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Molecular Characterization of a Partial Masculinization in Embryonic Ovaries Grafted into Male Nude Mice

ABSTRACT: The fetal ovarian grafts under the kidney capsule of adult male mice undergo a partial sex-reversal showing ectopic SOX9-positive Sertoli cell-like cells around 15-20 days post-transplantation. However, the molecular bases of such masculinization of fetal ovaries in the paternal environment were unclear. We examined the temporal changes of the gene expression profiles of the grafted fetal ovaries during the partial masculinizing process in the male nude mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE88797 | GEO | 2019/02/04

REPOSITORIES: GEO

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Mus musculus

Project description:Molecular Characterization of a Partial Masculinization in Embryonic Ovaries Grafted into Male Nude Mice

| PRJNA348671 | ENA

Molecular and genetic characterization of partial masculinization in embryonic ovaries grafted into male nude mice.

Project description:In most of mammalian embryos, gonadal sex differentiation occurs inside the maternal uterus before birth. In several fetal ovarian grafting experiments using male host mice, an experimental switch from the maternal intrauterine to male-host environment gradually induces partial masculinization of the grafted ovaries even under the wild-type genotype. However, either host-derived factors causing or molecular basis underlying this masculinization of the fetal ovaries are not clear. Here, we demonstrate that ectopic appearance of SOX9-positive Sertoli cell-like cells in grafted ovaries was mediated by the testosterone derived from the male host. Neither Sox8 nor Amh activity in the ovarian tissues is essential for such ectopic appearance of SOX9-positive cells. The transcriptome analyses of the grafted ovaries during this masculinization process showed early downregulation of pro-ovarian genes such as Irx3, Nr0b1/Dax1, Emx2, and Fez1/Lzts1 by days 7-10 post-transplantation, and subsequent upregulation of several pro-testis genes, such as Bhlhe40, Egr1/2, Nr4a2, and Zc3h12c by day 20, leading to a partial sex reversal with altered expression profiles in one-third of the total numbers of the sex-dimorphic pre-granulosa and Sertoli cell-specific genes at 12.5 dpc. Our data imply that the paternal testosterone exposure is partially responsible for the sex-reversal expression profiles of certain pro-ovarian and pro-testis genes in the fetal ovaries in a temporally dependent manner.

| S-EPMC6402656 | biostudies-literature

RUNX1 safeguards the identity of the fetal ovary through an interplay with FOXL2

Project description:We discovered that expression of the transcription factor RUNX1 is enriched in the fetal ovary in various vertebrate species. In the mouse, RUNX1 marks the supporting cell lineage and becomes granulosa cell-specific as the gonads differentiate. To understand the function of Runx1 during fetal development of the ovary, we ablated Runx1 specifically in the somatic cell lineage of the fetal ovaries using Sf1-Cre . We compared ovarian differentiation in wild type, Runx1 and Foxl2 single knockouts, and Runx1/Foxl2 double knockout ovaries. Transcriptome comparisons of newborn ovaries revealed that loss of Runx1 or Foxl2 affected a similar set of genes: 41% of the genes affected by the loss of Runx1 were also changed by the loss of Foxl2. Despite these transcriptomic changes, granulosa cell identity was maintained during fetal life in both Runx1 or Foxl2 single knockout ovaries. However, the combined loss of Runx1/Foxl2 resulted in masculinization of the ovaries during fetal life. To further characterize the impacts of the combined loss of Runx1 and Foxl2 on ovarian differentiation, we compared the transcriptome of Runx1/Foxl2 DKO newborn ovaries with the transcriptomes of control, Runx1, or Foxl2 single KO ovaries.

