Regulation ofHeliothis virescens prothoracic glands byCardiochiles nigriceps polydnavirus

Abstract

Heliothis virescens (F.) Larvae parasitized by the endophagous braconid Cardiochiles nigriceps Viereck fail to attain the pupal stage. This developmental alteration is caused by both an inactivation of prothoracic glands of last‐instar larvae and an altered ecdysone metabolism. Decrease in ecdysteroidogenesis in vitro was already evident in glands explanted from larvae that have attained the early cell formation stage (day 4 of fifth instar), 6 h after parasitoid oviposition. Ecdysteroidogenesis nearly ceased by 24 h after parasitoid oviposition. The degree of this biosynthetic depression increased as the time between parasitization and gland dissection increased. A time‐course study allowed us to determine if both the degree of phosphorylation of regulatory target proteins, the rate of general protein synthesis and ecdysteroidogenesis decreased in concert over time. The results provide further evidence in support of the hypothesis that these cellular activities in prothoracic gland cells are functionally correlated in steroidogenic responses. Treatment with calyx fluid and venom of C. nigriceps duplicates the parasitism‐induced inactivation of host prothoracic glands. A 6‐h conditioning in vitro of pupally committed host prothoracic glands with these parasitoid female reproductive secretions resulted in a significant depression of their ecdysteroid production. However, glands lost their sensitivity to calyx fluid and venom treatment when explanted from hosts that had already attained the cell formation stage. This was further supported by the fact that nearly all the host larvae parasitized on day 4 of fifth instar (cell formation stage) pupated, while parasitization on day 3 resulted in only 11% pupation. The coupled trioxsalen/UV irradiation treatment of C. nigriceps calyx fluid and venom eliminated their negative effect on biosynthetic activity in vitro by host prothoracic glands. This result indirectly demonstrates that C. nigriceps polydnavirus is the major regulating factor involved in the host prothoracic gland inactivation. Arch. Insect Biochem. Physiol. 38:1–10, 1998. © 1998 Wiley‐Liss, Inc.

Quantitative analysis of hemocyte morphological abnormalities associated with Campoletis sonorensis parasitization

“…Virus replication is not observed in parasitized hosts (Strand et al 1992;Theilmann and Summers 1986) although transcription of viral genes occurs in infected cells. Virus infection and expression of polydnavirusencoded proteins is required for successful parasitization and induces pathologies such as altered host development (Cusson et al 2000;Pennacchio et al 1998;Soller and Lanzrein 1996), reduced humoral immunity (Shelby et al 2000), and abrogation of cellular immunity (Cui et al 2000;Strand 1994). …”

Protein tyrosine phosphatases of Toxoneuron nigriceps bracovirus as potential disrupters of host prothoracic gland function

“…nigriceps was reared in the laboratory according to the methodology described by Vinson et al (1973). H. virescens larvae were maintained on an artificial diet previously described (Pennacchio et al, 1998a). Rearing temperature was 29 ± 1°C for both the host and parasitized host larvae, while T. nigriceps adults were kept at 25 ± 1°C.…”

“…The reduced biosynthetic activity of host PTGs is caused by the combined action of the venom and calyx fluid (Tanaka and Vinson, 1991), and infection of gland cells by transcriptionally active TnBV was found to be responsible for this alteration (Pennacchio et al, 1998a). The reduced biosynthetic activity of host PTGs was correlated with a marked underphosphorylation of proteins playing a central role in the prothoracicotropic hormone (PTTH) signal transduction pathway (Pennacchio et al, 1997(Pennacchio et al, , 1998b(Pennacchio et al, , 2001.…”

Infection by a symbiotic polydnavirus induces wasting and inhibits metamorphosis of the mothPseudoplusia includens

“…Most studies have focused on the hypothesis that the wasp or its associated PDV produce molecules which directly reduce ecdysteroid titers by altering processing or release of PTTH Tanaka and Vinson, 1987;Zitnan et al, 1995;Kelly et al, 1998), disrupting ecdysteroid biosynthesis by prothoracic glands (Pennacchio et al, 1998;Pennacchio et al, 2001;Fallabella et al, 2003), or metabolizing ecdysteroids in circulation (Grossniklaus-Burgin et al, 1998;Coudron et al, 1990). An alternative hypothesis is that inhibition of pupation is an indirect response to virus-and/or parasitoid-induced alterations in host growth or nutritional physiology (Thompson, …”