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Journal articles on the topic 'RNA splicing'

To see the other types of publications on this topic, follow the link: RNA splicing.

Author: Grafiati

Published: 4 June 2021

Last updated: 26 July 2024

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1

van den Hoogenhof, Maarten M. G., Yigal M. Pinto, and Esther E. Creemers. "RNA Splicing." Circulation Research 118, no. 3 (February 5, 2016): 454–68. http://dx.doi.org/10.1161/circresaha.115.307872.

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2

Newman, Andy. "RNA splicing." Current Biology 8, no. 25 (December 1998): R903—R905. http://dx.doi.org/10.1016/s0960-9822(98)00005-0.

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3

Zong, Xinying, Vidisha Tripathi, and Kannanganattu V. Prasanth. "RNA splicing control." RNA Biology 8, no. 6 (November 2011): 968–77. http://dx.doi.org/10.4161/rna.8.6.17606.

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4

GUTHRIE, CHRISTINE. "Catalytic RNA and RNA Splicing." American Zoologist 29, no. 2 (May 1989): 557–67. http://dx.doi.org/10.1093/icb/29.2.557.

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5

Newman, Andy. "RNA enzymes for RNA splicing." Nature 413, no. 6857 (October 2001): 695–96. http://dx.doi.org/10.1038/35099665.

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6

David, Rachel. "Visualizing RNA splicing." Nature Reviews Molecular Cell Biology 14, no. 11 (October 23, 2013): 688. http://dx.doi.org/10.1038/nrm3689.

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7

Hryckiewicz, Katarzyna, Maciej Bura, Arleta Kowala-Piaskowska, Beata Bolewska, and Iwona Mozer-Lisewska. "HIV RNA splicing." HIV & AIDS Review 10, no. 3 (September 2011): 61–64. http://dx.doi.org/10.1016/j.hivar.2011.05.001.

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8

Koodathingal, Prakash, and Jonathan P. Staley. "Splicing fidelity." RNA Biology 10, no. 7 (July 2013): 1073–79. http://dx.doi.org/10.4161/rna.25245.

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9

Cordin, Olivier, and Jean D. Beggs. "RNA helicases in splicing." RNA Biology 10, no. 1 (January 2013): 83–95. http://dx.doi.org/10.4161/rna.22547.

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10

Einstein, Richard. "Splicing 2002: RNA splicing in human pathology." Pharmacogenomics 4, no. 1 (January 2003): 19–22. http://dx.doi.org/10.1517/phgs.4.1.19.22591.

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11

Witten, Joshua T., and Jernej Ule. "Understanding splicing regulation through RNA splicing maps." Trends in Genetics 27, no. 3 (March 2011): 89–97. http://dx.doi.org/10.1016/j.tig.2010.12.001.

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12

Busch, Anke, and Klemens J. Hertel. "Splicing predictions reliably classify different types of alternative splicing." RNA 21, no. 5 (March 24, 2015): 813–23. http://dx.doi.org/10.1261/rna.048769.114.

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13

Escobar-Hoyos, Luisa, Katherine Knorr, and Omar Abdel-Wahab. "Aberrant RNA Splicing in Cancer." Annual Review of Cancer Biology 3, no. 1 (March 4, 2019): 167–85. http://dx.doi.org/10.1146/annurev-cancerbio-030617-050407.

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RNA splicing, the enzymatic process of removing segments of premature RNA to produce mature RNA, is a key mediator of proteome diversity and regulator of gene expression. Increased systematic sequencing of the genome and transcriptome of cancers has identified a variety of means by which RNA splicing is altered in cancer relative to normal cells. These findings, in combination with the discovery of recurrent change-of-function mutations in splicing factors in a variety of cancers, suggest that alterations in splicing are drivers of tumorigenesis. Greater characterization of altered splicing in cancer parallels increasing efforts to pharmacologically perturb splicing and early-phase clinical development of small molecules that disrupt splicing in patients with cancer. Here we review recent studies of global changes in splicing in cancer, splicing regulation of mitogenic pathways critical in cancer transformation, and efforts to therapeutically target splicing in cancer.

