Expression data from mouse preimplantation cloned embryos
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE41358 | GEO | 2013/04/05
SECONDARY ACCESSION(S): PRJNA176881
REPOSITORIES: GEO
Similar Datasets
Project description:Transcriptiome analysis is an excellent approach to understand the mechanism underlying nuclear reprogramming in somatic-cell-cloned embryos. Analysis of the transcriptomic data from the oocyte to blastocyst stage revealed that specific genes were inappropriately reprogrammed at each stage. Sertoli cell-cloned embryos appear to develop normally because the progression of incorrect reprogramming is concealed throughout development. The time-lapse gene expression profiles provide valuable information for understanding reprogramming in SCNT embryos. Single mouse oocyte (MII metaphase), in vitro fertilized embryo (replicates = 3 / each stage) and Sertoli cell cloned embryo (replicates = 5 / each stage) from 1-cell stage to blastocyst stage (16, 32, 48, 62, 72, 84 hours after sperm addition or activation) was used for total RNA extraction. Totally 51 Affymetrix microarrays were used in the experiment.
2013-04-05 | E-GEOD-41358 | biostudies-arrayexpress
Project description:Cloned embryos produced by somatic cell nuclear transfer (SCNT) display a plethora of phenotypic characteristics that make them different from fertilized embryos, indicating defects in the process of nuclear reprogramming by the recipient ooplasm. To elucidate the extent and timing of nuclear reprogramming, we used microarrays to analyze the transcriptome of mouse SCNT embryos during the first two cell cycles. We identified a large number of genes mis-expressed in SCNT embryos. We found that genes involved in transcription and regulation of transcription are prominent among affected genes, and thus may be particularly difficult to reprogram, and these likely cause a ripple effect that alters the transcriptome of many other functions, including oxidative phosphorylation, transport across membrane, and mRNA transport and processing. Interestingly, we also uncovered widespread alterations in the maternal (i.e. non transcribed) mRNA population of SCNT embryos. We conclude that gene expression in early SCNT embryos is grossly abnormal, and that this is at least in part the result of incomplete reprogramming of transcription factor genes. Experiment Overall Design: for both 1 and 2 cell stage we analyzed 4 samples each of fertilized embryos cultured with and without a-amanitin, scnt embryos cultured with and without a-amanitin, and parthennogenic embryos.
2008-06-15 | E-GEOD-6595 | biostudies-arrayexpress
Project description:Cloned embryos produced by somatic cell nuclear transfer (SCNT) display a plethora of phenotypic characteristics that make them different from fertilized embryos, indicating defects in the process of nuclear reprogramming by the recipient ooplasm. To elucidate the extent and timing of nuclear reprogramming, we used microarrays to analyze the transcriptome of mouse SCNT embryos during the first two cell cycles. We identified a large number of genes mis-expressed in SCNT embryos. We found that genes involved in transcription and regulation of transcription are prominent among affected genes, and thus may be particularly difficult to reprogram, and these likely cause a ripple effect that alters the transcriptome of many other functions, including oxidative phosphorylation, transport across membrane, and mRNA transport and processing. Interestingly, we also uncovered widespread alterations in the maternal (i.e. non transcribed) mRNA population of SCNT embryos. We conclude that gene expression in early SCNT embryos is grossly abnormal, and that this is at least in part the result of incomplete reprogramming of transcription factor genes. Keywords: embryo kind comparison
2007-01-01 | GSE6595 | GEO
Project description:Trophoblast stem cells (TSCs) are derived from the trophoectoderm of blastocysts and maintain ability to self-renewal and differentiation. TSC is a good model to research placenta development in vitro. It will contribute to understanding and improving cloned placentomegaly to compare the transcription and methylation between cloned and natural fertilized embryos throughout TSC derivation process. In the present study, we used SCNT (NT) and SCNT with HDACi treatment (SNT) as cloned groups and natural fertilized (NF) embryos to derive TSCs and chosed 5-time points to peform RNA-seq and RRBS. We found only NT got a barriar in TSC maintenace and both cloned groups exhited abnormal accumulating DNA methylation and it might be resiponsible for some malformations of cloned placentas.
2021-03-01 | GSE163380 | GEO
Project description:Trophoblast stem cells (TSCs) are derived from the trophoectoderm of blastocysts and maintain ability to self-renewal and differentiation. TSC is a good model to research placenta development in vitro. It will contribute to understanding and improving cloned placentomegaly to compare the transcription and methylation between cloned and natural fertilized embryos throughout TSC derivation process. In the present study, we used SCNT (NT) and SCNT with HDACi treatment (SNT) as cloned groups and natural fertilized (NF) embryos to derive TSCs and chosed 5-time points to peform RNA-seq and RRBS. We found only NT got a barriar in TSC maintenace and both cloned groups exhited abnormal accumulating DNA methylation and it might be resiponsible for some malformations of cloned placentas.
