WBP11 is required for splicing the TUBGCP6 pre-mRNA to promote centriole duplication
| العنوان: | WBP11 is required for splicing the TUBGCP6 pre-mRNA to promote centriole duplication |
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| المؤلفون: | Kevin M. Clutario, Phillip M. Scott, Elizabeth M. Park, Scott A. Gerber, Andrew J. Holland, Kevin H. Zhan, Katelyn B. Cassidy |
| المصدر: | The Journal of Cell Biology |
| بيانات النشر: | Rockefeller University Press, 2019. |
| سنة النشر: | 2019 |
| مصطلحات موضوعية: | RNA Splicing Factors, Spliceosome, Centriole, RNA Splicing, Nuclear Receptor Coactivators, Mitosis, Biology, Article, 03 medical and health sciences, Splicing factor, 0302 clinical medicine, RNA Precursors, Humans, RNA, Messenger, Research Articles, Centrioles, 030304 developmental biology, Centrosome, 0303 health sciences, Cell Cycle, Intron, Cell Biology, HCT116 Cells, humanities, Introns, Cell biology, DNA-Binding Proteins, WBP11, Colonic Neoplasms, RNA splicing, Transcriptome, Microtubule-Associated Proteins, 030217 neurology & neurosurgery, HeLa Cells |
| الوصف: | Park et al. identify a role for a subset of mRNA splicing factors, including WBP11, in centriole biogenesis. WBP11 is required for the splicing of short, weak introns, including those found in TUBGCP6 pre-mRNA. Splicing of TUBGCP6, as well as other WBP11 targets, allows for faithful mitotic progression and centriole duplication. Centriole duplication occurs once in each cell cycle to maintain centrosome number. A previous genome-wide screen revealed that depletion of 14 RNA splicing factors leads to a specific defect in centriole duplication, but the cause of this deficit remains unknown. Here, we identified an additional pre-mRNA splicing factor, WBP11, as a novel protein required for centriole duplication. Loss of WBP11 results in the retention of ∼200 introns, including multiple introns in TUBGCP6, a central component of the γ-TuRC. WBP11 depletion causes centriole duplication defects, in part by causing a rapid decline in the level of TUBGCP6. Several additional splicing factors that are required for centriole duplication interact with WBP11 and are required for TUBGCP6 expression. These findings provide insight into how the loss of a subset of splicing factors leads to a failure of centriole duplication. This may have clinical implications because mutations in some spliceosome proteins cause microcephaly and/or growth retardation, phenotypes that are strongly linked to centriole defects. |
| تدمد: | 1540-8140 0021-9525 |
| DOI: | 10.1083/jcb.201904203 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ea628187e8c6a45011b5401b347ab567 https://doi.org/10.1083/jcb.201904203 |
| Rights: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....ea628187e8c6a45011b5401b347ab567 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15408140 00219525 |
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| DOI: | 10.1083/jcb.201904203 |