in vivo and regulates the development of many embryonic tissues. Retinoic acid signaling is active in the oral ectoderm-derived tissues of the neuroendocrine system, but its role there has not yet been fully explored. We show here that retinoic acid signaling is active during pituitary organogenesis and dependent on the pituitary transcription factor Prop1. Prop1-mutant mice show reduced expression of the aldehyde dehydrogenase gene Aldh1a2, which metabolizes the vitamin A-intermediate retinaldehyde into retinoic acid. In order to elucidate the specific function of RA signaling during neuroendocrine development, we studied a conditional deletion of Aldh1a2 and a dominant-negative mouse model of inhibited retinoic acid signaling during pituitary organogenesis. These models partially phenocopy Prop1-mutant mice by exhibiting embryonic pituitary dysmorphology and reduced hormone expression, especially of thyroid-stimulating hormone. These findings establish the critical role of retinoic acid in embryonic pituitary stem cell progression to differentiated hormone cells and raise the question of gene-by-environment interactions as contributors to pituitary development and disease.

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Project description:Hedgehog signaling is dispensable for adult hematopoietic stem cell function

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Mus musculus

Project description:Retinoic acid signaling in thymic epithelial cells regulates thymopoiesis

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Dynamic upregulation of retinoic acid RA signal in the early postnatal murine heart promotes cardiomyocyte cell cycle exit and maturation [PRVCMs_Cont-ATRA]

Project description:Retinoic acid (RA), the major active metabolite of vitamin A, is essential for organogenesis, homeostasis, and tissue morphogenesis. Despite the importance of RA signaling in embryo heart development, little is known about its function in the early postnatal period. For a comprehensive transcriptional evaluation of the effect of RA signaling on neonatal cardiomyocyte cell cycle arrest and maturation, we performed RNA-seq analysis of cultured perinatal cardiomyocytes treated with all-trans retinoic acid (ATRA) in vitro.

2024-08-13 | GSE263096 | GEO

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Project description:Transcriptomic analysis of murine embryos lacking endogenous retinoic acid signaling

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