Key result
PARP-1 interacts with the C-terminal domain of Sindbis virus nsP3 in replication complexes during virus amplification in neuronal cells, independent of PARP enzymic activity or nsP3 phosphorylation.
PARP-1 interacts with the C-terminal domain of Sindbis virus nsP3 in neuronal cells, suggesting a role in regulating viral RNA synthesis.
Preclinical interaction does not inform alphavirus therapy; leaves open whether PARP-1 targeting limits replication in vivo.
The alphavirus non-structural protein 3 (nsP3) has a conserved N-terminal macro domain and a variable highly phosphorylated C-terminal domain. nsP3 forms complexes with cellular proteins, but its role in virus replication is poorly understood and protein interaction domains have not been defined. As the N-terminal macro domain can bind poly(ADP-ribose) (PAR), and PAR polymerase-1 (PARP-1) is activated and autoribosylated during Sindbis virus (SINV) infection, it was hypothesized that PARP-1 and nsP3 may interact. Co-immunoprecipitation studies showed that PARP-1 interacted with nsP3 during SINV infection of NSC34 neuronal cells and was most abundantly present in replication complexes that contained plus- and minus-strand SINV RNAs 10-14 h after infection, prior to PARP-1 activation or automodification with PAR. Treatment with an inhibitor of PARP enzymic activity did not affect the interaction between nsP3 and PARP-1 or SINV replication. Co-expression of individual domains of nsP3 with PARP-1 showed that nsP3 interacted with PARP-1 through the C-terminal domain, not the N-terminal macro domain, and that phosphorylation was not required. It was concluded that PARP-1 interacts with the C-terminal domain of nsP3, is present in replication complexes during virus amplification and may play a role in regulating virus RNA synthesis in neuronal cells.
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Park et al. (2009) studied Sindbis virus infection. Sindbis virus infection vs. Mock-infected cells was evaluated on Protein-protein interaction between nsP3 and PARP-1. PARP-1 interacts with the C-terminal domain of Sindbis virus nsP3 in replication complexes during virus amplification in neuronal cells, independent of PARP enzymic activity or nsP3 phosphorylation.
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