Project description:Total gene expression analysis was performed on RNA from testes extracted from two litters of constitutive homozygous and heterozygous H3f3b knockout mice compared to WT littermates. Constitutive knockout mice were obtained by mating H3f3b Fl/Fl mice to Zp3Cre mice. Heterozygous knockout mice were crossed until homozygous knockout mice were obtained. Testes were surgically removed from 8 week old homozygous knockouts, heterozygous knockouts and WT, and RNA was extracted from one testis from each mouse for total gene expression.
Project description:Ikbkap/Elp1 regulates genes involved in spermatogenesis. Ikbkap deficiency causes male infertility by disrupting meiotic progression. In this dataset, we include the expression data for control and Ikbkap-knockout mouse testis. We analyzed the gene expression in control and Ikbkap-knockout testes using the the Affymetrix MoGene-1_0-st-v1 platform. Three replicates per genotype.
Project description:Abcg8 knockout mice, fed chow, are infertile. These mice also are susceptible to absorption and retention of xenosterols contained in the diet. Ezetimibe, a blocker of dieary sterol entry, can reverse the fertility in Abcg8 knockout mice. In order to identify if the xenosterols resulted in disruption of a specific set of genes in the testes, we compared wild-type testes, Abcg8 knockout testes, or testes from Abcg8 knockout mice fed chow supplemented with 0.005% ezetimibe. To identify genes of interest, we reasoned that any causative gene expression changes seen in Abcg8 knockout mice fed chow, resulting in xenosterol exposure and accumulation, leading to infertilty, would be reveresed back to a pattern seen in the wild-type mice, when Abcg8 knockout mice are raised on chow containing ezetimibe (which prevents xenosterol absorption in the intestine). The target of this drug, Npc1l1, is not expressed in the testes. Testes from wild-type mice, Abcg8 knockout mice, and Abcg8 knockout mice fed chow supplemented with ezetimibe were analyzed.
Project description:Abcg8 knockout mice, fed chow, are infertile. These mice also are susceptible to absorption and retention of xenosterols contained in the diet. Ezetimibe, a blocker of dieary sterol entry, can reverse the fertility in Abcg8 knockout mice. In order to identify if the xenosterols resulted in disruption of a specific set of genes in the testes, we compared wild-type testes, Abcg8 knockout testes, or testes from Abcg8 knockout mice fed chow supplemented with 0.005% ezetimibe. To identify genes of interest, we reasoned that any causative gene expression changes seen in Abcg8 knockout mice fed chow, resulting in xenosterol exposure and accumulation, leading to infertilty, would be reveresed back to a pattern seen in the wild-type mice, when Abcg8 knockout mice are raised on chow containing ezetimibe (which prevents xenosterol absorption in the intestine). The target of this drug, Npc1l1, is not expressed in the testes.
Project description:Expression changes in testes of 5 week old mice after knockout of Phf13 were analyzed using Affymetrix mouse genome 430 2.0 expression microarrays. Transcripts on the X- and Y-chromosome were significantly upregulated.
Project description:Expression changes in testes of 15-20 week old mice after knockout of Phf13 were analyzed using Affymetrix mouse genome 430 2.0 expression microarrays. Transcripts on the X- and Y-chromosome were significantly upregulated.
Project description:To investigate the role of DDX20 in spermatogenesis, we generated Ddx20 flox/flox Ddx4-Cre mice to make a germ cell-specific Ddx20 knockout, and isolated spermatogonia from four-day-old mouse testes by THY1 magnetic beads.We then performed gene expression profiling analysis using data obtained from RNA-seq of THY1 + spermatogonia.
Project description:We have sequenced mouse embryonic fibroblasts (MEFs) and 6 organs (testes, prostate, liver, heart, spleen, and eye) harvested from adult male wild type and Tug1 knockout (Tug1_tm1.1Vlcg) mice in a C57BL/6J/129S6 (N3-C57BL/6J, no Neo) background. Additional sequencing was done on the testes of a Tug1 rescue mouse, which contains a doxycycline inducible allele for Tug1 (tg(Tug1)) and CAGs-rtTA3 in the Tug1 knockout background (Tug1_tmn1.1Vlcg).
Project description:Spermatogonial stem cells (SSCs) provide a continuous spermatogenesis and male fertility. However, the underlying mechanisms of alternative splicing (AS) in mouse SSCs are still largely unclear. We demonstrated that SRSF1 is essential for gene expression and splicing in mouse SSCs. Specific deletion of Srsf1 in mouse germ cells impairs self-renewal and homing of SSCs leading to male infertility. Whole-mount staining data showed the absence of germ cells in the testes of adult cKO mice, which indicates severe non-obstructive azoospermia (NOA) in cKO mice. Expression of SSC-related genes (Gfra1, Pou5f1, Plzf, Dnd1, Stra8, and Taf4b) was significantly reduced in the testes of conditional knockout (cKO) mice. CLIP-seq data found that SSC-related genes (Plzf, Id4, Setdb1, Stra8, Tial1, Bcas2, Ddx5, Srsf10, Uhrf1, and Bud31) were bound by SRSF1 in the mouse testes. Moreover, multi-omics analysis suggests that SRSF1 directly binds and regulates the expression of Tial1 via AS to implement SSCs self-renewal and differentiation. Collectively, our data reveal the critical role of an SRSF1-mediated AS in SSCs self-renewal and differentiation, which may provide a framework to elucidate the molecular mechanisms of the post-transcriptional network underlying SSCs.