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SON controls mouse early embryonic development by regulating RNA splicing and histone methylation

ABSTRACT: Thousands of genes are activated at later 2-cell embryos, which means that numerous pre-mRNAs are generated during this time. These pre-mRNAs must be accurately spliced to ensure that the mature mRNAs are translated to functional proteins. However, little is known about the roles of pre-mRNA splicing and cellular factors modulating pre-mRNA splicing during early embryonic development. Here, we report that downregulation of SON, a large Ser/Arg (SR)-related protein, reduced embryonic development and caused deficient blastomere cleavage. These embryonic developmental defects resulted from dysregulated nuclear speckle organization and pre-mRNA splicing of a set of cell-cycle-related genes. Furthermore, SON downregulation disturbed the transcriptome (2128 upregulation and 1399 downregulation) in 4-cell embryos. Increased H3K4me3, H3K9me3 and H3K27me3 levels were found in 4-cell embryos after SON downregulation. Taken together, those results demonstrate that accurate pre-mRNA splicing is essential for early embryonic development, and SON plays important roles on nuclear speckle organization, pre-mRNA splicing, the transcriptome establishment and histone methylation reprogramming during early embryonic development.

ORGANISM(S): Mus musculus

PROVIDER: GSE273029 | GEO | 2025/07/31

REPOSITORIES: GEO

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Project description:Cold stress resulting from chilling and freezing temperatures substantially inhibits plant growth and reduces crop production worldwide. Tremendous research efforts have been focused on elucidating the molecular mechanisms of freezing tolerance in plants. Little is known about the molecular nature of chilling stress responses in plants. Here we found that two allelic mutants in a spliceosome component gene SmEb (smeb-1 and smeb-2) are defective in development and responses to chilling stress. RNA-seq analysis revealed that SmEb controls the splicing of many pre-mRNAs under chilling stress. The intron retentive COP1b splicing variant was dramatically induced by chilling stress in the smeb mutants. This nuclear-depleted COP1b lacks the nuclear speckle-localization capacity, supporting the regulatory role of COP1-HY5 interaction in hypocotyl elongation during chilling stress. Genetic evidence indicates that chilling-sensitive phenotype of the smeb mutants are partially rescued by the hy5 mutation. The transcription factor BES1 shows a dramatic defect in pre-mRNA splicing in the smeb mutants. Ectopic expression of the two BES1 splicing variants enhances the chilling sensitivity of the smeb-1 mutant. Biochemical and genetic analysis showed that CBFs act as negative upstream regulators of SmEb by directly suppressing its transcription. Together, our results demonstrate that proper alternative splicing of pre-mRNAs controlled by the spliceosome component SmEb is critical for plant development and chilling stress responses. Cold stress resulting from chilling and freezing temperatures substantially inhibits plant growth and reduces crop production worldwide. Tremendous research efforts have been focused on elucidating the molecular mechanisms of freezing tolerance in plants. Little is known about the molecular nature of chilling stress responses in plants. Here we found that two allelic mutants in a spliceosome component gene SmEb (smeb-1 and smeb-2) are defective in development and responses to chilling stress. RNA-seq analysis revealed that SmEb controls the splicing of many pre-mRNAs under chilling stress. The intron retentive COP1b splicing variant was dramatically induced by chilling stress in the smeb mutants. This nuclear-depleted COP1b lacks the nuclear speckle-localization capacity, supporting the regulatory role of COP1-HY5 interaction in hypocotyl elongation during chilling stress. Genetic evidence indicates that chilling-sensitive phenotype of the smeb mutants are partially rescued by the hy5 mutation. The transcription factor BES1 shows a dramatic defect in pre-mRNA splicing in the smeb mutants. Ectopic expression of the two BES1 splicing variants enhances the chilling sensitivity of the smeb-1 mutant. Biochemical and genetic analysis showed that CBFs act as negative upstream regulators of SmEb by directly suppressing its transcription. Together, our results demonstrate that proper alternative splicing of pre-mRNAs controlled by the spliceosome component SmEb is critical for plant development and chilling stress responses.

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SON controls mouse early embryonic development by regulating RNA splicing and histone methylation

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