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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: 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. Wild type strain-matched spermatids are used as a control (4 biological replicates), and 3 biological replicate samples are analysed for each genotype of interest (shSLY, shSLX1 and shSLX1shSLY)

ORGANISM(S): Mus musculus

SUBMITTER: Peter Ellis

PROVIDER: E-GEOD-39109 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

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

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

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

2011-05-11 | GSE29197 | GEO

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

2011-05-11 | GSE29200 | GEO

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

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. 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.

2011-05-11 | E-GEOD-29200 | biostudies-arrayexpress

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