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Dual mutations in the Autographa californica nucleopolyhedrovirus FP-25 and p35 genes result in plasma-membrane blebbing in Trichoplusia ni cells

Barbara J. Kelly^1,2,

Susan D. J. Chapple^1,2,

¹ Centre for Ecology and Hydrology Oxford, Mansfield Road, Oxford OX1 3SR, UK
² School of Biological and Molecular Sciences, Oxford Brookes University, The Headington Campus, Oxford OX3 0BP, UK

Correspondence
Robert D. Possee
rdpo{at}ceh.ac.uk

Spodoptera frugiperda cells infected with Autographa californica nucleopolyhedrovirus (AcMNPV) lacking a functional anti-apoptotic p35 protein undergo apoptosis. However, such mutants replicate normally in Trichoplusia ni (TN-368) cells. An AcMNPV plaque isolate (AcdefrT) was identified during propagation of a virus deficient in p35 in TN-368 cells. This virus exhibited enhanced budded-particle formation in TN-368 cells, but was partially defective for polyhedra production in the same cells. Virus replication in AcdefrT-infected TN-368 cells was accompanied by extensive plasma-membrane blebbing and caspase activation late in infection, both features of apoptosis. Rescue of the p35 locus of AcdefrT continued to result in a reduction in polyhedra and increase in budded virus production in TN-368 cells, but no plasma-membrane blebbing was observed. The mutation was mapped to the FP-25 gene locus. This gene mutation combined with the non-functional p35 was found to be responsible for the cell-blebbing effect observed in AcdefrT-infected TN-368 cells.

Present address: Department of Microbiology, The Moyne Institute of Preventative Medicine, Trinity College, Dublin 2, Ireland.

Present address: The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK.

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				B. Bryant and R. J. Clem Caspase inhibitor P35 is required for the production of robust baculovirus virions in Trichoplusia ni TN-368 cells J. Gen. Virol., March 1, 2009; 90(3): 654 - 661. [Abstract] [Full Text] [PDF]