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ZNHIT3 Regulates Translation to Ensure Cell Lineage Differentiation in Mouse Preimplantation Development

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE268043 | GEO | 2025/11/18

REPOSITORIES: GEO

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ZNHIT3 Regulates Translation to Ensure Cell Lineage Differentiation in Mouse Preimplantation Development [SMARMseq]

Project description:Upon fertilization, the mouse zygotic genome is activated and maternal RNAs as well as proteins are degraded. Early developmental programs are built on proteins encoded by zygotic mouse genes that are needed to guide early cell fate commitment. The box C/D snoRNA ribonucleoprotein (snoRNP) complex is required for rRNA biogenesis, ribosome assembly and pre-mRNA splicing essential for protein translation. Zinc finger, HIT type 3 (encoded by Znhit3) is previously identified as a component in the assembly of the box C/D snoRNP complex. Using gene-edited mice, it identifies Znhit3 as an early embryonic gene whose ablation reduces protein translation and prevents mouse embryos development beyond the morula stage. The absence of ZNHIT3 leads to decreased snoRNA and rRNA abundance which causes defects of ribosomes and mRNA splicing. Microinjection of Znhit3 cRNA partially rescues the phenotype and confirms that ZNHIT3 is required for mRNA translation during preimplantation development.

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ZNHIT3 Regulates Translation to Ensure Cell Lineage Differentiation in Mouse Preimplantation Development [scRNA-Seq]

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ZNHIT3 Regulates Translation to Ensure Cell Lineage Differentiation in Mouse Preimplantation Development [seRNA-Seq]

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ZNHIT3 Regulates Translation to Ensure Cell Lineage Differentiation in Mouse Preimplantation Development

Project description:ZNHIT3 Regulates Translation to Ensure Cell Lineage Differentiation in Mouse Preimplantation Development

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ZNHIT3 Regulates Translation to Ensure Cell Lineage Differentiation in Mouse Preimplantation Development [SMARMseq]

Project description:ZNHIT3 Regulates Translation to Ensure Cell Lineage Differentiation in Mouse Preimplantation Development [SMARMseq]

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ZNHIT3 Regulates Translation to Ensure Cell Lineage Differentiation in Mouse Preimplantation Development [scRNA-Seq]

Project description:ZNHIT3 Regulates Translation to Ensure Cell Lineage Differentiation in Mouse Preimplantation Development [scRNA-Seq]

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ZNHIT3 Regulates Translation to Ensure Cell Lineage Differentiation in Mouse Preimplantation Development [seRNA-Seq]

Project description:ZNHIT3 Regulates Translation to Ensure Cell Lineage Differentiation in Mouse Preimplantation Development [seRNA-Seq]

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WDR36 Regulates Trophectoderm Differentiation During Human Preimplantation Embryonic Development Through Glycolytic Metabolism.

Project description:Mammalian pre-implantation development is a complex process involving sophisticated regulatory dynamics. WD repeat domain 36 (WDR36) is known to play a critical role in mouse early embryonic development, but its regulatory function in human embryogenesis is still elusive due to limited access to human embryos. The human pluripotent stem cell-derived blastocyst-like structure, termed a blastoid, offers an alternative means to study human development in a dish. In this study, after verifying that WDR36 inhibition disrupted polarization in mouse early embryos, it is further demonstrated that WDR36 interference can block human blastoid formation, dominantly hindering the trophectoderm lineage commitment. Both transcriptomics and targeted metabolomics analyses revealed that WDR36 interference downregulated glucose metabolism. WDR36 can interact with glycolytic metabolic protein lactate dehydrogenase A (LDHA), thereby positively regulating glycolysis during the late stage of human blastoid formation. Taken together, the study has established a mechanistic connection between WDR36, glucose metabolism, and cell fate determination during early embryonic lineage commitment, which may provide potential insights into novel therapeutic targets for early adverse pregnancy interventions.

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CTR9/PAF1c regulates molecular lineage identity, histone H3K36 trimethylation and genomic imprinting during preimplantation development.

Project description:Genome-wide epigenetic reprogramming is required for successful preimplantation development. Inappropriate or deficient chromatin regulation can result in defective lineage specification and loss of genomic imprinting, compromising normal development. Here we report that two members of the RNA polymerase II associated factor, homolog (Saccharomyces cerevisiae) complex (PAF1 complex) components, Ctr9 and Rtf1, are required during mammalian preimplantation development. We demonstrate that Ctr9-deficient embryos fail to correctly specify lineages at the blastocyst stage. Expression of some lineage specific factors is markedly reduced in Ctr9 knockdown embryos, including Eomes, Elf5 and Sox2, while others are inappropriately expressed (Oct4, Nanog, Gata6, Fgf4 and Sox17). We also show that several imprinted genes (Mest, Peg3, Snrpn and Meg3) are aberrantly expressed although allele specific DNA methylation is not altered. We document a loss of histone H3 lysine 36 trimethylation (H3K36me3) in Ctr9-deficient embryos and confirm that knockdown of either Setd2 or Rtf1 results in similar phenotypes. These findings show that the PAF1 complex is required for mammalian development, likely through regulation of H3K36me3, and indicate functional conservation of the PAF1 complex from yeast to mammals in vivo.

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Essential roles of HDAC1 and 2 in lineage development and genome-wide DNA methylation during mouse preimplantation development.

Project description:Epigenetic modifications, including DNA methylation and histone modifications, are reprogrammed considerably following fertilization during mammalian early embryonic development. Incomplete epigenetic reprogramming is a major factor leading to poor developmental outcome in embryos generated by assisted reproductive technologies, such as somatic cell nuclear transfer. However, the role of histone modifications in preimplantation development is poorly understood. Here, we show that co-knockdown (cKD) of Hdac1 and 2 (but not individually) resulted in developmental failure during the morula to blastocyst transition. This outcome was also confirmed with the use of small-molecule HDAC1/2-specific inhibitor FK228. We observed reduced cell proliferation and increased incidence of apoptosis in cKD embryos, which were likely caused by increased acetylation of TRP53. Importantly, both RNA-seq and immunostaining analysis revealed a failure of lineage specification to generate trophectoderm and pluripotent cells. Among many gene expression changes, a substantial decrease of Cdx2 may be partly accounted for by the aberrant Hippo pathway occurring in cKD embryos. In addition, we observed an increase in global DNA methylation, consistent with increased DNA methyltransferases and UHRF1. Interestingly, deficiency of RBBP4 and 7 (both are core components of several HDAC1/2-containing epigenetic complexes) results in similar phenotypes as those of cKD embryos. Overall, HDAC1 and 2 play redundant functions required for lineage specification, cell viability and accurate global DNA methylation, each contributing to critical developmental programmes safeguarding a successful preimplantation development.

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