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The Multicopy Gene Sly Represses the Sex Chromosomes in the Male Mouse Germline after Meiosis part 2

ABSTRACT: Studies of mice with Y chromosome long arm deficiencies suggest that the male-specific region (MSYq) encodes information required for sperm differentiation and postmeiotic sex chromatin repression (PSCR). Several genes have been identified on MSYq, but because they are present in more than 40 copies each, their functions cannot be investigated using traditional gene targeting. Here, we generate transgenic mice producing small interfering RNAs that specifically target the transcripts of the MSYq-encoded multicopy gene Sly (Sycp3-like Y-linked). Microarray analyses performed on these Sly-deficient males and on MSYq-deficient males show a remarkable up-regulation of sex chromosome genes in spermatids. Total RNA isolated from testis of young adult males (4-8 weeks postpartum) with Yq deletions or shSLY targeted knockdown, compared to age- and strain-matched controls.

ORGANISM(S): Mus musculus

SUBMITTER: Peter Ellis

PROVIDER: E-GEOD-29200 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The multicopy gene Sly represses the sex chromosomes in the male mouse germline after meiosis.

Cocquet Julie J Ellis Peter J I PJ Yamauchi Yasuhiro Y Mahadevaiah Shantha K SK Affara Nabeel A NA Ward Monika A MA Burgoyne Paul S PS

PLoS biology 20091117 11

Studies of mice with Y chromosome long arm deficiencies suggest that the male-specific region (MSYq) encodes information required for sperm differentiation and postmeiotic sex chromatin repression (PSCR). Several genes have been identified on MSYq, but because they are present in more than 40 copies each, their functions cannot be investigated using traditional gene targeting. Here, we generate transgenic mice producing small interfering RNAs that specifically target the transcripts of the MSYq- ...[more]

PMID: 19918361

Similar Datasets

The Multicopy Gene Sly Represses the Sex Chromosomes in the Male Mouse Germline after Meiosis

Project description:Studies of mice with Y chromosome long arm deficiencies suggest that the male-specific region (MSYq) encodes information required for sperm differentiation and postmeiotic sex chromatin repression (PSCR). Several genes have been identified on MSYq, but because they are present in more than 40 copies each, their functions cannot be investigated using traditional gene targeting. Here, we generate transgenic mice producing small interfering RNAs that specifically target the transcripts of the MSYq-encoded multicopy gene Sly (Sycp3-like Y-linked). Microarray analyses performed on these Sly-deficient males and on MSYq-deficient males show a remarkable up-regulation of sex chromosome genes in spermatids. Two sets of samples were examined: (1) Total RNA isolated from separated round spermatids of young adult males (8 weeks postpartum) with Yq deletions or shSLY targeted knockdown, compared to age- and strain-matched controls. (2) Total RNA isolated from whole testis of juvenile males (17 days post partum) with shSLY targeted knockdown, compared to age- and strain-matched controls.

2011-05-11 | E-GEOD-29198 | biostudies-arrayexpress

The Multicopy Gene Sly Represses the Sex Chromosomes in the Male Mouse Germline after Meiosis

2011-05-11 | GSE29198 | GEO

The Multicopy Gene Sly Represses the Sex Chromosomes in the Male Mouse Germline after Meiosis part 2

2011-05-11 | GSE29200 | GEO

Deficiency in the multicopy Sycp3-like X-linked genes Slx and Slxl1 causes major defects in spermatid differentiation

Project description:The gene Sly is present in multiple copies on the mouse Y chromosome and encodes a protein that is required for the epigenetic regulation of postmeiotic sex chromosome expression. The X chromosome carries two multicopy genes related to Sly: Slx and Slxl1. Here we investigate the role of Slx/Slxl1 using transgenically-delivered small interfering RNAs to disrupt their function. We show that Slx and Slxl1 are important for normal sperm differentiation and male fertility. Slx/Slxl1 deficiency leads to delay in spermatid elongation and sperm release. A high proportion of delayed spermatids are eliminated via apoptosis, with a consequent reduced sperm count. The remaining spermatozoa are abnormal with impaired motility and fertilizing abilities. Microarray analyses reveal that Slx/Slxl1 deficiency affects the metabolic processes occurring in the spermatid cytoplasm but does not lead to a global perturbation of sex chromosome expression; this is in contrast with the effect of Sly deficiency which leads to an up-regulation of X and Y chromosome genes. Total RNA isolated from separated round spermatids of young adult males (8 weeks postpartum) with shSLX or shSLY targeted knockdown, compared to age- and strain-matched controls.

