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Chromatin remodeler INO80 mediates trophectoderm permeability barrier to modulate morula-to-blastocyst transition

ABSTRACT: Chromatin remodeler INO80 mediates trophectoderm permeability barrier to modulate morula-to-blastocyst transition

PROVIDER: PRJNA736249 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14765714_1.fastq.gz	Fastqsanger.gz
	SRR14765714_2.fastq.gz	Fastqsanger.gz
	SRR14765715_1.fastq.gz	Fastqsanger.gz
	SRR14765715_2.fastq.gz	Fastqsanger.gz
	SRR14765716_1.fastq.gz	Fastqsanger.gz

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Chromatin remodeler INO80 mediates trophectoderm permeability barrier to modulate morula-to-blastocyst transition

Project description:INO80 promotes blastocyst development through regulating expression of key genes required for lineage specification, tight junction assembly, and fluid accumulation.

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Chromatin remodeler INO80 mediates trophectoderm permeability barrier to modulate morula-to-blastocyst transition.

Project description:Inositol requiring mutant 80 (INO80) is a chromatin remodeler that regulates pluripotency maintenance of embryonic stem cells and reprogramming of somatic cells into pluripotent stem cells. However, the roles and mechanisms of INO80 in porcine pre-implantation embryonic development remain largely unknown. Here, we show that INO80 modulates trophectoderm epithelium permeability to promote porcine blastocyst development. The INO80 protein is highly expressed in the nuclei during morula-to-blastocyst transition. Functional studies revealed that RNA interference (RNAi)-mediated knockdown of INO80 severely blocks blastocyst formation and disrupts lineage allocation between the inner cell mass and trophectoderm. Mechanistically, single-embryo RNA sequencing revealed that INO80 regulates multiple genes, which are important for lineage specification, tight junction assembly, and fluid accumulation. Consistent with the altered expression of key genes required for tight junction assembly, a permeability assay showed that paracellular sealing is defective in the trophectoderm epithelium of INO80 knockdown blastocysts. Importantly, aggregation of 8-cell embryos from the control and INO80 knockdown groups restores blastocyst development and lineage allocation via direct complementation of the defective trophectoderm epithelium. Taken together, these results demonstrate that INO80 promotes blastocyst development by regulating the expression of key genes required for lineage specification, tight junction assembly, and fluid accumulation.

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Project description:In humans, the embryonic genome activation (EGA) program is functional by day 3 after fertilization. The 6-8 cell stage embryo (day 3 post-fertilization) starts the process of “compaction” that leads to the generation of the tightly organized cell mass of the morula and is followed by differentiation of the morula into a blastocyst. The transition from day 3 embryos to day 5 blastocysts is likely to be controlled by many and specific changes in the expression of different genes. We used mRNA amplification technique and compared the transcriptomes of day 3 human embryos and trophectoderm (TE) cells from day 5 human blastocysts to identify transcripts that are differentially expressed during the embryo-to-TE transition and involved in the TE specification. These six embryo samples were compared to our five human trophectoderm samples that are available in GEO under the following accession numbers: GSM706168 GSM706169 GSM706170 GSM706171 GSM706172

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