Baculovirus infection blocks the progression of fat body degradation during metamorphosis in Bombyx mori

Baculovirus infection blocks the progression of fat body degradation during metamorphosis in... The effect of baculovirus infection into silkworm pupa particularly on programmed fat body degradation during metamorphosis was investigated. Pupal fat body degradation did not occur following infection with Bombyx mori nucleo-polyhedrovirus (BmNPV). There were no histolytic differences between the fat body tissues of mock and BmNPV infected papae until 48 h postinfection (p.i.). Between 48 and 72 h p.i., significant differences were observed. In order to determine whether the histolysis of fat body was due to apoptosis, genomic DNAs were purified at various p.i. times and analyzed. Rapid genomic DNA fragmentation was observed at 24 and 48 h after pupation in both mock and BmNPV infected pupae. However, BmNPV infection clearly inhibited DNA fragmentation and ladder formation at 72 h and later times p.i. Furthermore, pulse-labeling analysis showed that BmNPV infection restored protein synthesis in fat body cells. These results suggested that fat body degradation during pupal-adult development was due to apoptosis, and that BmNPV was able to evoke a cellular response in these cells. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Virology Springer Journals

Baculovirus infection blocks the progression of fat body degradation during metamorphosis in Bombyx mori

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Publisher
Springer-Verlag
Copyright
Copyright © Wien by 2000 Springer-Verlag/
Subject
Legacy
ISSN
0304-8608
eISSN
1432-8798
D.O.I.
10.1007/s007050070054
Publisher site
See Article on Publisher Site

Abstract

The effect of baculovirus infection into silkworm pupa particularly on programmed fat body degradation during metamorphosis was investigated. Pupal fat body degradation did not occur following infection with Bombyx mori nucleo-polyhedrovirus (BmNPV). There were no histolytic differences between the fat body tissues of mock and BmNPV infected papae until 48 h postinfection (p.i.). Between 48 and 72 h p.i., significant differences were observed. In order to determine whether the histolysis of fat body was due to apoptosis, genomic DNAs were purified at various p.i. times and analyzed. Rapid genomic DNA fragmentation was observed at 24 and 48 h after pupation in both mock and BmNPV infected pupae. However, BmNPV infection clearly inhibited DNA fragmentation and ladder formation at 72 h and later times p.i. Furthermore, pulse-labeling analysis showed that BmNPV infection restored protein synthesis in fat body cells. These results suggested that fat body degradation during pupal-adult development was due to apoptosis, and that BmNPV was able to evoke a cellular response in these cells.

Journal

Archives of VirologySpringer Journals

Published: Sep 1, 2000

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