scholarly journals Male-specific expression ofAldh1a1in mouse and chicken fetal testes: Implications for retinoid balance in gonad development

2009 ◽  
Vol 238 (8) ◽  
pp. 2073-2080 ◽  
Author(s):  
Josephine Bowles ◽  
Chun-Wei Feng ◽  
Deon Knight ◽  
Craig A. Smith ◽  
Kelly N. Roeszler ◽  
...  
Keyword(s):  
Gonad Development ◽  
Specific Expression ◽  
Male Specific

scholarly journals A male-specific role for SOX9 in vertebrate sex determination

Development ◽  
1996 ◽  
Vol 122 (9) ◽  
pp. 2813-2822 ◽  
Author(s):  
J. Kent ◽  
S.C. Wheatley ◽  
J.E. Andrews ◽  
A.H. Sinclair ◽  
P. Koopman
Keyword(s):  
Sex Determination ◽  
In Situ Hybridisation ◽  
Gonad Development ◽  
Adult Life ◽  
Cell Lineage ◽  
Polyclonal Antiserum ◽  
Cell Type Specificity ◽  
Sox9 Expression ◽  
Specific Expression ◽  
Male Specific

Mutation analyses of patients with campomelic dysplasia, a bone dysmorphology and XY sex reversal syndrome, indicate that the SRY-related gene SOX9 is involved in both skeletal development and sex determination. To clarify the role SOX9 plays in vertebrate sex determination, we have investigated its expression during gonad development in mouse and chicken embryos. In the mouse, high levels of Sox9 mRNA were found in male (XY) but not female (XX) genital ridges, and were localised to the sex cords of the developing testis. Purified fetal germ cells lacked Sox9 expression, indicating that Sox9 expression is specific to the Sertoli cell lineage. Sex specificity of SOX9 protein expression was confirmed using a polyclonal antiserum. The timing and cell-type specificity of Sox9 expression suggests that Sox9 may be directly regulated by SRY. Male-specific expression of cSOX9 mRNA during the sex determination period was also observed in chicken genital ridges. The conservation of sexually dimorphic expression in two vertebrate classes which have significant differences in their sex determination mechanisms, points to a fundamental role for SOX9 in testis determination in vertebrates. Sox9 expression was maintained in the mouse testis during fetal and adult life, but no expression was seen at any stage by in situ hybridisation in the developing ovary. Male-specific expression was also observed in the cells surrounding the Mullerian ducts and in the epididymis, and expression in both sexes was detected in the developing collecting ducts of the metanephric kidney. These results suggest that SOX9 may have a wider role in the development of the genitourinary system.

scholarly journals Unconventional Translation Initiation Factor EIF2A is required for Drosophila spermatogenesis

2021 ◽  
Author(s):  
David D Lowe ◽  
Denise Montell
Keyword(s):  
Mammalian Cells ◽  
Translation Initiation Factor ◽  
Initiation Factor ◽  
Male Sterile ◽  
Specific Expression ◽  
Transposon Insertion ◽  
Stress Related Genes ◽  
Male Specific ◽  
Multicellular Organisms

The eukaryotic initiation factor EIF2A is an unconventional translation factor required for initiation of protein synthesis from non-AUG codons from a variety of transcripts, including oncogenes and stress related genes in mammalian cells. Its function in multicellular organisms has not been reported. Here, we identify and characterize mutant alleles of the CG7414 gene, which encodes the Drosophila EIF2A ortholog. We identified that CG7414 undergoes sex-specific splicing that regulates its male-specific expression. We characterized a Mi{Mic} transposon insertion that disrupts the coding regions of all predicted isoforms and is a genetic null allele, and a PBac transposon insertion into an intron, which is a hypomorph. The Mi{Mic} allele is homozygous lethal, while the viable progeny from the hypomorphic PiggyBac allele are male sterile and female fertile. In dEIF2A mutant flies, sperm failed to individualize due to defects in F-actin cones and failure to form and maintain cystic bulges, ultimately leading to sterility. These results demonstrate that EIF2A is essential in a multicellular organism, both for normal development and spermatogenesis, and provide an entree into the elucidation of the role of EIF2A and unconventional translation in vivo.

scholarly journals Loss of Mafb and Maf distorts myeloid cell ratios and disrupts fetal mouse testis vascularization and organogenesis

