Abstract
Kaposi’s sarcoma-associated herpesvirus (KSHV) is an oncogenic γ-herpesivrus, the causative agent of Kaposi’s sarcoma and body cavity lymphomas. During infection KSHV produces a highly abundant long non-coding polyadenylated RNA that is retained in the nucleus known as PAN RNA. Long noncoding RNAs (lncRNA) are key regulators of gene expression and are known to interact with specific chromatin modification complexes, working in cis and trans to regulate gene expression. Data strongly supports a model where PAN RNA is a multifunctional regulatory transcript that controls KSHV gene expression by mediating the modification of chromatin by targeting the KSHV repressed genome.
Highlights
Kaposi’s sarcoma-associated herpesvirus (KSHV) was first identified as the etiological agent of Kaposi’s sarcoma in 1994 [1], and it wasn’t long after that before researchers first identified a highly abundant viral RNA from cells that were infected with KSHV [2,3]
The ability of PAN RNA to disregulate the expression of immune response genes and those involved in formation of the inflammasome suggested that PAN RNA had a global affect on cellular and viral gene expression programs
The interaction of PAN RNA with viral encoded processivity factor ORF59 may aid in the targeting UTX/JMJD3 to viral genes during lytic gene expression; (C) PAN RNA’s interaction with polycomb repressive complex 2 (PRC2) targets H3K27 for methylation and acts to repress gene expression
Summary
Kaposi’s sarcoma-associated herpesvirus (KSHV) was first identified as the etiological agent of Kaposi’s sarcoma in 1994 [1], and it wasn’t long after that before researchers first identified a highly abundant viral RNA from cells that were infected with KSHV [2,3]. Cytoplasmic and nuclear fractionation studies of 293T cells transfected with a T1.1 expression plasmid demonstrated that it was only detectable in the nuclear fraction and in situ hybridization studies localized PAN RNA to the nucleus of KSHV infected cells [2] These same studies quantitated the relative copy number of T1.1 transcripts to ~25,000 copies per cell based on the signal intensity of the same cells with cellular U12 RNA. An enhancer lncRNA facilities the signals from transcription factors to regulate gene expression Another interesting model of lncRNA’s, which goes along with its mechanisms of action, is that they can regulate nuclear organization to orchestrate and traffic protein complexes, genes, and chromosomes to appropriate locations allowing for proper activation or repression [15]. Isolation by RNA purification (ChIRP), and the more recent domain-specific chromatin isolation by RNA purification (dChIRP), are invaluable with respect to mapping specific lncRNA DNA interaction domains [20,21]
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