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14

Disney, Matthew D. "Short-circuiting RNA splicing." Nature Chemical Biology 4, no. 12 (December 2008): 723–24. http://dx.doi.org/10.1038/nchembio1208-723.

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15

Brow, David A., and Christine Guthrie. "Splicing a spliceosomal RNA." Nature 337, no. 6202 (January 1989): 14–15. http://dx.doi.org/10.1038/337014a0.

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16

Wang, Eric, and Iannis Aifantis. "RNA Splicing and Cancer." Trends in Cancer 6, no. 8 (August 2020): 631–44. http://dx.doi.org/10.1016/j.trecan.2020.04.011.

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17

Sharp, Phillip A. "RNA Splicing and Genes." JAMA: The Journal of the American Medical Association 260, no. 20 (November 25, 1988): 3035. http://dx.doi.org/10.1001/jama.1988.03410200091032.

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18

ABELSON, J. "RNA splicing in yeast." Cell Biology International Reports 14 (September 1990): 41. http://dx.doi.org/10.1016/0309-1651(90)90275-4.

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19

Sharp, P. A. "RNA splicing and genes." JAMA: The Journal of the American Medical Association 260, no. 20 (November 25, 1988): 3035–41. http://dx.doi.org/10.1001/jama.260.20.3035.

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20

Li, Zhaoxia, Jie Tang, Diane C. Bassham, and Stephen H. Howell. "Daily temperature cycles promote alternative splicing of RNAs encoding SR45a, a splicing regulator in maize." Plant Physiology 186, no. 2 (March 10, 2021): 1318–35. http://dx.doi.org/10.1093/plphys/kiab110.

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Abstract Elevated temperatures enhance alternative RNA splicing in maize (Zea mays) with the potential to expand the repertoire of plant responses to heat stress. Alternative RNA splicing generates multiple RNA isoforms for many maize genes, and here we observed changes in the pattern of RNA isoforms with temperature changes. Increases in maximum daily temperature elevated the frequency of the major modes of alternative splices (AS), in particular retained introns and skipped exons. The genes most frequently targeted by increased AS with temperature encode factors involved in RNA processing and plant development. Genes encoding regulators of alternative RNA splicing were themselves among the principal AS targets in maize. Under controlled environmental conditions, daily changes in temperature comparable to field conditions altered the abundance of different RNA isoforms, including the RNAs encoding the splicing regulator SR45a, a member of the SR45 gene family. We established an “in protoplast” RNA splicing assay to show that during the afternoon on simulated hot summer days, SR45a RNA isoforms were produced with the potential to encode proteins efficient in splicing model substrates. With the RNA splicing assay, we also defined the exonic splicing enhancers that the splicing-efficient SR45a forms utilize to aid in the splicing of model substrates. Hence, with rising temperatures on hot summer days, SR45a RNA isoforms in maize are produced with the capability to encode proteins with greater RNA splicing potential.

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21

Eul, Joachim, and Volker Patzel. "Homologous SV40 RNA trans-splicing." RNA Biology 10, no. 11 (November 2013): 1689–99. http://dx.doi.org/10.4161/rna.26707.

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22

Cheng, Soo-Chen. "RNA splicing for 30 years." RNA 21, no. 4 (March 16, 2015): 586–87. http://dx.doi.org/10.1261/rna.050021.115.

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23

Jacquier, Valentin, Manon Prévot, Thierry Gostan, Rémy Bordonné, Sofia Benkhelifa-Ziyyat, Martine Barkats, and Johann Soret. "Splicing efficiency of minor introns in a mouse model of SMA predominantly depends on their branchpoint sequence and can involve the contribution of major spliceosome components." RNA 28, no. 3 (December 10, 2021): 303–19. http://dx.doi.org/10.1261/rna.078329.120.

