PI3K/AKT signalling regulates mouse Inner Cell Mass (ICM) progenitor specification [FLASH-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1104168 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28797824_1.fastq.gz | Fastqsanger.gz | |||
| SRR28797824_2.fastq.gz | Fastqsanger.gz | |||
| SRR28797825_1.fastq.gz | Fastqsanger.gz | |||
| SRR28797825_2.fastq.gz | Fastqsanger.gz | |||
| SRR28797826_1.fastq.gz | Fastqsanger.gz |
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Project description:The inner cell mass (ICM) of early mouse embryos is specified into Epiblast (Epi) and primitive endoderm (PrE) lineages during blastocyst formation. The antagonistic transcription factors (TFs) NANOG and GATA6 in combination with FGF/ERK signaling are central actors in ICM fate choice. However, what initiates the specification of the bipotent ICM progenitor and whether other factors are involved in this process is not fully understood yet. Here, we report the key role of PI3K in mouse ICM progenitors specification. Surprisingly, while the PI3K/AKT signaling pathway is known for almost two decades to participate to the maintenance of pluripotency in stem cells, no role for this pathway in ICM cell fate decisions has been reported so far. This is likely due to the dynamic and asynchronous nature of ICM specification combined with the pleiotropic and rapidly evolving functions mediated by PI3K/AKT. By limiting the perturbations of the pathway to a short time-window corresponding to the early phase of ICM specification, we unravelled a dual role of PI3K in ICM progenitor, being required on the one hand for the maintenance of pluripotency TFs and, on the other hand, for the competence to engage into PrE differentiation in response to FGF signaling. Thus, our work identifies PI3K as a novel critical regulator of ICM progenitor specification in the mouse embryo.
2024-10-25 | GSE265767 | GEO
Project description:The inner cell mass (ICM) of early mouse embryos is specified into Epiblast (Epi) and primitive endoderm (PrE) lineages during blastocyst formation. The antagonistic transcription factors (TFs) NANOG and GATA6 in combination with FGF/ERK signaling are central actors in ICM fate choice. However, what initiates the specification of the bipotent ICM progenitor and whether other factors are involved in this process is not fully understood yet. Here, we report the key role of PI3K in mouse ICM progenitors specification. Surprisingly, while the PI3K/AKT signaling pathway is known for almost two decades to participate to the maintenance of pluripotency in stem cells, no role for this pathway in ICM cell fate decisions has been reported so far. This is likely due to the dynamic and asynchronous nature of ICM specification combined with the pleiotropic and rapidly evolving functions mediated by PI3K/AKT. By limiting the perturbations of the pathway to a short time-window corresponding to the early phase of ICM specification, we unravelled a dual role of PI3K in ICM progenitor, being required on the one hand for the maintenance of pluripotency TFs and, on the other hand, for the competence to engage into PrE differentiation in response to FGF signaling. Thus, our work identifies PI3K as a novel critical regulator of ICM progenitor specification in the mouse embryo.
2024-10-25 | GSE234578 | GEO
Project description:PI3K/AKT signalling regulates mouse Inner Cell Mass (ICM) progenitor specification [scRNA-seq]
| PRJNA982080 | ENA
Project description:Inner cell mass (ICM) cells of two independent E3.5 blastocysts were profiled by transcriptome sequencing to assess the expression of extracellular matrix components.
