Trans-splicing and Sl RNAS in C. elegans

1990 ◽  
Vol 14 (2-3) ◽  
pp. 115-115 ◽  
Author(s):  
David Hirsh ◽  
X. -Y. Huang
Keyword(s):  
1990 ◽  
Vol 10 (4) ◽  
pp. 1764-1768
Author(s):  
R F Liou ◽  
T Blumenthal

The nematode Caenorhabditis elegans has an unusual small nuclear RNA, containing a 100-nucleotide RNA molecule, spliced leader RNA, which donates its 5' 22 nucleotides to a variety of recipient RNAs by a trans-splicing reaction. The spliced leader RNA has a 5' trimethylguanosine (TMG) cap, which becomes the 5' end of trans-spliced mRNAs. We found that mature trans-spliced mRNAs were immunoprecipitable with anti-TMG cap antibodies and that TMG-containing dinucleotides specifically competed with the trans-spliced mRNAs for antibody binding. We also found that these mRNAs retained their TMG caps throughout development and that the TMG-capped mRNAs were polysome associated. Since the large majority of C. elegans mRNAs are not trans-spliced, the addition of the spliced leader and its TMG cap to a limited group of recipient RNAs may create a functionally distinct subset of mRNAs.


RNA ◽  
2007 ◽  
Vol 13 (4) ◽  
pp. 511-520 ◽  
Author(s):  
M. MacMorris ◽  
M. Kumar ◽  
E. Lasda ◽  
A. Larsen ◽  
B. Kraemer ◽  
...  
Keyword(s):  

RNA ◽  
2007 ◽  
Vol 13 (9) ◽  
pp. 1409-1426 ◽  
Author(s):  
J. H. Graber ◽  
J. Salisbury ◽  
L. N. Hutchins ◽  
T. Blumenthal

2020 ◽  
Vol 6 (50) ◽  
pp. eabc1450
Author(s):  
C. Cassart ◽  
C. Yague-Sanz ◽  
F. Bauer ◽  
P. Ponsard ◽  
F. X. Stubbe ◽  
...  

Serine 2 phosphorylation (S2P) within the CTD of RNA polymerase II is considered a Cdk9/Cdk12-dependent mark required for 3′-end processing. However, the relevance of CTD S2P in metazoan development is unknown. We show that cdk-12 lesions or a full-length CTD S2A substitution results in an identical phenotype in Caenorhabditis elegans. Embryogenesis occurs in the complete absence of S2P, but the hatched larvae arrest development, mimicking the diapause induced when hatching occurs in the absence of food. Genome-wide analyses indicate that when CTD S2P is inhibited, only a subset of growth-related genes is not properly expressed. These genes correspond to SL2 trans-spliced mRNAs located in position 2 and over within operons. We show that CDK-12 is required for maximal occupancy of cleavage stimulatory factor necessary for SL2 trans-splicing. We propose that CTD S2P functions as a gene-specific signaling mark ensuring the nutritional control of the C. elegans developmental program.


2018 ◽  
Author(s):  
Charles Nelson ◽  
Victor Ambros

SUMMARYlet-7 is a microRNA whose sequence and roles as a regulator of developmental progression are conserved throughout bilaterians. In most systems, transcription of the let-7 locus occurs relatively early in development, whilst processing of let-7 primary transcript into mature microRNA arises later and is associated with cellular differentiation. In C. elegans and other animals, the RNA binding protein LIN-28 post-transcriptionally inhibits let-7 biogenesis at early developmental stages. The mechanisms by which LIN-28 and other factors developmentally regulate let-7 biogenesis are not fully understood. Nor is it understood how the developmental regulation of let-7 might influence the expression or activities of other microRNAs of the same seed family. Here we show that in C. elegans, the primary let-7 transcript (pri-let-7) is trans-spliced to SL1 splice leader at a position downstream of the let-7 precursor stem-loop, producing a short, polyadenylated downstream mRNA. The trans-splicing event negatively impacts the biogenesis of mature let-7 microRNA in cis, likely by destabilizing the upstream pri-let-7 fragment. Moreover, the trans-spliced downstream mRNA contains complimentary sequences to multiple members of the let-7 seed family (let-7fam), and thereby serves as a sponge to negatively regulate let-7fam function in trans. Thus, this study provides evidence for a mechanism by which splicing of a microRNA primary transcript can negatively regulate said microRNA in cis as well as other microRNAs in trans.HIGHLIGHTSThe let-7 primary transcript is trans-spliced to produce an RNA that functions as a sponge that negatively regulates the let-7-family microRNAs.Trans-splicing of this RNA negatively impacts let-7 microRNA biogenesis.LIN-28 regulates this trans-splicing event


2017 ◽  
Author(s):  
Nicolas Tourasse ◽  
Jonathan R. M. Millet ◽  
Denis Dupuy

ABSTRACTAlmost twenty years after the completion of the C. elegans genome sequence, gene structure annotation is still an ongoing process with new evidence for gene variants still being regularly uncovered by additional in-depth transcriptome studies. While alternative splice forms can allow a single gene to encode several functional isoforms the question of how much spurious splicing is tolerated is still heavily debated.Here we gathered a compendium of 1,682 publicly available C. elegans RNA-seq datasets to increase the dynamic range of detection of RNA isoforms and obtained robust measurements of the relative abundance of each splicing event. While most of the splicing reads come from reproducibly detected splicing events, a large fraction of purported junctions are only supported by a very low number of reads. We devised an automated curation method that takes into account the expression level of each gene to discriminate robust splicing events from potential biological noise. We found that rarely used splice sites disproportionately come from highly expressed genes and are significantly less conserved in other nematode genomes than splice sites with a higher usage frequency.Our increased detection power confirmed trans-splicing for at least 84% of C. elegans protein coding genes. The genes for which trans-splicing was not observed are overwhelmingly low expression genes, suggesting that the mechanism is pervasive but not full captured by organism-wide RNA-Seq.We generated annotated gene models including quantitative exon usage information for the entire C. elegans genome. This allows users to visualize at a glance the relative expression of each isoform for their gene of interest.


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