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Spinal muscular atrophy (SMA) is a devastating neurodegenerative disease caused by reduced amounts of the ubiquitously expressed Survival of Motor Neuron (SMN) protein. In agreement with its crucial role in the biogenesis of spliceosomal snRNPs, SMN-deficiency is correlated to numerous splicing alterations in patient cells and various tissues of SMA mouse models. Among the snRNPs whose assembly is impacted by SMN-deficiency, those involved in the minor spliceosome are particularly affected. Importantly, splicing of several, but not all U12-dependent introns has been shown to be affected in different SMA models. Here, we have investigated the molecular determinants of this differential splicing in spinal cords from SMA mice. We show that the branchpoint sequence (BPS) is a key element controlling splicing efficiency of minor introns. Unexpectedly, splicing of several minor introns with suboptimal BPS is not affected in SMA mice. Using in vitro splicing experiments and oligonucleotides targeting minor or major snRNAs, we show for the first time that splicing of these introns involves both the minor and major machineries. Our results strongly suggest that splicing of a subset of minor introns is not affected in SMA mice because components of the major spliceosome compensate for the loss of minor splicing activity.

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24

Siam, Ahmad, Mai Baker, Leah Amit, Gal Regev, Alona Rabner, Rauf Ahmad Najar, Mercedes Bentata, et al. "Regulation of alternative splicing by p300-mediated acetylation of splicing factors." RNA 25, no. 7 (April 15, 2019): 813–24. http://dx.doi.org/10.1261/rna.069856.118.

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25

Zhang, X. H. F., M. A. Arias, S. Ke, and L. A. Chasin. "Splicing of designer exons reveals unexpected complexity in pre-mRNA splicing." RNA 15, no. 3 (January 20, 2009): 367–76. http://dx.doi.org/10.1261/rna.1498509.

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26

ZHENG, C. L. "MAASE: An alternative splicing database designed for supporting splicing microarray applications." RNA 11, no. 12 (December 1, 2005): 1767–76. http://dx.doi.org/10.1261/rna.2650905.

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27

Lazarev, D., and J. L. Manley. "Concurrent splicing and transcription are not sufficient to enhance splicing efficiency." RNA 13, no. 9 (July 13, 2007): 1546–57. http://dx.doi.org/10.1261/rna.595907.

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28

Gudikote, Jayanthi P., J. Saadi Imam, Ramon F. Garcia, and Miles F. Wilkinson. "RNA splicing promotes translation and RNA surveillance." Nature Structural & Molecular Biology 12, no. 9 (August 21, 2005): 801–9. http://dx.doi.org/10.1038/nsmb980.

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29

Majerciak, Vladimir, Beatriz Alvarado-Hernandez, Alexei Lobanov, Maggie Cam, and Zhi-Ming Zheng. "Genome-wide regulation of KSHV RNA splicing by viral RNA-binding protein ORF57." PLOS Pathogens 18, no. 7 (July 14, 2022): e1010311. http://dx.doi.org/10.1371/journal.ppat.1010311.

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RNA splicing plays an essential role in the expression of eukaryotic genes. We previously showed that KSHV ORF57 is a viral splicing factor promoting viral lytic gene expression. In this report, we compared the splicing profile of viral RNAs in BCBL-1 cells carrying a wild-type (WT) versus the cells containing an ORF57 knock-out (57KO) KSHV genome during viral lytic infection. Our analyses of viral RNA splice junctions from RNA-seq identified 269 RNA splicing events in the WT and 255 in the 57KO genome, including the splicing events spanning large parts of the viral genome and the production of vIRF4 circRNAs. We found that the 57KO alters the RNA splicing efficiency of targeted viral RNAs. Two most susceptible RNAs to ORF57 splicing regulation are the K15 RNA with multiple exons and introns and the bicistronic RNA encoding both viral thymidylate synthase (ORF70) and membrane-associated E3-ubiquitin ligase (K3). ORF70-K3 RNA bears two introns, of which the first intron is within the ORF70 coding region as an alternative intron and the second intron in the intergenic region between the ORF70 and K3 as a constitutive intron. In the WT cells expressing ORF57, most ORF70-K3 transcripts retain the first intron to maintain an intact ORF70 coding region. In contrast, in the 57KO cells, the first intron is substantially spliced out. Using a minigene comprising of ORF70-K3 locus, we further confirmed ORF57 regulation of ORF70-K3 RNA splicing, independently of other viral factors. By monitoring protein expression, we showed that ORF57-mediated retention of the first intron leads to the expression of full-length ORF70 protein. The absence of ORF57 promotes the first intron splicing and expression of K3 protein. Altogether, we conclude that ORF57 regulates alternative splicing of ORF70-K3 bicistronic RNA to control K3-mediated immune evasion and ORF70 participation of viral DNA replication in viral lytic infection.