2014-05-15 | E-MTAB-2555 | biostudies-arrayexpress
Project description:The inner cell mass (ICM) of the early blastocyst at E3.5, a source of ES cell derivation, is a morphologically homogeneous population of undifferentiated pluripotent cells that give rise to all embryonic lineages. The immediate application of the newly developed V1V3 method to single cells in this stage of mouse embryos revealed the presence of two populations of cells, one with primitive endoderm expression and the other with pluripotent epiblast-like gene expression. The genes expressed differentially between these two populations were well preserved in morphologically differentiated primitive endoderm and epiblast in the embryos one day later (E4.5), demonstrating that the method successfully detects subtle but essential differences in gene expression at the single-cell level among seemingly homogeneous cell populations. This study provides a strategy to analyze biophysical events in medicine as well as in neural, stem cell, and developmental biology, where small numbers of distinctive or diseased cells play critical roles. Experiment Overall Design: We isolated blastocysts at E3.5 and dissociated the ICM into single cells by trypsin-EDTA treatment. To prepare cDNA samples, we then randomly picked a total of 55 single cells. cDNAs were synthesized and amplified by the V1V3 method, and screened by gene-specific PCR using Oct4 and Cdx2 to remove trophectoderm cells, and 50 cells were identified as Oct4-positive and Cdx2-negative, ICM cells.
2008-06-13 | E-GEOD-4307 | biostudies-arrayexpress
Project description:Aneuploidy has been well documented in blastocyst embryos, but prior studies have been limited in scale and/or lack mechanistic data. We previously reported preclinical validation of microarray 24-chromosome preimplantation genetic screening (PGS) in a 24-hour protocol. The method diagnoses chromosome copy number, structural chromosome aberrations, parental source of aneuploidy, and distinguishes certain meiotic from mitotic errors. In this study our objective was to examine aneuploidy in human blastocysts and determine correspondence of karyotypes between trophectoderm (TE) and inner cell mass (ICM). We disaggregated 51 blastocysts from seventeen couples into ICM and one or two TE fractions. The average maternal age was 31. Next, we ran 24-chromosome microarray molecular karyotyping on all of the samples, and then performed a retrospective analysis of the data. The average per-chromosome confidence was 99.95%. Approximately 80% of blastocysts were euploid. The majority of aneuploid embryos were simple aneuploid, i.e., one or two whole-chromosome imbalances. Structural chromosome aberrations, which are common in cleavage stage embryos, occurred in only three blastocysts (5.8%). All TE biopsies derived from the same embryos were concordant. Forty-nine of fifty-one (96.1%) inner cell mass (ICM) samples were concordant with TE biopsies derived from the same embryos. Discordance between TE and ICM occurred only in the two embryos with structural chromosome aberration. We conclude that trophectoderm karyotype is an excellent predictor of inner cell mass karyotype. Discordance between TE and ICM occurred only in embryos with structural chromosome aberrations.
2010-09-28 | GSE22864 | GEO
Project description:This study describes the generation and analysis of the transcriptional profile of bovine inner cell mass (ICM) and trophectoderm (TE), obtained from in vivo developed embryos by using a bovine-embryo specific array (EmbryoGENE) containing 37,238 probes.
2015-12-02 | GSE75555 | GEO
Project description:Aneuploidy has been well documented in blastocyst embryos, but prior studies have been limited in scale and/or lack mechanistic data. We previously reported preclinical validation of microarray 24-chromosome preimplantation genetic screening (PGS) in a 24-hour protocol. The method diagnoses chromosome copy number, structural chromosome aberrations, parental source of aneuploidy, and distinguishes certain meiotic from mitotic errors. In this study our objective was to examine aneuploidy in human blastocysts and determine correspondence of karyotypes between trophectoderm (TE) and inner cell mass (ICM). We disaggregated 51 blastocysts from seventeen couples into ICM and one or two TE fractions. The average maternal age was 31. Next, we ran 24-chromosome microarray molecular karyotyping on all of the samples, and then performed a retrospective analysis of the data. The average per-chromosome confidence was 99.95%. Approximately 80% of blastocysts