Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of preimplantation mouse embryos to study the requirement of the MAP kinase signaling pathway for preimplantation development.

ABSTRACT: We examined expression profiles of genes that could be regulated by the MAPK pathways during mouse preimplantation development. We used Affymetrix GeneChips for microarray analysis, and three independent experiments were carried out. 8-cell stage embryos were treated or untreated with MAPK inhibitors, and blastocyst stage embryos were recruited for the study. Hybridization was carried out with the GeneChip Mouse Expression Set 430 or GeneChip Mouse Genome 430 2.0 Array following Affymetrix instructions. The array was then washed and stained using the GeneChip fluidics station according to the manufacture's instructions. Hybridized arrays were scanned using an Affymetrix GeneChip Scanner. Expression analysis was performed using GeneChip Operating Software 1.0 (Affymetrix) and scaled to an average probe set intensity of 500.

ORGANISM(S): Mus musculus

SUBMITTER: Eisuke Nishida

PROVIDER: E-GEOD-2229 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Requirement of the MAP kinase signaling pathways for mouse preimplantation development.

Maekawa Momoko M Yamamoto Takuya T Tanoue Takuji T Yuasa Yasuhito Y Chisaka Osamu O Nishida Eisuke E

Development (Cambridge, England) 20050316 8

Mammalian preimplantation development involves several crucial events, such as compaction and blastocyst formation, but little is known about essential genes that regulate this developmental process. Here, we have focused on MAP kinase signaling pathways as potential regulatory pathways for the process. Our results show that inhibition of the JNK pathway or of the p38 MAP kinase pathway, but not of the ERK pathway, results in inhibition of cavity formation, and that JNK and p38 are active during ...[more]

PMID: 15772134

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Project description:Preimplantation development is a crucial step for successful implantation and pregnancy. Although both compaction and blastocyst formation have been extensively studied, mechanisms regulating early cell division stages before compaction have remained unclear. Here, we show that ERK MAP kinase function is required for early embryonic cell division and normal cell-cell adhesion before compaction. Our analysis demonstrates that inhibition of ERK activation in the late 2-cell stage embryos leads to a reversible arrest in G2 phase in the 4-cell stage. The G2 arrested, 4-cell stage embryos show weakened cell-cell adhesion as compared to control embryos. Remarkably, microarray analyses show that most of the programmed changes of upregulated and downregulated gene expression during the 4- to 8-cell stages normally proceed in the 4-cell stage-arrested embryos, except for a portion of the genes whose expression profiles closely parallel the stages of embryonic development when arrested in G2 and released to resume development. These parallel genes include the genes encoding intercellular adhesion molecules, whose expression is found to be positively regulated by the ERK pathway. We also show that while ERK inactivation in the 8-cell stage embryos does not lead to cell division arrest, it does cause cell division arrest when cadherin-mediated cell-cell adhesion is disrupted. These results demonstrate an essential role of ERK function in the G2/M transition and the expression of adhesion molecules during the 2-cell to 8-cell stage embryos, and suggest a loose parallelism between the gene expression programs and the developmental stages before compaction. Experiment Overall Design: We examined expression profiles of genes during early cell division stages in mouse preimplantation development. We performed the genome-wide analysis by using Affymetrix GeneChip oligonucleotide microarrays, and examined the effect of the ERK pathway inhibitor U0126 on the expression profiles. Two independent experiments were carried out. We collected embryos at six points as follows; control embryos at day 1.5 (cont. 1.5, 2-cell stage), day 2.5 (cont. 2.5, 4- to 8-cell), and day 3.5 (cont. 3.5, morula to blastocyst), and the U0126-treated embryos at day 2.5 (U2.5, 4-cell arrested), embryos released from the U0126-induced arrest at day 3.5 (U3.5, 8-cell) and at day 4.5 (U4.5, morula to blastocyst). Hybridization was carried out with the Mouse Genome 430 2.0 array following Affymetrix instructions. Hybridized arrays were scanned using an Affymetrix GeneChip Scanner. Expression analysis was performed using GeneChip Operating Software v. 1.2 (GCOS) and GeneSpring 7.3.

Dataset Information

Transcription profiling of preimplantation mouse embryos to study the requirement of the MAP kinase signaling pathway for preimplantation development.

Publications

Requirement of the MAP kinase signaling pathways for mouse preimplantation development.

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