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30

Hinkle, Emma R., Hannah J. Wiedner, Eduardo V. Torres, Micaela Jackson, Adam J. Black, R. Eric Blue, Sarah E. Harris, et al. "Alternative splicing regulation of membrane trafficking genes during myogenesis." RNA 28, no. 4 (January 26, 2022): 523–40. http://dx.doi.org/10.1261/rna.078993.121.

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Alternative splicing transitions occur during organ development, and, in numerous diseases, splicing programs revert to fetal isoform expression. We previously found that extensive splicing changes occur during postnatal mouse heart development in genes encoding proteins involved in vesicle-mediated trafficking. However, the regulatory mechanisms of this splicing-trafficking network are unknown. Here, we found that membrane trafficking genes are alternatively spliced in a tissue-specific manner, with striated muscles exhibiting the highest levels of alternative exon inclusion. Treatment of differentiated muscle cells with chromatin-modifying drugs altered exon inclusion in muscle cells. Examination of several RNA-binding proteins revealed that the poly-pyrimidine tract binding protein 1 (PTBP1) and quaking regulate splicing of trafficking genes during myogenesis, and that removal of PTBP1 motifs prevented PTBP1 from binding its RNA target. These findings enhance our understanding of developmental splicing regulation of membrane trafficking proteins which might have implications for muscle disease pathogenesis.

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31

Kim, Eddo, Amir Goren, and Gil Ast. "Alternative splicing and disease." RNA Biology 5, no. 1 (January 2008): 17–19. http://dx.doi.org/10.4161/rna.5.1.5944.

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32

Ke, Shengdong, and Lawrence A. Chasin. "Context-dependent splicing regulation." RNA Biology 8, no. 3 (May 2011): 384–88. http://dx.doi.org/10.4161/rna.8.3.14458.

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33

Vicens, Q., P. J. Paukstelis, E. Westhof, A. M. Lambowitz, and T. R. Cech. "Toward predicting self-splicing and protein-facilitated splicing of group I introns." RNA 14, no. 10 (August 28, 2008): 2013–29. http://dx.doi.org/10.1261/rna.1027208.

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34

Prudêncio, Pedro, Rosina Savisaar, Kenny Rebelo, Rui Gonçalo Martinho, and Maria Carmo-Fonseca. "Transcription and splicing dynamics during early Drosophila development." RNA 28, no. 2 (October 19, 2021): 139–61. http://dx.doi.org/10.1261/rna.078933.121.

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Widespread cotranscriptional splicing has been demonstrated from yeast to human. However, most studies to date addressing the kinetics of splicing relative to transcription used either Saccharomyces cerevisiae or metazoan cultured cell lines. Here, we adapted native elongating transcript sequencing technology (NET-seq) to measure cotranscriptional splicing dynamics during the early developmental stages of Drosophila melanogaster embryos. Our results reveal the position of RNA polymerase II (Pol II) when both canonical and recursive splicing occur. We found heterogeneity in splicing dynamics, with some RNAs spliced immediately after intron transcription, whereas for other transcripts no splicing was observed over the first 100 nt of the downstream exon. Introns that show splicing completion before Pol II has reached the end of the downstream exon are necessarily intron-defined. We studied the splicing dynamics of both nascent pre-mRNAs transcribed in the early embryo, which have few and short introns, as well as pre-mRNAs transcribed later in embryonic development, which contain multiple long introns. As expected, we found a relationship between the proportion of spliced reads and intron size. However, intron definition was observed at all intron sizes. We further observed that genes transcribed in the early embryo tend to be isolated in the genome whereas genes transcribed later are often overlapped by a neighboring convergent gene. In isolated genes, transcription termination occurred soon after the polyadenylation site, while in overlapped genes, Pol II persisted associated with the DNA template after cleavage and polyadenylation of the nascent transcript. Taken together, our data unravel novel dynamic features of Pol II transcription and splicing in the developing Drosophila embryo.