were euploid. The majority of aneuploid embryos were simple aneuploid, i.e., one or two whole-chromosome imbalances. Structural chromosome aberrations, which are common in cleavage stage embryos, occurred in only three blastocysts (5.8%). All TE biopsies derived from the same embryos were concordant. Forty-nine of fifty-one (96.1%) inner cell mass (ICM) samples were concordant with TE biopsies derived from the same embryos. Discordance between TE and ICM occurred only in the two embryos with structural chromosome aberration. We conclude that trophectoderm karyotype is an excellent predictor of inner cell mass karyotype. Discordance between TE and ICM occurred only in embryos with structural chromosome aberrations. We thawed all fractions at 22°C, and then added Arcturus PicoPure Lysis Buffer (Molecular Devices, Sunnyvale, CA) to each of the biopsies. The tubes were incubated at 56°C for one hour, and then heat inactivated at 95°C for 10 minutes. DNA from the lysed biospsies was amplified using a commercial kit (GE Healthcare, Waukesha, WI) for multiple displacement amplification (MDA). MDA reactions were incubated at 30°C for 2.5 hours and then heat-inactivated at 65°C for five minutes. The amplified samples were genotyped using Illumina (San Diego, CA, USA) Infinium II genotyping microarrays (CytoSNP-12 chips) using a modified 24-hour protocol, as described previously*. Previously, we developed a genotyping microarray molecular karyotyping technology that uses parental genetic data to increase accuracy and determine mechanism and source of aneuploidy*. The algorithm uses parental genotypes and the observed distribution of unprocessed single cell microarray channel intensities to diagnose whole-chromosome imbalances and structural chromosome aberrations*. Because parental genotypes are available, the algorithm readily identifies parental source of whole-chromosome imbalances and structural chromosome aberrations. Additionally, the algorithm uses parental information, high confidence disomic single cell measurements on children, and recombination probabilities (genome.ucsc.edu) to determine the phase of the parental chromosomes. The phased data is then used to determine whether certain trisomies and uniparental disomies were mitotic or meiotic in origin*. *Johnson DS, Gemelos G, Baner J, Ryan A, Cinnioglu C, Banjevic M, Ross R, Alper M, Barrett B, Frederick J, Potter D, Behr B, Rabinowitz M. (2010). Preclinical validation of a microarray method for full molecular karyotyping of blastomeres in a 24-hour protocol. Human Reproduction January 24 [Epub ahead of print].
2010-09-28 | E-GEOD-22864 | biostudies-arrayexpress
Project description:The goal of this study is elucidating the mechanisms of the primitive endoderm (PrE, founder of the yolk sac) segregates from the epiblast (EPI, founder of the foetus). Within the uterus and ex vivo, precursors of the EPI and PrE emerge in an unsorted manner in inner cell mass (ICM). Coincident with identity acquisition, the cells physically sort, resulting in PrE establishing a single layer of cells covering the cavity-facing surface of the ICM with the EPI enclosed between the PrE and polar trophectoderm. The mechanism that determines this spatial segregation between EPI and PrE is still poorly understood. To achieve this goal, we have compared mouse embryonic day (E) 3.75 ICM cells’ transcriptome profiling to other existing mouse E3.5 and E4.5 ICM cells’ RNA-seq data. We have identified the timing of EPI and PrE lineages specification and maturation and each stage- and lineage-specific genes expression profiles.
2022-01-09 | GSE148462 | GEO
Project description:Networks of interacting co-regulated genes distinguish the inner cell mass (ICM) from the differentiated trophectoderm (TE) in the preimplantation blastocyst, in a species specific manner. In mouse the ground state pluripotency of the ICM appears to be maintained in murine embryonic stem cells (ESCs) derived from the ICM. This is not the case for human ESCs. In order to gain insight into this phenomenon, we have used network analysis to quantify how similar human (h)ESCs are to the human ICM. Using the hESC lines MAN1, HUES3 and HUES7 we have shown that all have only a limited overlap with ICM specific gene expression, but that this overlap is enriched for network properties that correspond to key aspects of function including transcription factor activity and the hierarchy of network modules. These analyses provide an important framework which highlights the developmental origins of hESCs.
2019-03-31 | GSE121982 | GEO