Mus musculus
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ABSTRACT:
PROVIDER: PRJNA344298 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The Rodent-Specific MicroRNA Cluster within the Sfmbt2 Gene is Imprinted and Essential for Placental Development [mRNA E11.5]
| PRJNA323831 | ENA
Project description:The Rodent-Specific MicroRNA Cluster within the Sfmbt2 Gene Is Imprinted and Essential for Placental Development
| PRJNA323829 | ENA
Project description:The Rodent-Specific MicroRNA Cluster within the Sfmbt2 Gene is Imprinted and Essential for Placental Development [miRNA]
| PRJNA323832 | ENA
Project description:Abnormal placentation in cloned animals remains an unsolved problem. We demonstrated the involvement of micro RNAs (miRNAs) in the abnormal enlargement (hyperplasia) of placentas in cloned mice. Using a comparative transcriptome analysis of cloned placentas, we noted the consistent upregulation of clustered miRNAs within Sfmbt2, a paternally expressed imprinted gene. This region was biallelically activated by loss of imprinting (LOI) in cloned placentas. Deletion of the maternal allele of the whole miRNA cluster resulted in the correction of their expression levels and upregulation of their putative target genes with antitumor or apoptotic functions. Consequently, the placental size was reduced to the normal level and histology was ameliorated. In contrast, correcting the expression of the LOI genes (Sfmbt2, Gab1, and Scl38a4) in cloned placentas had no impact on placental size. Thus, we identified that LOI of clustered miRNAs within Sfmbt2 in cloned placentas was the major cause of abnormal placental enlargement.
2020-02-29 | GSE129541 | GEO
Project description:Abnormal placentation in cloned animals remains an unsolved problem. We demonstrated the involvement of micro RNAs (miRNAs) in the abnormal enlargement (hyperplasia) of placentas in cloned mice. Using a comparative transcriptome analysis of cloned placentas, we noted the consistent upregulation of clustered miRNAs within Sfmbt2, a paternally expressed imprinted gene. This region was biallelically activated by loss of imprinting (LOI) in cloned placentas. Deletion of the maternal allele of the whole miRNA cluster resulted in the correction of their expression levels and upregulation of their putative target genes with antitumor or apoptotic functions. Consequently, the placental size was reduced to the normal level and histology was ameliorated. In contrast, correcting the expression of the LOI genes (Sfmbt2, Gab1, and Scl38a4) in cloned placentas had no impact on placental size. Thus, we identified that LOI of clustered miRNAs within Sfmbt2 in cloned placentas was the major cause of abnormal placental enlargement.
2020-02-29 | GSE129939 | GEO
Project description:MicroRNAs (miRNAs) represent small noncoding RNAs that are involved in physiologic and developmental processes by negatively regulating expression of target genes. They exist as individual miRNA genes or as polycistronically transcribed gene clusters. The largest miRNA cluster in mice is located in intron 10 of the Sfmbt2 gene, and contains 72 miRNA precursor sequences within approximately 50 kb. Although this miRNA cluster emerged recently in the rodent genome, probably coincidentally with the acquisition of the imprinted control of Sfmbt2, very little is known about its functions. In this study, we generated mice lacking the entire Sfmbt2 miRNA cluster to elucidate its functions during development. Like the Sfmbt2 gene, the Sfmbt2 miRNAs were expressed in the placenta predominantly from the paternal allele. Loss of the paternal allele resulted in severely impaired development of the spongiotrophoblast layer, which usually comprises about half of the fetal placenta. This phenotype was associated with fetal developmental delay or lethality, leading to significant decreases in the number of fetuses and their weights at term. Microarray analysis identified that at least 30 miRNAs in the cluster were actively transcribed in wild-type placentas. Among the predicted targets of these miRNAs, 132 genes were upregulated in the miRNA-deleted placentas. Some of the genes most significantly upregulated, including Gkn2 and Runx1, are known to inhibit cell proliferation by inducing cell cycle arrest or apoptosis. Thus, the Sfmbt2 miRNAs play essential roles in promoting trophoblastic cell proliferation in the placenta, cooperating with the host gene under the same paternal expression control.
2017-02-01 | GSE82054 | GEO
Project description:MicroRNAs (miRNAs) represent small noncoding RNAs that are involved in physiologic and developmental processes by negatively regulating expression of target genes. They exist as individual miRNA genes or as polycistronically transcribed gene clusters. The largest miRNA cluster in mice is located in intron 10 of the Sfmbt2 gene, and contains 72 miRNA precursor sequences within approximately 50 kb. Although this miRNA cluster emerged recently in the rodent genome, probably coincidentally with the acquisition of the imprinted control of Sfmbt2, very little is known about its functions. In this study, we generated mice lacking the entire Sfmbt2 miRNA cluster to elucidate its functions during development. Like the Sfmbt2 gene, the Sfmbt2 miRNAs were expressed in the placenta predominantly from the paternal allele. Loss of the paternal allele resulted in severely impaired development of the spongiotrophoblast layer, which usually comprises about half of the fetal placenta. This phenotype was associated with fetal developmental delay or lethality, leading to significant decreases in the number of fetuses and their weights at term. Microarray analysis identified that at least 30 miRNAs in the cluster were actively transcribed in wild-type placentas. Among the predicted targets of these miRNAs, 132 genes were upregulated in the miRNA-deleted placentas. Some of the genes most significantly upregulated, including Gkn2 and Runx1, are known to inhibit cell proliferation by inducing cell cycle arrest or apoptosis. Thus, the Sfmbt2 miRNAs play essential roles in promoting trophoblastic cell proliferation in the placenta, cooperating with the host gene under the same paternal expression control.
