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Abstract
In the early fetal stage, the gonads are bipotent and only later become the ovary or testis, depending on the genetic sex. Despite many studies examining how sex determination occurs from biopotential gonads, the spatial and temporal organization of bipotential gonads and their progenitors is poorly understood. Here, using lineage tracing in mice, we find that the gonads originate from a T+ primitive streak through WT1+ posterior intermediate mesoderm and appear to share origins anteriorly with the adrenal glands and posteriorly with the metanephric mesenchyme. Comparative single-cell transcriptomic analyses in mouse and cynomolgus monkey embryos reveal the convergence of the lineage trajectory and genetic programs accompanying the specification of biopotential gonadal progenitor cells. This process involves sustained expression of epithelial genes and upregulation of mesenchymal genes, thereby conferring an epithelial-mesenchymal hybrid state. Our study provides key resources for understanding early gonadogenesis in mice and primates.
Highlights
The formation of sexual dimorphism involves critical and pervasive events in sexually reproducing animals, thereby ensuring reproductive success
The embryonic gonads initially form as sexually bipotent structures known as genital ridges (GRs), which consist of GR progenitor cells (GPCs)
Descendants of T+ cells contribute to the gonads and related organs in a temporally distinct manner In vertebrate embryos, the body axis progressively extends during development in an anterior to posterior direction, such that new tissues are continuously deposited at the posterior end and are fueled by proliferating T+ progenitors residing in the primitive streak (PS), from which the anterior mesodermal organs exit early and posterior organs exit late (Deschamps and Duboule, 2017; Takasato and Little, 2015)
Summary
The formation of sexual dimorphism involves critical and pervasive events in sexually reproducing animals, thereby ensuring reproductive success. Prior studies have identified key genetic determinants of nascent GR formation, including Gata, Nr5a1, Lhx, Emx, Six1/4, Cbx, and Tcf (Birk et al, 2000; Cui et al, 2004; Fujimoto et al, 2013; Hu et al, 2013; Kusaka et al, 2010; Luo et al, 1994; Miyamoto et al, 1997). Mutations in these genes result in gonadal depletion/hypoplasia. The developmental origin of GATA4+ GPCs and the cellular trajectories leading to GPCs from their progenitors remain unknown
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