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35

Tang, Zhichao, Junxing Zhao, Zach J. Pearson, Zarko V. Boskovic, and Jingxin Wang. "RNA-Targeting Splicing Modifiers: Drug Development and Screening Assays." Molecules 26, no. 8 (April 14, 2021): 2263. http://dx.doi.org/10.3390/molecules26082263.

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RNA splicing is an essential step in producing mature messenger RNA (mRNA) and other RNA species. Harnessing RNA splicing modifiers as a new pharmacological modality is promising for the treatment of diseases caused by aberrant splicing. This drug modality can be used for infectious diseases by disrupting the splicing of essential pathogenic genes. Several antisense oligonucleotide splicing modifiers were approved by the U.S. Food and Drug Administration (FDA) for the treatment of spinal muscular atrophy (SMA) and Duchenne muscular dystrophy (DMD). Recently, a small-molecule splicing modifier, risdiplam, was also approved for the treatment of SMA, highlighting small molecules as important warheads in the arsenal for regulating RNA splicing. The cellular targets of these approved drugs are all mRNA precursors (pre-mRNAs) in human cells. The development of novel RNA-targeting splicing modifiers can not only expand the scope of drug targets to include many previously considered “undruggable” genes but also enrich the chemical-genetic toolbox for basic biomedical research. In this review, we summarized known splicing modifiers, screening methods for novel splicing modifiers, and the chemical space occupied by the small-molecule splicing modifiers.

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36

Wickland, Daniel P., Colton McNinch, Erik Jessen, Brian Necela, Barath Shreeder, Yi Lin, Keith L. Knutson, and Yan W. Asmann. "Comprehensive profiling of cancer neoantigens from aberrant RNA splicing." Journal for ImmunoTherapy of Cancer 12, no. 5 (May 2024): e008988. http://dx.doi.org/10.1136/jitc-2024-008988.

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BackgroundCancer neoantigens arise from protein-altering somatic mutations in tumor and rank among the most promising next-generation immuno-oncology agents when used in combination with immune checkpoint inhibitors. We previously developed a computational framework, REAL-neo, for identification, quality control, and prioritization of both class-I and class-II human leucocyte antigen (HLA)-presented neoantigens resulting from somatic single-nucleotide mutations, small insertions and deletions, and gene fusions. In this study, we developed a new module, SPLICE-neo, to identify neoantigens from aberrant RNA transcripts from two distinct sources: (1) DNA mutations within splice sites and (2) de novo RNA aberrant splicings.MethodsFirst, SPLICE-neo was used to profile all DNA splice-site mutations in 11,892 tumors from The Cancer Genome Atlas (TCGA) and identified 11 profiles of splicing donor or acceptor site gains or losses. Transcript isoforms resulting from the top seven most frequent profiles were computed using novel logic models. Second, SPLICE-neo identified de novo RNA splicing events using RNA sequencing reads mapped to novel exon junctions from either single, double, or multiple exon-skipping events. The aberrant transcripts from both sources were then ranked based on isoform expression levels and z-scores assuming that individual aberrant splicing events are rare. Finally, top-ranked novel isoforms were translated into protein, and the resulting neoepitopes were evaluated for neoantigen potential using REAL-neo. The top splicing neoantigen candidates binding to HLA-A*02:01 were validated using in vitro T2 binding assays.ResultsWe identified abundant splicing neoantigens in four representative TCGA cancers: BRCA, LUAD, LUSC, and LIHC. In addition to their substantial contribution to neoantigen load, several splicing neoantigens were potent tumor antigens with stronger bindings to HLA compared with the positive control of antigens from influenza virus.ConclusionsSPLICE-neo is the first tool to comprehensively identify and prioritize splicing neoantigens from both DNA splice-site mutations and de novo RNA aberrant splicings. There are two major advances of SPLICE-neo. First, we developed novel logic models that assemble and prioritize full-length aberrant transcripts from DNA splice-site mutations. Second, SPLICE-neo can identify exon-skipping events involving more than two exons, which account for a quarter to one-third of all skipping events.

