scholarly journals Histone Acetylation and Gene Expression Analysis of Sex lethal Mutants in Drosophila

Genetics ◽  
2000 ◽  
Vol 155 (2) ◽  
pp. 753-763
Author(s):  
Utpal Bhadra ◽  
Manika Pal-Bhadra ◽  
James A Birchler
Keyword(s):  
Gene Expression ◽  
Sex Determination ◽  
Sex Chromosome ◽  
Autosomal Gene ◽  
Single Sex ◽  
Dosage Effects ◽  
Male Specific Lethal ◽  
Sex Lethal ◽  
Male Specific ◽  
Sex Determination Mechanisms

Abstract The evolution of sex determination mechanisms is often accompanied by reduction in dosage of genes on a whole chromosome. Under these circumstances, negatively acting regulatory genes would tend to double the expression of the genome, which produces compensation of the single-sex chromosome and increases autosomal gene expression. Previous work has suggested that to reduce the autosomal expression to the female level, these dosage effects are modified by a chromatin complex specific to males, which sequesters a histone acetylase to the X. The reduced autosomal histone 4 lysine 16 (H4Lys16) acetylation results in lowered autosomal expression, while the higher acetylation on the X is mitigated by the male-specific lethal complex, preventing overexpression. In this report, we examine how mutations in the principal sex determination gene, Sex lethal (Sxl), impact the H4 acetylation and gene expression on both the X and autosomes. When Sxl expression is missing in females, we find that the sequestration occurs concordantly with reductions in autosomal H4Lys16 acetylation and gene expression on the whole. When Sxl is ectopically expressed in SxlM mutant males, the sequestration is disrupted, leading to an increase in autosomal H4Lys16 acetylation and overall gene expression. In both cases we find relatively little effect upon X chromosomal gene expression.

The msl-2 dosage compensation gene of Drosophila encodes a putative DNA-binding protein whose expression is sex specifically regulated by Sex-lethal

Development ◽  
1995 ◽  
Vol 121 (10) ◽  
pp. 3245-3258 ◽  
Author(s):  
G.J. Bashaw ◽  
B.S. Baker
Keyword(s):  
Dna Binding ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Ring Finger ◽  
The Other ◽  
Male Specific Lethal ◽  
Alternatively Spliced ◽  
Sex Lethal ◽  
Specific Regulation ◽  
Male Specific

In Drosophila dosage compensation increases the rate of transcription of the male's X chromosome and depends on four autosomal male-specific lethal genes. We have cloned the msl-2 gene and shown that MSL-2 protein is co-localized with the other three MSL proteins at hundreds of sites along the male polytene X chromosome and that this binding requires the other three MSL proteins. msl-2 encodes a protein with a putative DNA-binding domain: the RING finger. MSL-2 protein is not produced in females and sequences in both the 5′ and 3′ UTRs are important for this sex-specific regulation. Furthermore, msl-2 pre-mRNA is alternatively spliced in a Sex-lethal-dependent fashion in its 5′ UTR.

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 Sex differences in gene expression and proliferation are dependent on the epigenetic modifier HP1γ

2019 ◽  
Author(s):  
Pui-Pik Law ◽  
Ping-Kei Chan ◽  
Kirsten McEwen ◽  
Huihan Zhi ◽  
Bing Liang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Sex Differences ◽  
Sex Chromosome ◽  
Chromosome Complement ◽  
Autosomal Gene ◽  
Sexually Dimorphic ◽  
Heterochromatin Protein 1 ◽  
Epigenetic Modifier ◽  
Early Embryos ◽  
Males And Females

SummarySex differences in growth rate in very early embryos have been recognized in a variety of mammals and attributed to sex-chromosome complement effects as they occur before overt sexual differentiation. We previously found that sex-chromosome complement, rather than sex hormones regulates heterochromatin-mediated silencing of a transgene and autosomal gene expression in mice. Here, sex dimorphism in proliferation was investigated. We confirm that male embryonic fibroblasts proliferate faster than female fibroblasts and show that this proliferation advantage is completely dependent upon heterochromatin protein 1 gamma (HP1γ). To determine whether this sex-regulatory effect of HP1γ was a more general phenomenon, we performed RNA sequencing on MEFs derived from males and females, with or without HP1γ. Strikingly, HP1γ was found to be crucial for regulating nearly all sexually dimorphic autosomal gene expression because deletion of the HP1γ gene in males abolished sex differences in autosomal gene expression. The identification of a key epigenetic modifier as central in defining gene expression differences between males and females has important implications for understanding physiological sex differences and sex bias in disease.