2021-03-01 | GSE163379 | GEO
Project description:Somatic cell nuclear transfer (SCNT) enables the genome of a differentiated somatic cell to be reprogrammed to totipotency. However, this process is extremely inefficient, and the underlying mechanism of the epigenetic rearrangements following SCNT remains largely unknown. Here, we generated a genome-wide DNA methylome of mouse SCNT preimplantation embryos. Surprisingly, we identified widespread re-methylated regions (rDMRs) in 2- to 4-cell stage cloned embryos, which caused mis-expression of genes and retrotransposons important for zygotic genome activation and embryo development. Knocking-down DNA methyltransferases can specifically rescue the re-methylation defects of SCNT embryos and evidently improve the poor developmental capacity of cloned embryos. In addition, inactivation of DNA methyltransferases combined with overexpression of histone demethylases led to a more significant reduction in DNA methylation as well as exhibited a synergistic enhancement effect on the full-term development of nuclear transfer embryos. Our study therefore reveals that aberrant re-methylation functions as an unavoidable barrier for SCNT embryo development, and that the removal of multiple epigenetic barriers would be a promising approach to achieve the highest cloning efficiency.
2018-08-14 | GSE108708 | GEO
Project description:Somatic cell nuclear transfer (SCNT) enables the genome of a differentiated somatic cell to be reprogrammed to totipotency. However, this process is extremely inefficient, and the underlying mechanism of the epigenetic rearrangements following SCNT remains largely unknown. Here, we generated a genome-wide DNA methylome of mouse SCNT preimplantation embryos. Surprisingly, we identified widespread re-methylated regions (rDMRs) in 2- to 4-cell stage cloned embryos, which caused mis-expression of genes and retrotransposons important for zygotic genome activation and embryo development. Knocking-down DNA methyltransferases can specifically rescue the re-methylation defects of SCNT embryos and evidently improve the poor developmental capacity of cloned embryos. In addition, inactivation of DNA methyltransferases combined with overexpression of histone demethylases led to a more significant reduction in DNA methylation as well as exhibited a synergistic enhancement effect on the full-term development of nuclear transfer embryos. Our study therefore reveals that aberrant re-methylation functions as an unavoidable barrier for SCNT embryo development, and that the removal of multiple epigenetic barriers would be a promising approach to achieve the highest cloning efficiency.
2018-08-14 | GSE116103 | GEO
Project description:Somatic cell nuclear transfer (SCNT) in mammals has been mostly unsuccessful. In this study, we measured and compared transcription profiles of cloned and fertilized embryos using RNA sequencing. Before zygotic genome activation (ZGA), fewer genes were activated in the cloned embryos than in vitro fertilization (IVF), leading to insufficient activation of protein transport and degradation functions. In blastocysts, terms of “embryo development” and “adherens junction” represented major differences for repressed genes in SCNT compared to IVF. Vitamin C (Vc) was found to relax donor cell chromatin and promote cloned embryo development. RNA sequencing indicated that Vc treatment restored some abnormal genes and processes in the cloned embryos. Processes of autophagy, RNA-editing and cell junction were not fully established, but they were improved by Vc treatment. Overexpression of ZNF641, one of the completely restored genes by Vc treatment, improved the cloned embryos’ potential. Finally, Vc treatment rescued some long non-coding RNAs that were aberrantly expressed in the cloned embryos. Collectively, many important genes and biological processes were abnormal in the cloned embryos, some of which can be improved by Vc treatment. This investigation provides several practical aspects that could be useful for improving cloning efficiency and its future applications.
2020-12-12 | GSE123705 | GEO
Project description:Somatic cell nuclear transfer (SCNT) enables the genome of a differentiated somatic cell to be reprogrammed to totipotency. However, this process is extremely inefficient, and the underlying mechanism of the epigenetic rearrangements following SCNT remains largely unknown. Here, we generated a genome-wide DNA methylome of mouse SCNT preimplantation embryos. Surprisingly, we identified widespread re-methylated regions (rDMRs) in 2- to 4-cell stage cloned embryos, which caused mis-expression of genes and retrotransposons important for zygotic genome activation and embryo development. Knocking-down DNA methyltransferases can specifically rescue the re-methylation defects of SCNT embryos and evidently improve the poor developmental capacity of cloned embryos. In addition, inactivation of DNA methyltransferases combined with overexpression of histone demethylases led to a more significant reduction in DNA methylation as well as exhibited a synergistic enhancement effect on the full-term development of nuclear transfer embryos. Our study therefore reveals that aberrant re-methylation functions as an unavoidable barrier for SCNT embryo development, and that the removal of multiple epigenetic barriers would be a promising approach to achieve the highest cloning efficiency.
2018-08-14 | GSE108710 | GEO
Project description:Somatic cell nuclear transfer (SCNT) enables the genome of a differentiated somatic cell to be reprogrammed to totipotency. However, this process is extremely inefficient, and the underlying mechanism of the epigenetic rearrangements following SCNT remains largely unknown. Here, we generated a genome-wide DNA methylome of mouse SCNT preimplantation embryos. Surprisingly, we identified widespread re-methylated regions (rDMRs) in 2- to 4-cell stage cloned embryos, which caused mis-expression of genes and retrotransposons important for zygotic genome activation and embryo development. Knocking-down DNA methyltransferases can specifically rescue the re-methylation defects of SCNT embryos and evidently improve the poor developmental capacity of cloned embryos. In addition, inactivation of DNA methyltransferases combined with overexpression of histone demethylases led to a more significant reduction in DNA methylation as well as exhibited a synergistic enhancement effect on the full-term development of nuclear transfer embryos. Our study therefore reveals that aberrant re-methylation functions as an unavoidable barrier for SCNT embryo development, and that the removal of multiple epigenetic barriers would be a promising approach to achieve the highest cloning efficiency.
2018-08-14 | GSE116104 | GEO