2021 ◽  
Author(s):  
Shu-Yun Li ◽  
Xiaowei Gu ◽  
Anna Heinrich ◽  
Emily G. Hurley ◽  
Blanche Capel ◽  
...  
Keyword(s):  
Sertoli Cells ◽  
Immune Cell ◽  
Gonad Development ◽  
Myeloid Cell ◽  
Cell Types ◽  
Double Knockout ◽  
Fetal Mouse ◽  
Testis Differentiation ◽  
Male Specific ◽  
Testis Cord

AbstractTestis differentiation is initiated when Sry in pre-Sertoli cells directs the gonad toward a male-specific fate. Sertoli cells are essential for testis development, but cell types within the interstitial compartment, such as immune and endothelial cells, are also critical for organ formation. Our previous work implicated macrophages in fetal testis morphogenesis, but little is known about genes underlying immune cell development during organogenesis. Here we examine the role of the immune-associated genes Mafb and Maf in mouse fetal gonad development, and we demonstrate that deletion of these genes leads to aberrant hematopoiesis manifested by supernumerary gonadal monocytes. Mafb;Maf double knockout embryos underwent initial gonadal sex determination normally, but exhibited testicular hypervascularization, testis cord formation defects, Leydig cell deficit, and a reduced number of germ cells. In general, Mafb and Maf alone were dispensable for gonad development; however, when both genes were deleted, we observed significant defects in testicular morphogenesis, indicating that Mafb and Maf work redundantly during testis differentiation. These results demonstrate previously unappreciated roles for Mafb and Maf in immune and vascular development and highlight the importance of interstitial cells in gonadal differentiation.Summary statementDeletion of Mafb and Maf genes leads to supernumerary monocytes in fetal mouse gonads, resulting in vascular, morphogenetic, and differentiation defects during testicular organogenesis.

scholarly journals Vertebrate sex determination: many means to an end

Reproduction ◽  
2002 ◽  
pp. 447-457 ◽  
Author(s):  
BC Morrish ◽  
AH Sinclair
Keyword(s):  
Sex Determination ◽  
Regulatory Network ◽  
Gonadal Dysgenesis ◽  
Developmental Process ◽  
Gonad Development ◽  
Complex Interplay ◽  
Specific Expression ◽  
Sex Specificity ◽  
Bipotential Gonad

The differentiation of a testis or ovary from a bipotential gonadal primordium is a developmental process common to mammals, birds and reptiles. Since the discovery of SRY, the Y-linked testis-determining gene in mammals, extensive efforts have failed to find its orthologue in other vertebrates, indicating evolutionary plasticity in the switch that triggers sex determination. Several other genes are known to be important for sex determination in mammals, such as SOX9, AMH, WT1, SF1, DAX1 and DMRT1. Analyses of these genes in humans with gonadal dysgenesis, mouse models and using in vitro cell culture assays have revealed that sex determination results from a complex interplay between the genes in this network. All of these genes are conserved in other vertebrates, such as chickens and alligators, and show gonad-specific expression in these species during the period of sex determination. Intriguingly, the sequence, sex specificity and timing of expression of some of these genes during sex determination differ among species. This finding indicates that the interplay between genes in the regulatory network leading to gonad development differs between vertebrates. However, despite this, the development of a testis or ovary from a bipotential gonad is remarkably similar across vertebrates.

Drosophila Male-Specific Lethal 2 Protein Controls Sex-Specific Expression of the roX Genes

Genetics ◽  
2004 ◽  
Vol 166 (4) ◽  
pp. 1825-1832 ◽  
Author(s):  
Barbara P Rattner ◽  
Victoria H Meller
Keyword(s):  
Gene Expression ◽  
Transcriptional Regulation ◽  
X Chromosome ◽  
Specific Expression ◽  
Linked Gene ◽  
Male And Female ◽  
Male Specific Lethal ◽  
Msl Complex ◽  
Male Specific ◽  
Rox Rna

Abstract The MSL complex of Drosophila upregulates transcription of the male X chromosome, equalizing male and female X-linked gene expression. Five male-specific lethal proteins and at least one of the two noncoding roX RNAs are essential for this process. The roX RNAs are required for the localization of MSL complexes to the X chromosome. Although the mechanisms directing targeting remain speculative, the ratio of MSL protein to roX RNA influences localization of the complex. We examine the transcriptional regulation of the roX genes and show that MSL2 controls male-specific roX expression in the absence of any other MSL protein. We propose that this mechanism maintains a stable MSL/roX ratio that is favorable for localization of the complex to the X chromosome.