scholarly journals A partially sex-reversed giant kelp sheds light into the mechanisms of sexual differentiation in a UV sexual system

2021 ◽  
Author(s):  
Dieter Mueller ◽  
Enora Gachet ◽  
Olivier Godfroy ◽  
Josselin Gueno ◽  
Guillaume Cossard ◽  
...  
Keyword(s):  
Gene Expression ◽  
Sex Determination ◽  
Sexual Differentiation ◽  
Expression Patterns ◽  
Specific Region ◽  
Autosomal Gene ◽  
Giant Kelp ◽  
Developmental Programs ◽  
Male And Female ◽  
Developmental Program

In UV sexual systems, sex is determined during the haploid phase of the life cycle and males have a V chromosome whereas females have a U chromosome. Previous work in the brown algal model Ectocarpus revealed that the V chromosome has a dominant role in male sex determination and suggested that the female developmental program may occur by default, triggered in the absence of the male master sex determination gene(s). Here, we describe the identification of a genetically male giant kelp strain presenting phenotypic features typical of a female, despite lacking the U-specific region. The conversion to the female developmental program is however incomplete, because gametes of this feminised male are unable to produce the sperm-attracting pheromone lamoxirene. We identify the transcriptomic patterns underlying the male and female specific developmental programs, and reveal the faster evolutionary rates of male-biased genes compared to female-biased and unbiased genes. Moreover, we show that the phenotypic feminisation of the variant strain is associated with both feminisation and de-masculinisation of gene expression patterns. Importantly, the feminisation phenotype was associated with the dramatic downregulation of two V-specific genes including a candidate sex-determining gene on the V-specific region. Our results reveal the transcriptional changes associated with sexual differentiation in a UV system with marked sexual dimorphism, and contribute to disentangling the role of sex-linked genes and autosomal gene expression in the initiation of the male and female developmental programs. Overall, the data presented here imply that the U-specific region in the giant kelp is not required to initiate the female developmental program, but is critical to produce fully functional eggs, arguing against the idea that female is the default sex in this species.

scholarly journals Differential regulation of mouse hippocampal gene expression sex differences by chromosomal content and gonadal sex

2021 ◽  
Author(s):  
Sarah R Ocanas ◽  
Victor A Ansere ◽  
Kyla B Tooley ◽  
Niran Hadad ◽  
Ana J Chucair-Elliott ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Sex Differences ◽  
Sex Chromosomes ◽  
Sex Chromosome ◽  
Chromosome Complement ◽  
Experimental Models ◽  
Ctcf Binding ◽  
Autosomal Gene ◽  
Sex Effects

Sex differences in the brain as they relate to health and disease are often overlooked in experimental models. Many neurological disorders, like Alzheimer's disease (AD), multiple sclerosis (MS), and autism, differ in prevalence between males and females. Sex differences originate either from differential gene expression on sex chromosomes or from hormonal differences, either directly or indirectly. To disentangle the relative contributions of genetic sex (XX v. XY) and gonadal sex (ovaries v. testes) to the regulation of hippocampal sex effects, we use the "sex-reversal" Four Core Genotype (FCG) mouse model which uncouples sex chromosome complement from gonadal sex. Transcriptomic and epigenomic analyses of hippocampal RNA and DNA from ~12 month old FCG mice, reveals differential regulatory effects of sex chromosome content and gonadal sex on X- versus autosome-encoded gene expression and DNA modification patterns. Gene expression and DNA methylation patterns on the X chromosome were driven primarily by sex chromosome content, not gonadal sex. The majority of DNA methylation changes involved hypermethylation in the XX genotypes (as compared to XY) in the CpG context, with the largest differences in CpG islands, promoters, and CTCF binding sites. Autosomal gene expression and DNA modifications demonstrated regulation by sex chromosome complement and gonadal sex. These data demonstrate the importance of sex chromosomes themselves, independent of hormonal status, in regulating hippocampal sex effects. Future studies will need to further interrogate specific CNS cell types, identify the mechanisms by which sex chromosome regulate autosomes, and differentiate organizational from activational hormonal effects.

scholarly journals TWO CLOSELY LINKED MUTATIONS IN DROSOPHILA MELANOGASTER THAT ARE LETHAL TO OPPOSITE SEXES AND INTERACT WITH DAUGHTERLESS

Genetics ◽  
1978 ◽  
Vol 90 (4) ◽  
pp. 683-697
Author(s):  
Thomas W Cline
Keyword(s):  
Maternal Effect ◽  
Spontaneous Mutation ◽  
Dominant Male ◽  
Lethal Effects ◽  
Male Specific Lethal ◽  
Constitutive Mutation ◽  
Sex Lethal ◽  
The Right ◽  
Female Specific ◽  
Male Specific

