A viral adaptor protein modulating casein kinase II activity induces cytopathic effects in permissive cells.

摘要: Autonomous parvoviruses induce severe morphological and physiological alterations in permissive host cells, eventually leading to cell lysis release of progeny virions. Viral cytopathic effects (CPE) result from specific rearrangements destruction cytoskeletal micro- intermediate filaments. We recently reported that inhibition endogenous casein kinase II (CKII) protects target cells parvovirus minute virus mice (MVM)-induced CPE, pointing this as an effector MVM toxicity. The present work shows the parvoviral NS1 protein mediates CKII-dependent death. can act adaptor molecule, linking cellular CKIIα tropomyosin thus modulating substrate specificity kinase. This action results altered phosphorylation pattern both vitro living cells. capacity CPE was impaired by mutations abolishing binding with either or tropomyosin. cytotoxic function confirmed fusion peptides, where tropomyosin-binding domain are physically linked. These peptides were able mimic its ability death transformed MVM-permissive