Strand-Specific RNA-Seq Provides Greater Resolution of Transcriptome Profiling
It seems that antisense tran-scriptional ‘hot spots’ are located around nucleosome-free regions such as those associated with promoters, indicating that it is likely that antisense transcripts carry out important regulatory functions.
Furthermore, antisense transcripts have been documented that partner with active promoter sites or those that are in close proximity of transcription start sites [17, 22, 23]. While antisense transcripts occur at lower abundances than their sense transcripts, all evidence points to non-coding antisense transcripts playing a pivotal role in regulation of the transcriptome [19].
There exist a variety of pathways in which antisense transcripts can act as regulatory elements. It is possible to divide these pathways into three broad categories; transcription modulation, hybridization of sense-antisense RNA partners and chromatin modification.
The act of antisense transcription, rather than asRNA molecule itself
can modulate gene expression levels. During transcription RNA polymerase
binds to the promoter region of the gene and proceeds along the strand.
If transcription occurs on the DNA sense strand and antisense strand
simultaneously it can result in the RNA polymerases colliding.
Splicing is controlled by the presence of exonic splicing
enhancers/silencers and intronic enhancer/silencers, the ratios of these
elements impact on the splicing pattern [27].
These elements contain motifs that will recruit splicing machinery to
the site. If sections of the transcript containing these elements are
masked, by hybridization with an antisense transcript, then the splicing
patterns of the sense transcript will be changed.
RNA duplex formation in the cytoplasm may alter the ability of a
transcript to be translated. It is possible that the duplex formation
blocks the ability of the transcript to associate with the ribosome
hence altering the efficiency of the translation machinery.
It has been suggested that long ncRNAs, such as those produced by
antisense transcription, may interact with histone modifying enzymes via
the formation of specific RNA secondary structures [36].
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