H2B ubiquitylation modulates spliceosome assembly and function in budding yeast.

H2B ubiquitylation modulates spliceosome assembly and function in budding yeast.
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DOI:
10.1111/boc.201400003
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发表时间:
2014-04
影响因子:
2.7
通讯作者:
Dargemont C
Dargemont C
中科院分区:
生物学4区
文献类型:
--
作者:
Hérissant L;Moehle EA;Bertaccini D;Van Dorsselaer A;Schaeffer-Reiss C;Guthrie C;Dargemont C

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剪接发生在共转录过程中,但一个主要的未解决的问题是,体内转录模板染色质的各种修饰在多大程度上有助于剪接的调节。在这里,我们进行了全基因组分析,表明抑制特定标记- H2B泛素化,H3K4甲基化和H3K36甲基化-会干扰出芽酵母的剪接,每种修饰都会产生基因特异性作用。此外,纯化核mRNPs的半定量质谱分析和含内含子基因的染色质免疫沉淀分析表明,H2B泛素化,而不是Set1-、Set2-或dot1依赖性H3甲基化,刺激早期剪接因子(即U1和U2 snRNPs)募集到新生rna上。这些结果表明,组蛋白修饰通过不同的途径影响不同基因亚群的剪接。
Commitment to splicing occurs co-transcriptionally, but a major unanswered question is the extent to which various modifications of chromatin, the template for transcription in vivo, contribute to the regulation of splicing. Here we perform genome-wide analyses showing that inhibition of specific marks – H2B ubiquitylation, H3K4 methylation, and H3K36 methylation – perturbs splicing in budding yeast, with each modification exerting gene-specific effects. Furthermore, semi-quantitative mass spectrometry on purified nuclear mRNPs and chromatin immunoprecipitation analysis on intron-containing genes indicated that H2B ubiquitylation, but not Set1-, Set2- or Dot1-dependent H3 methylation, stimulates recruitment of the early splicing factors, namely U1 and U2 snRNPs, onto nascent RNAs. These results suggest that histone modifications impact splicing of distinct subsets of genes using distinct pathways.
人类中的相互内含子和外显子组蛋白修饰区。
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