Gene expression of mouse embryonic gonad [Nanos2_Stra8]
Ontology highlight
ABSTRACT: To examine whether the meiosis was solo factor responsible for the disruption of the male gonocyte differenitiation in the Nanos2-/- male germ cells, we deleted Stra8 function from Nanos2-null background and performed expression microarray analysis of the Nanos2+/-/Stra8+/- , Nanos2-/-/Stra8+/-, and Nanos2-/-/Stra8-/- male emnbryonic gonads at E14.5.
Project description:To examine whether the meiosis was solo factor responsible for the disruption of the male gonocyte differenitiation in the Nanos2-/- male germ cells, we deleted Stra8 function from Nanos2-null background and performed expression microarray analysis of the Nanos2+/-/Stra8+/- , Nanos2-/-/Stra8+/-, and Nanos2-/-/Stra8-/- male emnbryonic gonads at E14.5. Biological duplicates were examined at each stage, genotype, and sex for each experiment.
Project description:To analyze the function of retinoic acid and Stra8 in the male germ cell differentiation, we performed expression microarray analysis of the Cyp26b1-/-/Stra8-/- male gonads at E14.5.
Project description:To analyze the function of retinoic acid and Stra8 in the male germ cell differentiation, we performed expression microarray analysis of the Cyp26b1-/-/Stra8-/- male gonads at E14.5. Biological duplicates were examined at each genotype for each experiment.
Project description:To elucidate the function of NANOS2 to regulate the transcriptome in embryonic male germ cells, we performed expression microarray analysis of the embyornic gonads of the Nanos2+/-, Nanos2-/- male and wild type female from E12.5 to E15.5. The Nanos2+/- and Nanos2-/- female gonads at E15.5 were analyzed as a negative control.
Project description:To elucidate the function of NANOS2 to regulate the transcriptome in embryonic male germ cells, we performed expression microarray analysis of the embyornic gonads of the Nanos2+/-, Nanos2-/- male and wild type female from E12.5 to E15.5. The Nanos2+/- and Nanos2-/- female gonads at E15.5 were analyzed as a negative control. Biological duplicates were examined at each stage, genotype, and sex for each experiment.
Project description:To identify Nanos2-associated mRNAs, we performed microarray analysis of mRNAs coprecipitated with FLAG-tagged NANOS2 with male gonad from Tg-Nanos2 enhancer-3xFLAG-Nanos2-3'UTR at E14.5.
Project description:To identify Nanos2-associated mRNAs, we performed microarray analysis of mRNAs coprecipitated with FLAG-tagged NANOS2 with male gonad from Tg-Nanos2 enhancer-3xFLAG-Nanos2-3'UTR at E14.5. Biological duplicates were examined at each sample.
Project description:In mouse embryos, sex-specific differentiation of primordial germ cells (PGCs) begins with distinct cell cycle regulations: while PGCs in female (XX) gonads enter meiosis, PGCs in male (XY) gonads defer meiosis and arrest cell cycle1,2. The mitotic quiescence in XY gonads requires Nanos2, an evolutionarily conserved RNA-binding protein implicated in RNA degradation3-5; however, underlying mechanisms including the identity of its target mRNAs in vivo remain unknown. Here we show that Nanos2 negatively regulates Dazl (Deleted in azoospermia-like), a germline-specific gene encoding an RNA-binding protein that is implicated in translational control and meiotic initiation6,7. Comprehensive microarray analyses identified Dazl as one of the genes that were up-regulated in Nanos2-deficient XY gonads, but down-regulated in Nanos2-expressing XX gonads. Analysis of a BAC transgenic mouse line, in which the 3’UTR of Dazl can be removed by Flp-Frt recombination system, showed that repression of Dazl is likely achieved by the association of Nanos2 with Dazl’s 3’UTR. Elevated levels of Dazl expression in the transgenic XY PGCs resulted in abnormal progression of cell cycles including meiosis, reminiscent of the phenotype observed in Nanos2-/- XY gonads. This phenotype was suppressed by inhibiting retinoic acid (RA) signaling, suggesting that Nanos2 represses Dazl to prevent RA-induced cell cycle progression in XY PGCs. Furthermore, we show that a part of Nanos2-associated mRNAs, most of which are up-regulated in Nanos2-/- XY gonads, can also associate with Dazl, and that excess Dazl impedes localization of Nanos2 to processing-bodies where RNA degradation takes place, suggesting that repression of Dazl is required for Nanos2 to efficiently degrade its target mRNAs. These data provide the first link between the two RNA-binding proteins that play pivotal roles in sexual differentiation of murine PGCs.
Project description:In mouse embryos, sex-specific differentiation of primordial germ cells (PGCs) begins with distinct cell cycle regulations: while PGCs in female (XX) gonads enter meiosis, PGCs in male (XY) gonads defer meiosis and arrest cell cycle1,2. The mitotic quiescence in XY gonads requires Nanos2, an evolutionarily conserved RNA-binding protein implicated in RNA degradation3-5; however, underlying mechanisms including the identity of its target mRNAs in vivo remain unknown. Here we show that Nanos2 negatively regulates Dazl (Deleted in azoospermia-like), a germline-specific gene encoding an RNA-binding protein that is implicated in translational control and meiotic initiation6,7. Comprehensive microarray analyses identified Dazl as one of the genes that were up-regulated in Nanos2-deficient XY gonads, but down-regulated in Nanos2-expressing XX gonads. Analysis of a BAC transgenic mouse line, in which the 3’UTR of Dazl can be removed by Flp-Frt recombination system, showed that repression of Dazl is likely achieved by the association of Nanos2 with Dazl’s 3’UTR. Elevated levels of Dazl expression in the transgenic XY PGCs resulted in abnormal progression of cell cycles including meiosis, reminiscent of the phenotype observed in Nanos2-/- XY gonads. This phenotype was suppressed by inhibiting retinoic acid (RA) signaling, suggesting that Nanos2 represses Dazl to prevent RA-induced cell cycle progression in XY PGCs. Furthermore, we show that a part of Nanos2-associated mRNAs, most of which are up-regulated in Nanos2-/- XY gonads, can also associate with Dazl, and that excess Dazl impedes localization of Nanos2 to processing-bodies where RNA degradation takes place, suggesting that repression of Dazl is required for Nanos2 to efficiently degrade its target mRNAs. These data provide the first link between the two RNA-binding proteins that play pivotal roles in sexual differentiation of murine PGCs.
Project description:To investigate the biochemical function of NANOS2, we performed expression microarray analysis of the embyornic male gonad of Nanos2 hetero, Nanos2 KO, and Nanos2 KO_Tg 3M-CM-^WFLAG-tagged Nanos2-M-NM-^TN10, which is truncated form of Nanos2 in the N-terminal region, transgenic mice. 3M-CM-^WFLAG-tagged Nanos2-M-NM-^TN10 protein function was validated by rescue experiment in the Nanos2-null male gonad of mouse embryo at E14.5. Biological duplicates were examined at each genotype, Nanos2 hetero, Nanos2 KO, and Nanos2 KO_Tg 3M-CM-^WFLAG-tagged Nanos2-M-NM-^TN10 for each experiment.