Single cell RNAseq of mouse E12.5 fetal ovarian somatic cells
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ABSTRACT:
PROVIDER: PRJNA998546 | ENA |
REPOSITORIES: ENA
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Project description:From fish to human, FOXL2 is considered one of the most conserved markers of ovarian granulosa cell identity. To determine if the sole expression of FOXL2 can determine ovarian differentiation, we created a mouse model that allows the conditional expression of FOXL2. Rosa26-CAG-LSL-Foxl2 mice were crossed to Sf1-Cre mice to induce the expression of FOXL2 in the SF1+ somatic cells of the fetal gonads.When FOXL2 was induced in the somatic cells of the undifferentiated testis, the Sertoli cells and consequently the other cell lineages composing the fetal gonads were feminized, resulting in a partial testis-to-ovary sex reversal We created a mouse genetic model that conditionaly express FOXL2 in the somatic cells of the fetal gonads. All embryos used in this study resulted from the crossing between Rosa26-CAG-LSL-Foxl2+/f and Sf1-cre+/Tg mice. XX and XY fetal gonads were collected at embryonic day E14.5. This microarray analysis led to the identification of the genes misregulated upon ectopic induction of FOXL2 in the fetal testis, and showed that FOXL2 expression resulted in feminization of both somatic and germ cells of the fetal gonad.
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Project description:In mammal, female reproductive health is largely related to fetal ovarian development, along with tight coordination of transcriptional and metabolic regulations, as well as cell-cell communications. Mice is an ideal modal for the understanding of network mechanism in this process, thus providing essential information on the diagnosis and therapy of female reproductive diseases, as well as on oogenesis in vitro. To plot the landscape of mouse fetal ovarian development, STRT-seq was applied for ovarian cells isolated from E11.5 to E18.5 female gonads using Blimp1-mVenus and Stella-ECFP (BVSC) mice. Based on the expression patterns of well-known marker genes, 9 germ cell clusters and 8 somatic cell clusters were annotated, presenting a continuous distribution across fetal ovarian development. To summarize, we constructed a systematic cell-fate transition of mouse female fetal ovarian cells at single-cell resolution, including stage-specifically activated TFs, cellular metabolism pathway, and cell–cell communication network in ovarian microenvironment.
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Project description:We performed RNA-seq on testicular somatic cells from fetal activin A-deficient mice (Inhba KO) and wildtype littermates at embryonic ages E13.5 and E15.5. Activin A deficiency predominantly affects the Sertoli cell transcriptome. New candidate targets include Minar1, Sel1l3, Vnn1, Sfrp4, Masp1, Nell1, Tthy1 and Prss12. Importantly, the testosterone (T) biosynthetic enzymes present in fetal Sertoli cells, Hsd17b1 and Hsd17b3, were identified as activin-responsive. Activin-deficient testes contained elevated androstenedione (A4), displayed an Inhba gene dose-dependent A4/T ratio, and contained 11-keto androgens.
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