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37

Fergany, Alzahraa A. M., and Victor V. Tatarskiy. "RNA Splicing: Basic Aspects Underlie Antitumor Targeting." Recent Patents on Anti-Cancer Drug Discovery 15, no. 4 (December 29, 2020): 293–305. http://dx.doi.org/10.2174/1574892815666200908122402.

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Background: RNA splicing, a fundamental step in gene expression, is aimed at intron removal and ordering of exons to form the protein’s reading frame. Objective: This review is focused on the role of RNA splicing in cancer biology; the splicing abnormalities that lead to tumor progression emerge as targets for therapeutic intervention. Methods: We discuss the role of aberrant mRNA splicing in carcinogenesis and drug response. Results and Conclusion: Pharmacological modulation of RNA splicing sets the stage for treatment approaches in situations where mRNA splicing is a clinically meaningful mechanism of the disease.

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38

Verma, Dinesh, and Sankar Swaminathan. "Epstein-Barr Virus SM Protein Functions as an Alternative Splicing Factor." Journal of Virology 82, no. 14 (May 7, 2008): 7180–88. http://dx.doi.org/10.1128/jvi.00344-08.

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ABSTRACT Alternative splicing of RNA increases the coding potential of the genome and allows for additional regulatory control over gene expression. The full extent of alternative splicing remains to be defined but is likely to significantly expand the size of the human transcriptome. There are several examples of mammalian viruses regulating viral splicing or inhibiting cellular splicing in order to facilitate viral replication. Here, we describe a viral protein that induces alternative splicing of a cellular RNA transcript. Epstein-Barr virus (EBV) SM protein is a viral protein essential for replication that enhances EBV gene expression by enhancing RNA stability and export. SM also increases cellular STAT1 expression, a central mediator of interferon signal transduction, but disproportionately increases the abundance of the STAT1β splicing isoform, which can act as a dominant-negative suppressor of STAT1α. SM induces splicing of STAT1 at a novel 5′ splice site, resulting in a STAT1 mRNA incapable of producing STAT1α. SM-induced alternative splicing is dependent on the presence of an RNA sequence to which SM binds directly and which can confer SM-dependent splicing on heterologous RNA. The cellular splicing factor ASF/SF2 also binds to this region and inhibits SM-RNA binding and SM-induced alternative splicing. These results suggest that viruses may regulate cellular gene expression at the level of alternative mRNA splicing in order to facilitate virus replication or persistence in vivo.

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39

LENASI, T. "Distal regulation of alternative splicing by splicing enhancer in equine -casein intron 1." RNA 12, no. 3 (March 1, 2006): 498–507. http://dx.doi.org/10.1261/rna.7261206.

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40

Karlin, Kristen. "Abstract IA022: Mechanisms of splicing dysregulation and dependency in cancer." Molecular Cancer Therapeutics 23, no. 6_Supplement (June 10, 2024): IA022. http://dx.doi.org/10.1158/1538-8514.synthleth24-ia022.

