title: Oocyte destruction is activated during viral infection.
abstract: Viral infection has been associated with a starvation-like state in Drosophila melanogaster. Because starvation and inhibiting TOR kinase activity in vivo result in blocked oocyte production, we hypothesized that viral infection would also result in compromised oogenesis. Wild-type flies were injected with flock house virus (FHV) and survival and embryo production were monitored. Infected flies had a dose-responsive loss of fecundity that corresponded to a global reduction in Akt/TOR signaling. Highly penetrant egg chamber destruction mid-way through oogenesis was noted and FHV coat protein was detected within developing egg chambers. As seen with in vivo TOR inhibition, oogenesis was partially rescued in loss of function discs large and merlin mutants. As expected, mutants in genes known to be involved in virus internalization and trafficking [Clathrin heavy chain (chc) and synaptotagmin] survive longer during infection. However, oogenesis was rescued only in chc mutants. This suggests that viral response mechanisms that control fly survival and egg chamber survival are separable. The genetic and signaling requirements for oocyte destruction delineated here represent a novel host-virus interaction with implications for the control of both fly and virus populations.
authors.affiliation: Department of Obstetrics, Gynecology, and Reproductive Sciences/Division of Reproductive Endocrinology and Infertility, Yale School of Medicine, New Haven, Connecticut, USA.
authors.forename: Travis C
authors.initials: TC
authors.lastname: Thomson
authors.forename: Anette
authors.initials: A
authors.lastname: Schneemann
authors.forename: Joshua
authors.initials: J
authors.lastname: Johnson
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D033922:Clathrin Heavy Chains / Q000235:genetics; D029721:Drosophila Proteins / Q000235:genetics / Q000378:metabolism; D004331:Drosophila melanogaster / Q000235:genetics / Q000502:physiology* / Q000821:virology*; D005260:Female; D005298:Fertility; D051379:Mice; D009154:Mutation; D030381:Nodaviridae / Q000472:pathogenicity*; D009865:Oocytes / Q000502:physiology* / Q000821:virology; D009866:Oogenesis; D010053:Ovary / Q000821:virology; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D013217:Starvation; D050857:Synaptotagmins / Q000235:genetics; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism
chemical_list: D029721:Drosophila Proteins; D033922:Clathrin Heavy Chains; D050857:Synaptotagmins; D051057:Proto-Oncogene Proteins c-akt; D058570:TOR Serine-Threonine Kinases