2011-05-11 | E-GEOD-29197 | biostudies-arrayexpress

Deficiency in the multicopy Sycp3-like X-linked genes Slx and Slxl1 causes major defects in spermatid differentiation

2011-05-11 | GSE29197 | GEO

Male mice lacking Teshl lncRNA exhibit inactivation of Y chromosomal multicopy genes and female distortion-biased sex ratio change in offspring

Project description:Deletion of multicopy genes located in the male-specific region of the mouse Y chromosome long arm (MSYq) is associated with sperm head abnormalities and male infertility. Heat shock factor 2 (HSF2) regulates the transcription of multicopy genes in MSYq. Little is known how HSF2-dependent regulation of the MSYq genes occurs only in testis. Testis harbors the largest number of tissue-specific long noncoding RNAs (lncRNAs). Here, we report that the novel mouse testis-specific lncRNA NR_038002 is conserved in humans and displayed a spatiotemporal expression pattern in the nucleus of elongating spermatids. NR_038002-deficient male mice produced sperm with abnormal head morphology and exhibited reduced fertility accompanied by female-biased sex ratio change in offspring. Molecular analyses revealed that NR_038002 interacts with HSF2, and thereby activates the expression of the MSYq genes, such as Sycp3 like Y-linked (Sly) and spermiogenesis-specific transcript on the Y (Ssty). We designate NR_038002 as Teshl (testis-specific HSF2-interacting lncRNA). Taken together, our study establishes a molecular relationship of Teshl-HSF2-MSYq, and provides evidence for the critical role of the Teshl-HSF2 complex in acquiring the normal quality of Y-bearing sperm, leading to balanced offspring sex ratio

2021-01-01 | GSE162652 | GEO

A genetic basis for a postmeiotic X vs. Y chromosome intragenomic conflict in the mouse

Project description:The Y-encoded multicopy gene Sly has been shown to repress X and Y genes in spermatids, among which are its X-linked homologs Slx and Slxl1, via modulation of post-meiotic sex chromain (PMSC). In this experiment, we compared expression in spermatids from mice that are deficient for Sly (shSLY), for Slx/Slxl1 (shSLX1) or both (shSLX1shSLY). We observed that Slx/Slxl1 has an opposite role to that of Sly, and stimulates expression of X and Y genes in spermatids when Sly is absent. Slx/Slxl1 deficiency rescues the sperm differentiation defects and near sterility caused by Sly deficiency and vice versa. Slx/Slxl1 deficiency also causes a sex ratio distortion towards the production of male offspring that is corrected by Sly deficiency.

2012-07-06 | GSE39109 | GEO

A genetic basis for a postmeiotic X vs. Y chromosome intragenomic conflict in the mouse

2012-07-05 | E-GEOD-39109 | biostudies-arrayexpress

Rapid de novo evolution of X chromosome dosage compensation in Silene latifolia, a plant with young sex chromosomes

Project description:Silene latifolia is a dioecious plant with heteromorphic sex chromosomes that have originated only ~10 MYA and is a promising model organism to study sex chromosome evolution in plants. Previous work suggests that S. latifolia XY chromosomes have gradually stopped recombining and the Y chromosome is undergoing degeneration as in animal sex chromosomes. However, this work has been limited by the paucity of sex-linked genes available. Here, we used 35 Gb of RNA-seq data from multiple males (XY) and females (XX) of a S. latifolia inbred line to detect sex-linked SNPs and identified more than 1700 sex-linked contigs (with X-linked and Y-linked alleles). Analyses using known sex-linked and autosomal genes, together with simulations indicate that these newly identified sex-linked contigs are reliable. Using read numbers, we then estimated expression levels of X-linked and Y-linked alleles in males and found an overall trend of reduced expression of Y-linked alleles, consistent with a widespread ongoing degeneration of the S. latifolia Y chromosome. By comparing expression intensities of X-linked alleles in males and females, we found that X-linked allele expression increases as Y-linked allele expression decreases in males, which makes expression of sex-linked contigs similar in both sexes. This phenomenon is known as dosage compensation and has so far only been observed in evolutionary old animal sex chromosome systems. Our results suggest that dosage compensation has evolved in plants and that it can quickly evolve de novo after the origin of sex chromosomes.

2012-08-24 | GSE35563 | GEO

Sex Chromosomes and Sex Phenotype Contribute to Biased DNA Methylation in Mouse Liver

Project description:Sex biases in the genome-wide distribution of DNA methylation and gene expression levels are some of the manifestations of sexual dimorphism in mammals. To advance our understanding of the mechanisms that contribute to sex biases in DNA methylation and gene expression, we conducted whole genome bisulfite sequencing (WGBS) as well as RNA-seq on liver samples from mice with different combinations of sex phenotype and sex-chromosome complement. We compared groups of animals with different sex phenotypes, but the same genetic sexes, and vice versa, same sex phenotypes, but different sex-chromosome complements. We also compared sex-biased DNA methylation in mouse and human livers. Our data show that sex phenotype, X-chromosome dosage, and the presence of Y chromosome shape the differences in DNA methylation between males and females. We also demonstrate that sex bias in autosomal methylation is associated with sex bias in gene expression, whereas X-chromosome dosage-dependent methylation differences are not, as expected for a dosage-compensation mechanism. Furthermore, we find partial conservation between the repertoires of mouse and human genes that are associated with sex-biased methylation, an indication that gene function is likely to be an important factor in this phenomenon.

2022-11-14 | GSE217666 | GEO

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