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Abstract Dysregulated RNA splicing is a hallmark feature of cancer. Much like mutational signatures in tumors, RNA mis-splicing patterns are widely heterogeneous and segregate tumors into clades, suggesting there are distinct mechanisms underlying these splicing aberrations. However, the mechanisms driving such distinct RNA splicing dysregulation remain largely unknown. Herein, we discovered that copy-number variation of essential splicing factors is a pervasive cause of splicing dysregulation, and in some tumor contexts, confers deep dependencies on RNA-binding proteins (RBPs) that converge on these mechanisms. Using a systematic chemical biology approach, we delineate how splicing RBPs participate in distinct types of RNA quality control in cells, and when disrupted, produce surprisingly unique patterns of RNA mis-splicing. These RBP-specific mis-splicing patters are common in distinct cancer types. Notably, unbiased genome-wide analysis revealed that RBP-specific mis-splicing patterns found in tumors were significantly associated with copy number loss of a network of functionally linked splicing factors. These splicing factors often reside on tumor suppressor loci that are frequently deleted in breast and other cancers, suggesting that copy number loss of essential splicing RBPs is a collateral event with selected loss of tumor suppressors. Importantly, RBP-specific mis-splicing signatures also segregate tumor models that are dependent on the concordant RBP, suggesting that these tumors evolve defects in RBP function that predispose them to further perturbation. Together, our work suggests that deletions of tumor suppressor loci may drive collateral dysregulation of RNA splicing through partial loss of splicing RBPs and provokes the hypothesis that these mis-splicing signatures may predict actionable dependencies in the cancers that harbor them. Citation Format: Kristen Karlin. Mechanisms of splicing dysregulation and dependency in cancer [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Expanding and Translating Cancer Synthetic Vulnerabilities; 2024 Jun 10-13; Montreal, Quebec, Canada. Philadelphia (PA): AACR; Mol Cancer Ther 2024;23(6 Suppl):Abstract nr IA022.

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41

Wersig, C., and A. Bindereif. "Reconstitution of functional mammalian U4 small nuclear ribonucleoprotein: Sm protein binding is not essential for splicing in vitro." Molecular and Cellular Biology 12, no. 4 (April 1992): 1460–68. http://dx.doi.org/10.1128/mcb.12.4.1460-1468.1992.

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We have developed an in vitro splicing complementation assay to investigate the domain structure of the mammalian U4 small nuclear RNA (snRNA) through mutational analysis. The addition of affinity-purified U4 snRNP or U4 RNA to U4-depleted nuclear extract efficiently restores splicing activity. In the U4-U6 interaction domain of U4 RNA, only stem II was found to be essential for splicing activity; the 5' loop is important for spliceosome stability. In the central domain, we have identified a U4 RNA sequence element that is important for splicing and spliceosome assembly. Surprisingly, an intact Sm domain is not essential for splicing in vitro. Our data provide evidence that several distinct regions of U4 RNA contribute to snRNP assembly, spliceosome assembly and stability, and splicing activity.

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42

Wersig, C., and A. Bindereif. "Reconstitution of functional mammalian U4 small nuclear ribonucleoprotein: Sm protein binding is not essential for splicing in vitro." Molecular and Cellular Biology 12, no. 4 (April 1992): 1460–68. http://dx.doi.org/10.1128/mcb.12.4.1460.

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We have developed an in vitro splicing complementation assay to investigate the domain structure of the mammalian U4 small nuclear RNA (snRNA) through mutational analysis. The addition of affinity-purified U4 snRNP or U4 RNA to U4-depleted nuclear extract efficiently restores splicing activity. In the U4-U6 interaction domain of U4 RNA, only stem II was found to be essential for splicing activity; the 5' loop is important for spliceosome stability. In the central domain, we have identified a U4 RNA sequence element that is important for splicing and spliceosome assembly. Surprisingly, an intact Sm domain is not essential for splicing in vitro. Our data provide evidence that several distinct regions of U4 RNA contribute to snRNP assembly, spliceosome assembly and stability, and splicing activity.

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43

Kitamura, Koji, and Keisuke Nimura. "Regulation of RNA Splicing: Aberrant Splicing Regulation and Therapeutic Targets in Cancer." Cells 10, no. 4 (April 16, 2021): 923. http://dx.doi.org/10.3390/cells10040923.

