Abstract
Non-coding antisense transcripts arise from the strand opposite the sense strand. Over 70% of the human genome generates non-coding antisense transcripts while less than 2% of the genome codes for proteins. Antisense transcripts and/or the act of antisense transcription regulate gene expression and genome integrity by interfering with sense transcription and modulating histone modifications or DNA methylation. Hence, they have significant pathological and physiological relevance. Indeed, antisense transcripts were found to be associated with various diseases including cancer, diabetes, cardiac and neurodegenerative disorders, and, thus, have promising potentials for prognostic and diagnostic markers and therapeutic development. However, it is not clearly understood how antisense transcription is initiated and epigenetically regulated. Such knowledge would provide new insights into the regulation of antisense transcription, and hence disease pathogenesis with therapeutic development. The recent studies on antisense transcription initiation and its epigenetic regulation, which are limited, are discussed here. Furthermore, we concisely describe how antisense transcription/transcripts regulate gene expression and genome integrity with implications in disease pathogenesis and therapeutic development.
Highlights
Eukaryotic transcription of the protein-coding genes is a highly coordinated and complex process initiated by an assembly of general transcription factors and RNA Polymerase II at the promoter by an activator protein, followed by elongation, and, termination [1,2,3,4,5,6,7]
Only a limited number of studies have focused on understanding the mechanisms of antisense transcription initiation and its regulation by the chromatin structure
NuA4 KAT, TBPs, TBP-associated factors (TAFs), TFIIB (Transcription factor IIB) and a Mediator are required for the recruitment of RNA polymerase II to the 3 -end of the GAL10 coding sequence to initiate antisense transcription [83,84]
Summary
Eukaryotic transcription of the protein-coding genes is a highly coordinated and complex process initiated by an assembly of general transcription factors and RNA Polymerase II at the promoter by an activator protein (activator), followed by elongation, and, termination [1,2,3,4,5,6,7] This process is tightly regulated by epigenetic factors and processes such as DNA methylation, histone modifications, and/or ATP-dependent chromatin remodeling [8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26]. The roles of antisense transcription/transcripts in the regulation of gene expression and genomic stability, with implications in disease pathogenesis and therapeutic development, are described below
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