(a) Cytoplasmic stress induces stress granule assembly mediated by PARP5a, PARP12, PARP13 and PARP14. microRNA mediated silencing is relieved upon cytoplasmic stress or viral infection, a process which requires PARP13 function. PARP7, PARP12, PARP13 and PARP14 directly inhibit translation in response to stress or upon viral infection. Viral RNA is additionally targeted to the RNA decay machinery by PARP13.
(b)During heat shock PARP1 regulates splicing by recruiting hnRNPs to poly(ADP-ribosyl)ated proteins. This results in the dissociation of the hnRNPs from their target mRNAs. Heat shock activated PARP1 also mediates poly(ADP-ribosyl)ation of poly(A)polymerase (PAP) resulting in decreased polyadenylation activity of the protein. RNAs lacking poly(A) tails fail to be exported to the cytoplasm and are degraded. During DNA damage, PARP2 binds to accumulated rRNA through its SAP domain activating its enzymatic activity.