ABSTRACT A new spontaneous mutation named Sex-lethal, Male-specific #1 (SxlM1) is described that is lethal to males, even in the presence of an Sxl  + duplication. Females homozygous for SxlM1 are fully viable. This dominant, male-specific lethal mutation is on the X chromosome approximately 0.007 map units to the right of a previously isolated female-specific mutation, Female-lethal, here renamed Sex-lethal, Female-specific #1 (SxlF1). SxlM1 and SxlF1 are opposite in nearly every respect, particularly with regard to their interaction with the maternal effect of the autosomal mutation, daughterless (da). Females that are homozygous for da produce defective eggs that cannot support female (XX) development. A single dose of SxlM1 enables daughters to survive this da female-specific lethal maternal effect. A duplication of the Sxl locus weakly mimics this action of SxlM1. In contrast, SxlF1 and a deficiency for Sxl, strongly enhance the female-lethal effects of da. The actions of SxlM1 and SxlF1 are explained by a model in which expression of the Sxl locus is essential for females, lethal for males, and under the control of a product of the da locus. It is suggested that SxlM1 is a constitutive mutation at the Sxl locus.

scholarly journals Identification of the master sex determining gene in Northern pike (Esox lucius) reveals restricted sex chromosome differentiation

2019 ◽  
Author(s):  
Qiaowei Pan ◽  
Romain Feron ◽  
Ayaka Yano ◽  
René Guyomard ◽  
Elodie Jouanno ◽  
...  
Keyword(s):  
Sex Determination ◽  
Sex Chromosomes ◽  
Sex Chromosome ◽  
Wild Population ◽  
Northern Pike ◽  
Esox Lucius ◽  
Telomeric Region ◽  
Male Genome ◽  
Long Reads ◽  
Male Specific

AbstractTeleost fishes, thanks to their rapid evolution of sex determination mechanisms, provide remarkable opportunities to study the formation of sex chromosomes and the mechanisms driving the birth of new master sex determining (MSD) genes. However, the evolutionary interplay between the sex chromosomes and the MSD genes they harbor is rather unexplored. We characterized a male-specific duplicate of the anti-Müllerian hormone (amh) as the MSD gene in Northern Pike (Esox lucius), using genomic and expression evidences as well as by loss-of-function and gain-of-function experiments. Using RAD-Sequencing from a family panel, we identified Linkage Group (LG) 24 as the sex chromosome and positioned the sex locus in its sub-telomeric region. Furthermore, we demonstrated that this MSD originated from an ancient duplication of the autosomal amh gene, which was subsequently translocated to LG24. Using sex-specific pooled genome sequencing and a new male genome sequence assembled using Nanopore long reads, we also characterized the differentiation of the X and Y chromosomes, revealing a small male-specific insertion containing the MSD gene and a limited region with reduced recombination. Our study depicts an unexpected level of limited differentiation within a pair of sex chromosomes harboring an old MSD gene in a wild population of teleost fish, highlights the pivotal role of genes from the amh pathway in sex determination, as well as the importance of gene duplication as a mechanism driving the turnover of sex chromosomes in this clade.Author SummaryIn stark contrast to mammals and birds, teleosts have predominantly homomorphic sex chromosomes and display a high diversity of sex determining genes. Yet, population level knowledge of both the sex chromosome and the master sex determining gene is only available for the Japanese medaka, a model species. Here we identified and provided functional proofs of an old duplicate of anti-Müllerian hormone (Amh), a member of the Tgf-β family, as the male master sex determining gene in the Northern pike, Esox lucius. We found that this duplicate, named amhby (Y-chromosome-specific anti-Müllerian hormone paralog b), was translocated to the sub-telomeric region of the new sex chromosome, and now amhby shows strong sequence divergence as well as substantial expression pattern differences from its autosomal paralog, amha. We assembled a male genome sequence using Nanopore long reads and identified a restricted region of differentiation within the sex chromosome pair in a wild population. Our results provide insight on the conserved players in sex determination pathways, the mechanisms of sex chromosome turnover, and the diversity of levels of differentiation between homomorphic sex chromosomes in teleosts.

scholarly journals Both Loss-of-Function and Gain-of-Function Mutations in snf Define a Role for snRNP Proteins in Regulating Sex-lethal Pre-mRNA Splicing in Drosophila Development

