scholarly journals Functional interconnections of Arabidopsis exon junction complex proteins and genes at multiple steps of gene expression

2011 ◽  
Vol 62 (14) ◽  
pp. 5025-5036 ◽  
Author(s):  
Eduardo F. Mufarrege ◽  
Daniel H. Gonzalez ◽  
Graciela C. Curi
Keyword(s):  
Gene Expression ◽  
Exon Junction Complex ◽  
Exon Junction

scholarly journals The exon junction complex core factor eIF4A3 is a key regulator of HPV16 gene expression

2021 ◽  
Vol 41 (4) ◽  
Author(s):  
Koceila Meznad ◽  
Philippe Paget-Bailly ◽  
Elise Jacquin ◽  
Anne Peigney ◽  
François Aubin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Translation Initiation Factor ◽  
Initiation Factor ◽  
Exon Junction Complex ◽  
Eukaryotic Translation ◽  
Protein Levels ◽  
Exon Junction ◽  
Complex Core ◽  
Eukaryotic Translation Initiation ◽  
E6 And E7

Abstract High-risk human papillomavirus (hrHPVs), particularly HPV16 and HPV18, are the etiologic factors of ano-genital cancers and some head and neck squamous cell carcinomas (HNSCCs). Viral E6 and E7 oncoproteins, controlled at both transcriptional and post-transcriptional levels, drive hrHPVs-induced carcinogenesis. In the present study, we investigated the implication of the DEAD-box helicase eukaryotic translation initiation factor 4A3 (eIF4A3,) an Exon Junction Complex factor, in the regulation of HPV16 gene expression. Our data revealed that the depletion of the factor eIF4A3 up-regulated E7 oncoprotein levels. We also showed that the inhibition of the nonsense-mediated RNA decay (NMD) pathway, resulted in the up-regulation of E7 at both RNA and protein levels. We therefore proposed that HPV16 transcripts might present different susceptibilities to NMD and that this pathway could play a key role in the levels of expression of these viral oncoproteins during the development of HPV-related cancers.

scholarly journals The exon junction complex and intron removal prevent re-splicing of mRNA

PLoS Genetics ◽  
2021 ◽  
Vol 17 (5) ◽  
pp. e1009563
Author(s):  
Brian Joseph ◽  
Eric C. Lai
Keyword(s):  
Gene Expression ◽  
Splice Site ◽  
Site Selection ◽  
Exon Junction Complex ◽  
Splice Sites ◽  
Splice Site Selection ◽  
Exon Junction ◽  
Intron Removal ◽  
Cryptic Splice Sites

Accurate splice site selection is critical for fruitful gene expression. Recently, the mammalian EJC was shown to repress competing, cryptic, splice sites (SS). However, the evolutionary generality of this remains unclear. Here, we demonstrate the Drosophila EJC suppresses hundreds of functional cryptic SS, even though most bear weak splicing motifs and are seemingly incompetent. Mechanistically, the EJC directly conceals cryptic splicing elements by virtue of its position-specific recruitment, preventing aberrant SS definition. Unexpectedly, we discover the EJC inhibits scores of regenerated 5’ and 3’ recursive SS on segments that have already undergone splicing, and that loss of EJC regulation triggers faulty resplicing of mRNA. An important corollary is that certain intronless cDNA constructs yield unanticipated, truncated transcripts generated by resplicing. We conclude the EJC has conserved roles to defend transcriptome fidelity by (1) repressing illegitimate splice sites on pre-mRNAs, and (2) preventing inadvertent activation of such sites on spliced segments.

scholarly journals The Exon Junction Complex and intron removal prevents resplicing of mRNA

2020 ◽  
Author(s):  
Brian Joseph ◽  
Eric C. Lai
Keyword(s):  
Gene Expression ◽  
Splice Site ◽  
Site Selection ◽  
Exon Junction Complex ◽  
Splice Sites ◽  
Splice Site Selection ◽  
Exon Junction ◽  
Exon Junctions ◽  
Intron Removal ◽  
Cryptic Splice Sites

AbstractAccurate splice site selection is critical for fruitful gene expression. Here, we demonstrate the Drosophila EJC suppresses hundreds of functional cryptic splice sites (SS), even though majority of these bear weak splicing motifs and appear incompetent. Mechanistically, the EJC directly conceals splicing elements through position-specific recruitment, preventing SS definition. We note that intron removal using strong, canonical SS yields AG|GU signatures at exon-exon junctions. Unexpectedly, we discover that scores of these minimal exon junction sequences are in fact EJC-suppressed 5’ and 3’ recursive SS, and that loss of EJC regulation from such transcripts triggers faulty mRNA resplicing. An important corollary is that intronless cDNA expression constructs from aforementioned targets yield high levels of unanticipated, truncated transcripts generated by resplicing. Consequently, we conclude the EJC has ancestral roles to defend transcriptome fidelity by (1) repressing illegitimate splice sites on pre-mRNAs, and (2) preventing inadvertent activation of such sites on spliced segments.

Structural insights into the exon junction complex

2008 ◽  
Vol 18 (1) ◽  
pp. 112-119 ◽  
Author(s):  
Hervé Le Hir ◽  
Gregers Rom Andersen
Keyword(s):  
Exon Junction Complex ◽  
Exon Junction ◽  
Structural Insights
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