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RNA splicing is a critical step in the maturation of precursor mRNA (pre-mRNA) by removing introns and exons. The combination of inclusion and exclusion of introns and exons in pre-mRNA can generate vast diversity in mature mRNA from a limited number of genes. Cancer cells acquire cancer-specific mechanisms through aberrant splicing regulation to acquire resistance to treatment and to promote malignancy. Splicing regulation involves many factors, such as proteins, non-coding RNAs, and DNA sequences at many steps. Thus, the dysregulation of splicing is caused by many factors, including mutations in RNA splicing factors, aberrant expression levels of RNA splicing factors, small nuclear ribonucleoproteins biogenesis, mutations in snRNA, or genomic sequences that are involved in the regulation of splicing, such as 5’ and 3’ splice sites, branch point site, splicing enhancer/silencer, and changes in the chromatin status that affect the splicing profile. This review focuses on the dysregulation of RNA splicing related to cancer and the associated therapeutic methods.

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CHEN, Wei, Liao-Fu LUO, Li-Rong ZHANG, and Yong-Qiang XING. "Nucleosome Positioning and RNA Splicing*." PROGRESS IN BIOCHEMISTRY AND BIOPHYSICS 36, no. 8 (October 16, 2009): 1035–40. http://dx.doi.org/10.3724/sp.j.1206.2008.00816.

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Davis, Richard E., Cara Hardwick, Paul Tavernier, Scott Hodgson, and Hardeep Singh. "RNA Trans-splicing in Flatworms." Journal of Biological Chemistry 270, no. 37 (September 15, 1995): 21813–19. http://dx.doi.org/10.1074/jbc.270.37.21813.

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Padgett, R. A., P. J. Grabowski, M. M. Konarska, S. Seiler, and P. A. Sharp. "Splicing of Messenger RNA Precursors." Annual Review of Biochemistry 55, no. 1 (June 1986): 1119–50. http://dx.doi.org/10.1146/annurev.bi.55.070186.005351.

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Sharp, P. "Splicing of messenger RNA precursors." Science 235, no. 4790 (February 13, 1987): 766–71. http://dx.doi.org/10.1126/science.3544217.

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Wilkinson, Max E., Clément Charenton, and Kiyoshi Nagai. "RNA Splicing by the Spliceosome." Annual Review of Biochemistry 89, no. 1 (June 20, 2020): 359–88. http://dx.doi.org/10.1146/annurev-biochem-091719-064225.

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Abstract:

The spliceosome removes introns from messenger RNA precursors (pre-mRNA). Decades of biochemistry and genetics combined with recent structural studies of the spliceosome have produced a detailed view of the mechanism of splicing. In this review, we aim to make this mechanism understandable and provide several videos of the spliceosome in action to illustrate the intricate choreography of splicing. The U1 and U2 small nuclear ribonucleoproteins (snRNPs) mark an intron and recruit the U4/U6.U5 tri-snRNP. Transfer of the 5′ splice site (5′SS) from U1 to U6 snRNA triggers unwinding of U6 snRNA from U4 snRNA. U6 folds with U2 snRNA into an RNA-based active site that positions the 5′SS at two catalytic metal ions. The branch point (BP) adenosine attacks the 5′SS, producing a free 5′ exon. Removal of the BP adenosine from the active site allows the 3′SS to bind, so that the 5′ exon attacks the 3′SS to produce mature mRNA and an excised lariat intron.

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Conboy, John G. "RNA splicing during terminal erythropoiesis." Current Opinion in Hematology 24, no. 3 (May 2017): 215–21. http://dx.doi.org/10.1097/moh.0000000000000329.

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Sharp, P. A., M. M. Konarksa, P. J. Grabowski, A. I. Lamond, R. Marciniak, and S. R. Seiler. "Splicing of Messenger RNA Precursors." Cold Spring Harbor Symposia on Quantitative Biology 52 (January 1, 1987): 277–85. http://dx.doi.org/10.1101/sqb.1987.052.01.033.

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