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Regions of the C. virginica mitochondrial genome denoted as non-coding regions were screened for introns that might mediate the splicing of the discontinuous LSU rRNA gene.
All of these results indicate that GC content is related to splice site usage and it may mediate the splicing process through RNA secondary structures.
First, mRNA secondary structures may mediate the splicing process via affecting the motif recognition rate to facilitate or prevent the binding of splicing regulators.
Thus far, we have little understanding of how heteroallelic Csd proteins mediate the splicing of female fem messenger RNAs (mRNAs) or how Fem proteins direct the splicing of honeybee dsx (Am-dsx) pre-mRNAs.
Trans-splicing occurs in plant mitochondria [ 49, 50], but in these cases the coding breakpoints are flanked by group II intron elements, which form secondary structures that mediate the splicing events.
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Given the observed epistasis between alleles of cdc40Δ and rad6Δ after MMS treatment [54], and the failure of the correctly spliced ANC1 transcript to complement a cdc40Δ mutant's damage sensitivity [53], it is worth exploring whether Cdc40 mediates the splicing of the MMS2 and/or UBC13 transcripts as well.
In response to ER stress, the endonuclease activity of IRE1 mediates the splicing of bZIP60 mRNA to generate an alternatively spliced transcript that lacks transmembrane domain-encoding sequences.
The exon junction complex (EJC) is believed to mediate the link between splicing and NMD in these systems.
The results further demonstrate a role of ROCK in mediating the Ca2+ dependent splicing repression at NRXN3α E11 and E20 and NRXN2α E11 in vitro and the experience related splicing of NRXN1/2/3α SS#4 exons and memory formation in vivo.
Activated IRE1 mediates the non-conventional splicing of an intron from the X box binding protein 1 (XBP1/HAC1) mRNA (Cox and Walter, 1996), and the IRE1-spliced XBP1 acts as a transcription factor to up-regulate the expression of ER chaperones such as BiP and other target genes to relieve the ER stress (Travers et al., 2000; Lee et al., 2003).
There was no consistent alteration in nucleosome occupancy between the wild-type and mutant alleles at a variety of donor and acceptor sites, which would be expected if nucleosome positioning at these sites played a role in mediating the effects of splice site mutations.
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