scholarly journals Mouse Gonad Development in the Absence of the Pro-Ovary Factor WNT4 and the Pro-Testis Factor SOX9

Cells ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 1103
Author(s):  
Furong Tang ◽  
Nainoa Richardson ◽  
Audrey Albina ◽  
Marie-Christine Chaboissier ◽  
Aitana Perea-Gomez
Keyword(s):  
Granulosa Cells ◽  
Gonad Development ◽  
Supporting Cell ◽  
Gonadal Development ◽  
Ovary Development ◽  
Double Knockout ◽  
Cell Identity ◽  
Knockout Mouse Model ◽  
Steroidogenic Cell ◽  
Male Specific

The transcription factors SRY and SOX9 and RSPO1/WNT4/β-Catenin signaling act as antagonistic pathways to drive testis and ovary development respectively, from a common gonadal primordium in mouse embryos. In this work, we took advantage of a double knockout mouse model to study gonadal development when Sox9 and Wnt4 are both mutated. We show that the XX gonad mutant for Wnt4 or for both Wnt4 and Sox9 develop as ovotestes, demonstrating that ectopic SOX9 function is not required for the partial female-to-male sex reversal caused by a Wnt4 mutation. Sox9 deletion in XY gonads leads to ovarian development accompanied by ectopic WNT/β-catenin signaling. In XY Sox9 mutant gonads, SRY-positive supporting precursors adopt a female-like identity and develop as pre-granulosa-like cells. This phenotype cannot be fully prevented by the deletion of Wnt4 or Rspo1, indicating that SOX9 is required for the early determination of the male supporting cell identity independently of repressing RSPO1/WNT4/β-Catenin signaling. However, in XY Sox9 Wnt4 double mutant gonads, pre-granulosa cells are not maintained, as they prematurely differentiate as mature granulosa cells and then trans-differentiate into Sertoli-like cells. Together, our results reveal the dynamics of the specific and independent actions of SOX9 and WNT4 during gonadal differentiation: SOX9 is essential in the testis for early specification of male-supporting cells whereas WNT4 functions in the ovary to maintain female-supporting cell identity and inhibit male-specific vascular and steroidogenic cell differentiation.

Conservation of male-specific expression of novel phosphoprotein phosphatases in Drosophila

2010 ◽  
Vol 220 (3-4) ◽  
pp. 123-128 ◽  
Author(s):  
Csaba Ádám ◽  
László Henn ◽  
Márton Miskei ◽  
Miklós Erdélyi ◽  
Péter Friedrich ◽  
...  
Keyword(s):  
Specific Expression ◽  
Phosphoprotein Phosphatases ◽  
Male Specific

scholarly journals Y disruption, autosomal hypomethylation and poor male lung cancer survival

2020 ◽  
Author(s):  
Saffron A.G. Willis-Owen ◽  
Clara Domingo Sabugo ◽  
Elizabeth Starren ◽  
Liming Liang ◽  
Maxim B. Freidin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Y Chromosome ◽  
Cancer Survival ◽  
Dna Hypomethylation ◽  
Specific Expression ◽  
Pulmonary Tissue ◽  
Risk Of Death ◽  
Increased Risk ◽  
Discovery Dataset ◽  
Male Specific

SummaryLung cancer is the most frequent cause of cancer death worldwide1. It is male predominant and for reasons that are unknown also associated with significantly worse outcomes in men2. Here we compared gene co-expression networks in affected and unaffected pulmonary tissue derived from 126 patients with Stage IA–IV lung cancer. We observed marked degradation of a sex-associated gene co-expression network in tumour tissue. The disturbance was linked to fractional loss of the Y chromosome and was detected in 28% of male tumours in the discovery dataset and 27% of male tumours in a 123 sample replication dataset. Depression of Y chromosome expression was accompanied by extensive autosomal DNA hypomethylation. The male specific H3K4 demethylase, KDM5D, was identified as an apex hub within this co-expression network. Male patients exhibiting relative tumour KDM5D deficiency had an increased risk of death in the discovery dataset (Hazard Ratio [HR] 3.80, 95% CI 1.40 – 10.3, P=0.009) and in an independent sample of 1,100 male lung tumours (HR 1.67, 95% CI 1.4-2.0, P=1.2⨯10−10). Our findings identify tumour-specific weakening of male-specific expression, in particular deficiency of KDM5D, as a common replicable prognostic marker and credible mechanism underlying sex disparity in cancer.

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