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Analysis of developmental imprinting dynamics in primates using SNP-free methods to identify imprinting defects in cloned placenta

ABSTRACT: Analysis of developmental imprinting dynamics in primates using SNP-free methods to identify imprinting defects in cloned placenta

PROVIDER: PRJNA668521 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12806700_1.fastq.gz	Fastqsanger.gz
	SRR12806700_2.fastq.gz	Fastqsanger.gz
	SRR12806701_1.fastq.gz	Fastqsanger.gz
	SRR12806701_2.fastq.gz	Fastqsanger.gz
	SRR12806702_1.fastq.gz	Fastqsanger.gz

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Analysis of developmental imprinting dynamics in primates using SNP-free methods to identify imprinting defects in cloned placenta

Project description:Our knowledge of genomic imprinting in primates is lagging behand that of mice largely due to the difficulties of allelic analyses in outbred animals. To understand imprinting dynamics in primates, we profiled transcriptomes, DNA methylomes and H3K27me3 in uniparental monkey embryos. We further developed single-nucleotide polymorphisms (SNP)-free methods, TARSII and CARSII, to identify germline differentially methylated regions (DMRs) in somatic tissues. Our comprehensive analyses showed that allelic DNA methylation, but not H3K27me3, is a major mark that correlates with paternal-biasedly expressed genes (PEGs) in uniparental monkey embryos. Interestingly, primate germline DMRs are different from PEG-associated DMRs in early embryos and are enriched in placenta. Strikingly, most placenta-specific germline DMRs are lost in placenta of cloned monkey. Collectively, our study establishes SNP-free germline DMR identification methods, defines developmental imprinting dynamics in primates and demonstrates imprinting defects in cloned monkey placenta, which provides important clues for improving primate cloning.

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Loss of Slc38a4 imprinting is a major cause of mouse SCNT placenta hyperplasia at late gestation

Project description:Placenta hyperplasia is commonly observed in cloned animals and is believed to impede the proper development of cloned embryos. However, the mechanism underlying this phenomenon is largely unknown. Here we show that placenta hyperplasia of cloned mouse embryos occurs in both middle and late gestation. Interestingly, restoring paternal-specific expression of an amino acid transporter Slc38a4, which loses maternal H3K27me3-dependent imprinting and becomes bi-allelically expressed in cloned placentae, rescued the overgrowth of cloned placentae at late gestation. Molecular analyses reveal that loss of Slc38a4 imprinting leads to over activation of the mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway in cloned placentae, which is likely due to the increased amino acids transportation by SLC38A4. Collectively, our study not only reveals loss of Slc38a4 imprinting is responsible for overgrowth of cloned placentae at late gestation, but also suggests the underlying mechanism involves increased amino acid transportation and over activation of mTORC1.

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Loss of H3K27me3 imprinting in the Sfmbt2 miRNA cluster causes enlargement of cloned mouse placentas

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.

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Project description:De novo copy number variations in cloned dogs from the same nuclear donor In this study, we aimed to identify de novo post-cloning CNV events and estimated the rate of CNV mosaicism in cloned dogs with the identical genetic background.

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De novo copy number variations in cloned dogs (Illumina SNP)

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Loss of H3K27me3 imprinting in the Sfmbt2 miRNA cluster causes enlargement of cloned mouse placentas

Project description:Loss of H3K27me3 imprinting in the Sfmbt2 miRNA cluster causes enlargement of cloned mouse placentas

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Loss of H3K27me3 imprinting in the Sfmbt2 miRNA cluster causes enlargement of cloned mouse placentas

Project description:Loss of H3K27me3 imprinting in the Sfmbt2 miRNA cluster causes enlargement of cloned mouse placentas

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