ZNHIT3 regulates translation to ensure mouse preimplantation development [seRNA-Seq]
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE267997 | GEO | 2025/11/18
REPOSITORIES: GEO
Dataset's files
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| GSE267997_RAW.tar | Raw | |||
| GSE267997_Znhit3_seRNAseq_gene_count_matrix.csv.gz | Csv | |||
| filelist.txt | Txt |
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Project description:Upon fertilization, the mouse zygotic genome is activated, accompanied by degradation of maternal proteins and RNAs. The development programs are built by accumulation of proteins from zygotic genes to guide the early cell fate commitments. Box C/D snoRNA ribonucleoprotein (snoRNP) complex is required for rRNA biogenesis, ribosome assembly and pre-mRNA splicing necessary for protein translation. Zinc finger, HIT type 3 (encoded by Znhit3) was previously identified to be one component in the assembly of the box C/D snoRNP complex. Using gene-edited mice, we identify Znhit3 as a pioneer embryonic gene whose ablation prevents mouse embryos development beyond the morula stage due to reduced protein translation. Znhit3 ablation impairs snoRNA and rRNA levels which leads to defects of ribosomes and failure of mRNA splicing. Our results provide clear evidence that ZNHIT3 is required for mouse preimplantation development by controlling proper mRNA translation into protein.
2025-11-18 | GSE267991 | GEO
Project description:Upon fertilization, the mouse zygotic genome is activated, accompanied by degradation of maternal proteins and RNAs. The development programs are built by accumulation of proteins from zygotic genes to guide the early cell fate commitments. Box C/D snoRNA ribonucleoprotein (snoRNP) complex is required for rRNA biogenesis, ribosome assembly and pre-mRNA splicing necessary for protein translation. Zinc finger, HIT type 3 (encoded by Znhit3) was previously identified to be one component in the assembly of the box C/D snoRNP complex. Using gene-edited mice, we identify Znhit3 as a pioneer embryonic gene whose ablation prevents mouse embryos development beyond the morula stage due to reduced protein translation. Znhit3 ablation impairs snoRNA and rRNA levels which leads to defects of ribosomes and failure of mRNA splicing. Our results provide clear evidence that ZNHIT3 is required for mouse preimplantation development by controlling proper mRNA translation into protein.
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Project description:Glioblastoma (GBM) ranks among the most lethal of human cancers, containing glioma stem cells (GSCs) that display therapeutic resistance. Here, we report that the lncRNA INHEG is highly expressed in GSCs compared to differentiated glioma cells (DGCs) and promotes GSC self-renewal through control of rRNA 2’-O-methylation. INHEG induces the interaction between a novel SUMO E3 ligase TAF15 and NOP58, a core component of snoRNP that guides rRNA methylation, to regulate NOP58 sumoylation and accelerate the C/D box snoRNP assembly. INHEG activation enhances rRNA 2’-O-methylation, thereby increasing the translation of oncogenic proteins including EGFR and IGF1R in glioma cells. Taken together, this study identifies a lncRNA that connects snoRNP-guided rRNA 2’-O-methylation to upregulated protein translation in GSCs, supporting a new axis for potential therapeutic targeting of gliomas.
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