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Developmental and sexual dimorphic atlas of the prenatal mouse external genitalia at the single cell level

ABSTRACT: Developmental and sexual dimorphic atlas of the prenatal mouse external genitalia at the single cell level

PROVIDER: PRJNA731171 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15425100.fastq.gz	Fastqsanger.gz
	SRR15425101.fastq.gz	Fastqsanger.gz
	SRR15425102.fastq.gz	Fastqsanger.gz
	SRR15425103.fastq.gz	Fastqsanger.gz
	SRR15425104.fastq.gz	Fastqsanger.gz

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Developmental and sexual dimorphic atlas of the prenatal mouse external genitalia at the single cell level

Project description:Before the onset of sexual differentiation, male and female external genitalia are morphologically indistinguishable. After the onset of sex-specific production of sex steroids by the gonads, the male and female external genitalia differentiate into either a penis or clitoris. Here we use single cell sequencing to investigate the similarities and differences of cell populations in the external genitalia during the critical sexual differentiation window in the mouse embryo. We found the male and female genitalia are largely similar in cell composition and gene expression at the bipotential stage of development. As sexual differentiation ensues, sex steroid-dependent and -independent differences in cell populations arise, leading to dimorphic establishment of the external genitalia.

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Project description:The hindlimb and external genitalia of present-day tetrapods are thought to derive from an ancestral common primordium that evolved to generate a wide diversity of structures adapted for efficient locomotion and mating in the ecological niche conquered by the species. We show that despite long evolutionary distance from the ancestral condition, the early primordium of the mouse external genitalia preserved the capacity to take hindlimb fates. In the absence of Tgfbr1, the pericloacal mesoderm generates an extra pair of hindlimbs at the expense of the external genitalia. It has been shown that the hindlimb and the genital primordia share many of their key regulatory factors. Tgfbr1 controls the response to those factors acting in a pioneer-like mode to modulate the accessibility status of regulatory elements that control the gene regulatory networks leading to the formation of genital or hindlimb structures. Our work uncovers a remarkable tissue plasticity with potential implications in the evolution of the hindlimb/genital area of tetrapods, and identifies a novel mechanism for Tgfbr1 activity that might also contribute to the control of other physiological or pathological processes.

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Developmental and sexual dimorphic atlas of the prenatal mouse external genitalia at the single-cell level.

Project description:Birth defects of the external genitalia are among the most common in the world. Proper formation of the external genitalia requires a highly orchestrated process that involves special cell populations and sexually dimorphic hormone signaling. It is clear what the end result of the sexually dimorphic development is (a penis in the male versus clitoris in the female); however, the cell populations involved in the process remain poorly defined. Here, we used single-cell messenger RNA sequencing in mouse embryos to uncover the dynamic changes in cell populations in the external genitalia during the critical morphogenetic window. We found that overall, male and female external genitalia are largely composed of the same core cellular components. At the bipotential stage of development (embryonic day or E14.5), few differences in cell populational composition exist between male and female. Although similar in cell population composition, genetic differences in key sexual differentiation developmental pathways arise between males and females by the early (E16.5) and late (E18.5) differentiation stages. These differences include discrete cell populations with distinct responsiveness to androgen and estrogen. By late sexual differentiation (E18.5), unique cell populations in both male and female genitalia become apparent and are enriched with androgen- and estrogen-responsive genes, respectively. These data provide insights into the morphogenesis of the external genitalia that could be used to understand diseases associated with defects in the external genitalia.

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