2019-07-17 | GSE129038 | GEO

Identification and characterization of novel and conserved microRNAs in self-grafted and grafted watermelon by high-throughput sequencing

Project description:In this study, Solexa sequencing technology has been used to discover small RNA populations of self-grafted watermelon and grafted watermelon (bottle gourd and squash were used as rootstocks). A total of 11,458,476, 11,614,094 and 9,339,089 raw reads representing 2,957,751, 2,880,328 and 2,964,990 unique sequences were obtained from the scions of self-grafted watermelon and watermelon grafted on-to bottle gourd and squash at two true-leaf stage, respectively. 39 known miRNAs belonging to 30 miRNA families and 80 novel miRNAs were identified in our small RNA dataset. Compared with self-grafted watermelon, 20 (5 known and 15 novel miRNAs) and 51 (21 known miRNAs and 30 novel miRNAs) miRNAs were expressed significantly different with higher abundance or lower abundance in watermelon grafted on to bottle gourd and squash, respectively. The differentially expressed miRNA target various transcriptional factors and other genes which involved in a wide range of biological processes. This study was firstly conducted to identify and compare miRNAs on genome-wide scale in watermelon grafting system. The miRNAs expressed differentially when watermelon was grafted onto different rootstocks suggesting that miRNAs might play an important role in diverse biological and metabolic processes in watermelon and grafting may possibly by changing miRNAs expression to regulate plant growth and response to stresses. The small RNA transcriptomes obtained in this study provided insights into molecular basis of miRNA regulation of genes expressed in self-grafted and grafted watermelon.

2011-10-26 | GSE33209 | GEO

RUNX1 safeguards the identity of the fetal ovary through an interplay with FOXL2

Project description:Sex determination of the gonads begins with fate specification of gonadal supporting cells into either ovarian granulosa cells or testicular Sertoli cells. This process of fate specification hinges on a balance of transcriptional control. We discovered that the transcription factor RUNX1 is enriched in the fetal ovary in rainbow trout, turtle, mouse, and human. In the mouse, RUNX1 marks the supporting cell lineage and becomes granulosa cell-specific as the gonads differentiate. RUNX1 plays complementary/redundant roles with FOXL2 to maintain fetal granulosa cell identity, and combined loss of RUNX1 and FOXL2 results in masculinization of the fetal ovaries. To determine whether interplay between RUNX1 and FOXL2 occurs at the chromatin level, we performed genome-wide analysis of RUNX1 chromatin occupancy in E14.5 ovaries. The top de novo motif identified in RUNX1 ChIP-seq matched the RUNX motif. We found that RUNX1 chromatin occupancy was partially overlapping with FOXL2 chromatin occupancy in fetal ovaries.

2019-04-02 | GSE128767 | GEO

Identification and characterization of novel and conserved microRNAs in self-grafted and grafted watermelon by high-throughput sequencing

2011-10-26 | E-GEOD-33209 | biostudies-arrayexpress

Total RNA sequencing of progenies of Col-0 grafted on msh1; Col-0 grafted on dcl2,3,4,msh1; Col-0 grafted on Col-0 in Arabidopsis [msh1_graft_leaf_RNA-seq]

Project description:Col-0 floral stem was grafted on the msh1 mutant (Col-0/msh1); on the dcl2,3,4,msh1 quadruple mutant (Col-0/dcl2,3,4,msh1); on Col-0 (Col-0/Col-0). Seeds were collected from the grafted Col-0 scion after grafts were established. Seed coming from the graft then were grown on the peat mix, leaf tissue was collected at the bolting and used for the total RNA sequencing.

2020-09-20 | GSE152565 | GEO

Treatment of C3H/HeJ grafted mice with baricitinib [topical]

Project description:The C3H/HeJ grafted model of alopecia areata was used to determine the efficacy of systemic baricitinib at preventing alopecia or treating established disease. The efficacy of topical baricitinib at treating established alopecia in the C3H/HeJ grafted model was also assessed. Microarrays were performed on skin RNA at week 0 and week 12 after starting treatment in all models.

2015-05-01 | GSE61554 | GEO

Treatment of C3H/HeJ grafted mice with baricitinib [systemic]

2015-05-01 | GSE61552 | GEO

Treatment of C3H/HeJ grafted mice with baricitinib [prevention]

2015-05-01 | GSE61551 | GEO