Primary specification of blastocyst trophectoderm by scRNA-seq: new insights into embryo implantation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA550362 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10062785_1.fastq.gz | Fastqsanger.gz | |||
| SRR10062785_2.fastq.gz | Fastqsanger.gz | |||
| SRR10062786_1.fastq.gz | Fastqsanger.gz | |||
| SRR10062786_2.fastq.gz | Fastqsanger.gz | |||
| SRR10062787_1.fastq.gz | Fastqsanger.gz |
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Project description:Mechanisms of implantation such as determination of the attachment pole, fetal-maternal communication, as well as underlying causes of implantation failure are largely unexplored. Here we performed single-cell RNA sequencing (scRNA-seq) on peri-implantation embryos from both humans and mice to explore trophectoderm development and embryo–endometrium crosstalk. We found that the transcriptomes of polar and mural trophectoderm (TE) diverged after embryos hatched from the zona pellucida in both species, with polar TE being more mature than mural TE. The implantation poles show similarities in cell cycle activities, as well as in expression of genes critical for implantation and placentation. Embryos that either fail to attach in vitro or fail to implant in vivo, show abnormalities in pathways related to energy production, protein metabolism and 18S rRNA m6A methylation. These findings uncover the gene expression characteristics of humans and mice TE differentiation during the peri-implantation period and provide new insights into embryo implantation.
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Project description:Mechanisms of implantation such as determination of the attachment pole, fetal-maternal communication, and underlying causes of implantation failure are largely unexplored. Here, we performed single-cell RNA sequencing on peri-implantation embryos from both humans and mice to explore trophectoderm (TE) development and embryo-endometrium cross-talk. We found that the transcriptomes of polar and mural TE diverged after embryos hatched from the zona pellucida in both species, with polar TE being more mature than mural TE. The implantation poles show similarities in cell cycle activities, as well as in expression of genes critical for implantation and placentation. Embryos that either fail to attach in vitro or fail to implant in vivo show abnormalities in pathways related to energy production, protein metabolism, and 18S ribosomal RNA m6A methylation. These findings uncover the gene expression characteristics of humans and mice TE differentiation during the peri-implantation period and provide new insights into embryo implantation.
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Project description:How embryonic blastomeres transition from totipotency to differentiation remains a fundamental question in developmental biology. Here, we uncover the transcription factor CEBPa as an orchestrator of this process. CEBPa expression is first activated by NR5A2 at the 2-cell to 4-cell transition and in a second wave peaks in the trophectoderm of blastocysts. Loss of CEBPa disrupts timely blastocyst formation and impairs trophectoderm development, while its forced expression in embryonic stem cells drives differentiation into trophectoderm-like cells. Mechanistically, CEBPa sequentially activates key trophectoderm enhancers in a dose-dependent manner. At the 4-cell stage, some of these trophectoderm enhancers are already active while others are primed or still closed, placing blastomeres in a state of alert. These findings establish CEBPa as a molecular switch that equips 4-cell blastomeres with the competence for trophectoderm differentiation, defining the earliest steps in cell fate bifurcation and shedding new light on the mechanisms driving embryonic lineage specification.
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Project description:How embryonic blastomeres transition from totipotency to differentiation remains a fundamental question in developmental biology. Here, we uncover the transcription factor CEBPa as an orchestrator of this process. CEBPa expression is first activated by NR5A2 at the 2-cell to 4-cell transition and in a second wave peaks in the trophectoderm of blastocysts. Loss of CEBPa disrupts timely blastocyst formation and impairs trophectoderm development, while its forced expression in embryonic stem cells drives differentiation into trophectoderm-like cells. Mechanistically, CEBPa sequentially activates key trophectoderm enhancers in a dose-dependent manner. At the 4-cell stage, some of these trophectoderm enhancers are already active while others are primed or still closed, placing blastomeres in a state of alert. These findings establish CEBPa as a molecular switch that equips 4-cell blastomeres with the competence for trophectoderm differentiation, defining the earliest steps in cell fate bifurcation and shedding new light on the mechanisms driving embryonic lineage specification.
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Project description:How embryonic blastomeres transition from totipotency to differentiation remains a fundamental question in developmental biology. Here, we uncover the transcription factor CEBPa as an orchestrator of this process. CEBPa expression is first activated by NR5A2 at the 2-cell to 4-cell transition and in a second wave peaks in the trophectoderm of blastocysts. Loss of CEBPa disrupts timely blastocyst formation and impairs trophectoderm development, while its forced expression in embryonic stem cells drives differentiation into trophectoderm-like cells. Mechanistically, CEBPa sequentially activates key trophectoderm enhancers in a dose-dependent manner. At the 4-cell stage, some of these trophectoderm enhancers are already active while others are primed or still closed, placing blastomeres in a state of alert. These findings establish CEBPa as a molecular switch that equips 4-cell blastomeres with the competence for trophectoderm differentiation, defining the earliest steps in cell fate bifurcation and shedding new light on the mechanisms driving embryonic lineage specification.
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Project description:How embryonic blastomeres transition from totipotency to differentiation remains a fundamental question in developmental biology. Here, we uncover the transcription factor CEBPa as an orchestrator of this process. CEBPa expression is first activated by NR5A2 at the 2-cell to 4-cell transition and in a second wave peaks in the trophectoderm of blastocysts. Loss of CEBPa disrupts timely blastocyst formation and impairs trophectoderm development, while its forced expression in embryonic stem cells drives differentiation into trophectoderm-like cells. Mechanistically, CEBPa sequentially activates key trophectoderm enhancers in a dose-dependent manner. At the 4-cell stage, some of these trophectoderm enhancers are already active while others are primed or still closed, placing blastomeres in a state of alert. These findings establish CEBPa as a molecular switch that equips 4-cell blastomeres with the competence for trophectoderm differentiation, defining the earliest steps in cell fate bifurcation and shedding new light on the mechanisms driving embryonic lineage specification.
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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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