Biochemical and developmental alterations of Heliothis virescens (F.) (lepidoptera, noctuidae) larvae induced by the endophagous parasitoid Cardiochiles nigriceps viereck (Hymenoptera, braconidae)

Abstract

All larval stages of Heliothi5 virescens (F.) parasitized by the endophagous larval parasitoid Cardiochiles nigriceps Viereck, a braconid species belonging to the subfamily Microgasterinae, exhibit developmental arrest at last instar and fail to pupate. The major part of larval development of the parasitoid is synchronized with the arrested host last larval instar and the parasitoid first molt is never observed before the host attains the late digging stage. At this time, the total ecdysteroid titer of the hemolymph of parasitized hosts is very low and subsequently shows a slow and gradual increase, characterized by a low titer of 20-hydroxyecdysone (20-HE) associated with consistent amounts of inactive ecdysteroid polar metabolites. Juvenile hormone esterase UHE) activity is high in both control and parasitized host larvae at the early digging stage of development, and juvenile hormone analogs UHA) applied to parasitized host last instar larvae appear to suppress the parasitoid molt. Concurrent with these changes was an increase in the hemolymph titer of proteins which was maintained at a high level in parasitized larvae in contrast to the observed decrease in control larvae at the cell formation stage of development.Neck-ligation of newly molted host 5th instar parasitized larvae, prior to both JHE release and the increase in protein titers, inhibited growth and molting of the parasitoid. In contrast, ligation after ]HE release and with high hemolymph protein Acknowledgments:is not necessary for the molt. Teratocytes of C. nigriceps seem to play an important role in the inactivation of 20-HE through its conversion to inactive polar metabolites, and along with female calyx fluid and venom which depress the secretory activity of the host prothoracic glands, they are the most important sources of host regulatory factors. 0 1994 Witey-Liss, Inc.

Lepidopteran Larval Midgut During Prepupal Instar: Digestion or Self-Digestion?

“…6,7 At early stages of the midgut replacement process, this PCD form could be, in theory, activated as a starvation-induced protective mechanism, enabling the prepupa to cope with food deprivation and to maintain cell homeostasis, by providing an alternative energy source. 8,9 However, the autophagic burst in H. virescens midgut takes place only after the 20-hydroxyecdysone commitment peak, 10 suggesting that this PCD modality is finely …”

Physiological and molecular interaction in the host–parasitoid system Heliothis virescens–Toxoneuron nigriceps: current status and future perspectives

“…The infection and active transcription of TnBV genome is required for host prothoracic gland (PTG) inactivation that results in a consistent reduction of ecdysteroid titre (Tanaka and Vinson, 1991;Pennacchio et al, 1997Pennacchio et al, , 1998. The reduced amount of bioactive 20-hydroxyecdysone still produced is selectively converted by teratocytes to inactive metabolites, which gradually accumulate during the final part of parasitoid's larval development (Pennacchio et al, 1994). Therefore, the combined action of host regulation factors of both maternal (TnBV) and embryonic (teratocytes) origin insures the near complete absence of 20-hydroxyecdysone in mature parasitized larvae, which become developmentally arrested.…”

“…1D). These cells freely float in the host haemocoel, and, as the parasitoid larva develops, they increase in size and ploidy level, without undergoing division (Dahlman and Vinson, 1993;Pennacchio et al, 1994). TnBV and teratocytes are the two major host regulation factors, respectively of maternal and embryonic origin, responsible for the physiological alterations induced by parasitization (Tanaka and Vinson, 1991;Pennacchio et al, 1998).…”

Toxoneuron nigriceps parasitization delays midgut replacement in fifth-instar Heliothis virescens larvae

“…Because parasitized host larvae show a concurrent delay of gut development with a failure of 20E surge (Pennacchio et al 1994), we wanted to assess the possible rescue effect of 20E injection into parasitized larvae (Fig. 6a) on day 4 of the fifth instar, which corresponds to the time interval when the peak that triggers pupation in unparasitized controls is observed.…”

“…The major endocrine changes registered are a significantly higher titer of juvenile hormone (JH) in parasitized host last-instar larvae (Li et al 2003), associated with the suppression of the 20-hydroxyecdysone (20E) peak, and a gradual accumulation over time of polar ecdysteroids ). This alteration is induced by the combined action of the bracovirus associated with T. nigriceps (TnBV), which strongly reduces ecdysone biosynthesis by the prothoracic glands of host last-instar larvae (Pennacchio et al 1997Pennacchio and Strand 2006), whereas the teratocytes, cells deriving from the dissociation of the embryonic serosal membrane, are responsible for the selective conversion of the 20E to inactive polar metabolites, which accumulate in the host hemolymph (Pennacchio et al 1994Pennacchio and Strand 2006). The most evident consequence of the disrupted endocrine balance is the developmental arrest of parasitized last-instar larvae of the host.…”