Genetics ◽  
1996 ◽  
Vol 144 (1) ◽  
pp. 95-108
Author(s):  
Helen K Salz ◽  
Thomas W Flickinger
Keyword(s):  
Sex Determination ◽  
Rna Splicing ◽  
Loss Of Function ◽  
Functional Homology ◽  
Snrnp Protein ◽  
A Cell ◽  
Sex Lethal ◽  
Mutant Phenotypes ◽  
Female Specific ◽  
Male Specific

Abstract The Drosophila snf gene encodes a protein with functional homology to the mammalian UlA and U2B″ snRNP proteins. Studies, based on the analysis of three viable alleles, have suggested a role for snf in establishing the female-specific splicing pattern of the sex determination switch gene, Sex-lethal. Here, we show that the non-sex-specific lethal null allele is required for female sex determination, arguing against the formal possibility that the viable alleles disrupt a function unrelated to snf's wild-type function. Moreover, we find snf is required for normal cell growth and/or survival, as expected for a protein involved in a cell-vital process such as RNA splicing. We also show that of the three viable alleles only one, snfJA2, is a partial loss-of-function mutation. The other two viable alleles, snf1621 and snfe8H, encode antimorphic proteins. We find the antimorphic proteins are mislocalized and correlate their mislocalization with their molecular lesions and mutant phenotypes. Finally, we provide genetic evidence that the antimorphic alleles interfere with the autoregulatory splicing function of the Sex-lethal protein. Based on these studies we suggest a model in which the snRNP protein, Snf, functions with Sex-lethal to block recognition of the regulated male-specific exon.

scholarly journals Algal Sex Determination and the Evolution of Anisogamy

2019 ◽  
Vol 73 (1) ◽  
pp. 267-291 ◽  
Author(s):  
James Umen ◽  
Susana Coelho
Keyword(s):  
Sex Determination ◽  
Sexual Reproduction ◽  
Green Algae ◽  
Life Histories ◽  
Mating Systems ◽  
Chromosome Evolution ◽  
Sex Chromosome ◽  
Photosynthetic Eukaryotes ◽  
Sex Determination Mechanisms ◽  
Shed Light

Algae are photosynthetic eukaryotes whose taxonomic breadth covers a range of life histories, degrees of cellular and developmental complexity, and diverse patterns of sexual reproduction. These patterns include haploid- and diploid-phase sex determination, isogamous mating systems, and dimorphic sexes. Despite the ubiquity of sexual reproduction in algae, their mating-type-determination and sex-determination mechanisms have been investigated in only a limited number of representatives. These include volvocine green algae, where sexual cycles and sex-determining mechanisms have shed light on the transition from mating types to sexes, and brown algae, which are a model for UV sex chromosome evolution in the context of a complex haplodiplontic life cycle. Recent advances in genomics have aided progress in understanding sexual cycles in less-studied taxa including ulvophyte, charophyte, and prasinophyte green algae, as well as in diatoms.

scholarly journals Multi-Tissue Transcriptome Analysis Identifies Key Sexual Development-Related Genes of the Ornate Spiny Lobster (Panulirus ornatus)

Genes ◽  
2020 ◽  
Vol 11 (10) ◽  
pp. 1150
Author(s):  
Tomer Ventura ◽  
Jennifer C. Chandler ◽  
Tuan V. Nguyen ◽  
Cameron J. Hyde ◽  
Abigail Elizur ◽  
...  
Keyword(s):  
Sex Determination ◽  
Sexual Development ◽  
Molecular Mechanisms ◽  
Sex Chromosome ◽  
Spiny Lobster ◽  
Homology Search ◽  
Previous Knowledge ◽  
Key Factors ◽  
Factors Associated ◽  
Sex Determination Mechanisms

Sexual development involves the successive and overlapping processes of sex determination, sexual differentiation, and ultimately sexual maturation, enabling animals to reproduce. This provides a mechanism for enriched genetic variation which enables populations to withstand ever-changing environments, selecting for adapted individuals and driving speciation. The molecular mechanisms of sexual development display a bewildering diversity, even in closely related taxa. Many sex determination mechanisms across animals include the key family of “doublesex- and male abnormal3-related transcription factors” (Dmrts). In a few exceptional species, a single Dmrt residing on a sex chromosome acts as the master sex regulator. In this study, we provide compelling evidence for this model of sex determination in the ornate spiny lobster Panulius ornatus, concurrent with recent reports in the eastern spiny lobster Sagmariasus verreauxi. Using a multi-tissue transcriptomic database established for P. ornatus, we screened for the key factors associated with sexual development (by homology search and using previous knowledge of these factors from related species), providing an in-depth understanding of sexual development in decapods. Further research has the potential to close significant gaps in our understanding of reproductive development in this ecologically and commercially significant order.

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