The role of the AcMNPV 25K gene, 'FP25,' in baculovirus polh and p10 expression

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Abstract

A previous study showed that an Autographa californica multicapsid nuclear polyhedrosis virus (AcMNPV) 25K mutant produced less polyhedrin protein than wild-type (Jarvis et al., J. Virol. 66, 6903-6911, 1992). In this study, the role of the 25K gene product (AcMNPV ORF 61) in baculovirus gene expression was further investigated. Five different viral 25K mutants expressed lower levels of polyhedrin protein and less CAT activity under the control of the polh promoter compared to wild-type. Polh RNA was equally stable in wild-type and mutant virus-infected cells while the rate of polh transcription was significantly reduced in mutant-infected cells. In comparison, steady-state levels of p10 RNA were not reduced in 25K mutant-infected cells, indicating that the reduction in polh RNA did not reflect a general effect on very late gene transcription. Expression of ie-1, which also appears to influence polh expression (Choi and Guarino, Virology 209, 90-98, 1995), was not influenced by 25K mutation. These results show that the 25K protein is important for maintaining optimal levels of polh transcription by a mechanism that does not involve maintaining ie-1 expression.

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Harrison, R. L., Jarvis, D. L., & Summers, M. D. (1996). The role of the AcMNPV 25K gene, “FP25,” in baculovirus polh and p10 expression. Virology, 226(1), 34–46. https://doi.org/10.1006/viro.1996.0625

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