Abstract
The awareness of genome complexity brought a radical approach to the study of transcriptome, opening eyes to single RNAs generated from two or more adjacent genes according to the present consensus. This kind of transcript was thought to originate only from chromosomal rearrangements, but the discovery of readthrough transcription opens the doors to a new world of fusion RNAs. In the last years many possible intergenic cis-splicing mechanisms have been proposed, unveiling the origins of transcripts that contain some exons of both the upstream and downstream genes. In some cases, alternative mechanisms, such as trans-splicing and transcriptional slippage, have been proposed. Five databases, containing validated and predicted Fusion Transcripts of Adjacent Genes (FuTAGs), are available for the scientific community. A comparative analysis revealed that two of them contain the majority of the results. A complete analysis of the more widely characterized FuTAGs is provided in this review, including their expression pattern in normal tissues and in cancer. Gene structure, intergenic splicing patterns and exon junction sequences have been determined and here reported for well-characterized FuTAGs. The available functional data and the possible roles in cancer progression are discussed.
Highlights
It is known that in human genomes the number of genes is significantly lower than the number of transcripts, due to a set of mechanisms such as alternative splicing, alternative promoter usage, alternative transcription termination sites, RNA editing, post-transcriptional alterations and so on
The activity of SF3B1 and SRRM1 was tested on five cis-SAGes by silencing experiment and the results suggested that SRRM1 acts as a negative regulator of readthrough expression, while SF3B1 acts as a positive regulator of cis-SAGe formation [72]
Fusion Transcripts of Adjacent Genes (FuTAGs) were considered as cancer-signature transcripts, but some studies suggest that they exist in physiological cells too, discrediting them as unique among cancer cells [73]
Summary
It is known that in human genomes the number of genes is significantly lower than the number of transcripts, due to a set of mechanisms such as alternative splicing, alternative promoter usage, alternative transcription termination sites, RNA editing, post-transcriptional alterations and so on These mechanisms converge in the so-called genome complexity [1]. Since in the several cases the exact mechanism of generation of those transcripts is not known, we prefer to use the generic term fusion transcripts of adjacent genes (FuTAGs), without taking into account the mechanism of formation. These fusion transcripts are categorized as intrachromosomal-single strand-0 gap [11]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