2017-02-01 | GSE82053 | GEO
Project description:MicroRNAs (miRNAs) represent small noncoding RNAs that are involved in physiologic and developmental processes by negatively regulating expression of target genes. They exist as individual miRNA genes or as polycistronically transcribed gene clusters. The largest miRNA cluster in mice is located in intron 10 of the Sfmbt2 gene, and contains 72 miRNA precursor sequences within approximately 50 kb. Although this miRNA cluster emerged recently in the rodent genome, probably coincidentally with the acquisition of the imprinted control of Sfmbt2, very little is known about its functions. In this study, we generated mice lacking the entire Sfmbt2 miRNA cluster to elucidate its functions during development. Like the Sfmbt2 gene, the Sfmbt2 miRNAs were expressed in the placenta predominantly from the paternal allele. Loss of the paternal allele resulted in severely impaired development of the spongiotrophoblast layer, which usually comprises about half of the fetal placenta. This phenotype was associated with fetal developmental delay or lethality, leading to significant decreases in the number of fetuses and their weights at term. Microarray analysis identified that at least 30 miRNAs in the cluster were actively transcribed in wild-type placentas. Among the predicted targets of these miRNAs, 132 genes were upregulated in the miRNA-deleted placentas. Some of the genes most significantly upregulated, including Gkn2 and Runx1, are known to inhibit cell proliferation by inducing cell cycle arrest or apoptosis. Thus, the Sfmbt2 miRNAs play essential roles in promoting trophoblastic cell proliferation in the placenta, cooperating with the host gene under the same paternal expression control.
2017-02-01 | GSE87302 | GEO
Project description:Genomic imprinting regulates parental origin-dependent mono-allelic gene expression. It is mediated by either germline differential methylation of DNA (canonical imprinting) or oocyte-derived H3K27me3 (non-canonical imprinting) in mice. Depletion of Eed, an essential component of Polycomb repressive complex 2, results in genome-wide loss of H3K27me3 in oocytes, which causes loss of non-canonical imprinting (LOI) in embryos. Although Eed maternal KO (matKO) embryos show partial lethality after implantation, it is unknown whether LOI itself contributes to the developmental phenotypes of these embryos, which makes it unclear whether non-canonical imprinting is developmentally relevant. Here, by combinatorial matKO of Xist, a non-canonical imprinted gene whose LOI causes aberrant transient maternal X chromosome inactivation (XCI) at preimplantation, we show that prevention of the transient maternal XCI greatly restores the development of Eed matKO embryos. Moreover, we find that the placentae of Eed matKO embryos are remarkably enlarged in a manner independent of Xist LOI. Heterozygous deletion screening of individual autosomal non-canonical imprinted genes suggests that LOI of the Sfmbt2 miRNA cluster-chromosome 2 miRNA cluster (C2MC), solute carrier family 38 member 4 (Slc38a4), and Gm32885 contributes to the placental enlargement. Taken together, our study provides evidence that Xist imprinting sustains embryonic development and autosomal non-canonical imprinting restrains placental overgrowth.
2022-06-30 | GSE199115 | GEO
Project description:Hybrid phenotypes that contribute to postzygotic reproductive isolation often exhibit pronounced asymmetry, both between reciprocal crosses and between the sexes in accordance with Haldane's rule. Inviability in mammalian hybrids is associated with parent-of-origin placental growth abnormalities for which misregulation of imprinted genes is the leading candidate mechanism. However, direct evidence for the involvement of imprinted genes in hybrid growth dysplasia is limited. We used transcriptome and reduced representation bisulfite sequencing to conduct the first genome-scale assessment of the contribution of imprinted genes to parent-of-origin placental growth dysplasia in the cross between the house mouse (Mus musculus domesticus) and the Algerian mouse (Mus spretus). Imprinted genes with transgressive expression and methylation were concentrated in the Kcnq1 cluster, which contains causal genes for prenatal growth abnormalities in mice and humans. Hypermethylation of the cluster’s imprinting control region, and consequent misexpression of the genes Phlda2 and Ascl2, is a strong candidate mechanism for transgressive placental undergrowth. Transgressive placental and gene regulatory phenotypes, including expression and methylation in the Kcnq1 cluster, were more extreme in hybrid males. While consistent with Haldane’s rule, male-biased defects are unexpected in rodent placenta because the X-chromosome is effectively hemizygous in both sexes. In search of an explanation we found evidence of leaky imprinted (paternal) X-chromosome inactivation in hybrid female placenta, an epigenetic disturbance that may buffer females from the effects of X-linked incompatibilities to which males are fully exposed. Sex differences in chromatin structure on the X and sex-biased maternal effects are non-mutually exclusive alternative explanations for adherence to Haldane’s rule in hybrid placenta. The results of this study contribute to understanding the genetic basis of hybrid inviability in mammals, and the role of imprinted genes in speciation.
2020-11-09 | GSE161051 | GEO