The RbFox RNA binding proteins regulate alternative splicing of genes governing mammalian development and organ function. They bind to the RNA sequence (U)GCAUG with high affinity but also non-canonical secondary motifs in a concentration dependent manner. However, the hierarchical requirement of RbFox motifs, which are widespread in the genome, is still unclear. Here we show that deep intronic, tightly clustered RbFox1 motifs cooperate and are important regulators of alternative exons splicing. Bioinformatic analysis revealed that (U)GCAUG-clusters are widely present in both mouse and human genes and are embedded in sequences binding the large assembly of splicing regulators (LASR). Integrative data analysis from eCLIP and RNAseq experiments showed a global increase in RNA isoform modulation of genes with Rbfox1 eCLIP-peaks associated with these clusters. Experimentally, by employing recombineering mutagenesis in a bacterial artificial chromosome containing the NTrk2 mouse region subjected to alternative splicing we showed that tightly clustered (U)GCAUG motifs in the middle of 50 Kb introns are necessary for RbFox1 regulation of NTrk2 gene isoforms expression. Moreover, our data raise the possibility that clustered (U)GCAUG-motifs promote the recruitment of RbFox proteins to form a Rbfox/LASR complex required for splicing. Altogether, these data suggest that clustered, distal intronic Rbfox-binding motifs embedded in LASR binding sequences are important determinants of RbFox1 function in the mammalian genome and provide a target for identification of pathogenic mutations.
Clusters of deep intronic RbFox motifs embedded in large assembly of splicing regulators sequences regulate alternative splicing.
大量剪接调控序列中嵌入的深内含子 RbFox 基序簇调控选择性剪接
阅读:18
作者:Tomassoni-Ardori Francesco, Palko Mary Ellen, Galloux Melissa, Tessarollo Lino
| 期刊: | PLoS Genetics | 影响因子: | 3.700 |
| 时间: | 2025 | 起止号: | 2025 Sep 9; 21(9):e1011855 |
| doi: | 10.1371/journal.pgen.1011855 | ||
特别声明
1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。
2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。
3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。
4、投稿及合作请联系:info@biocloudy.com。
