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  • Reduction of testis growth of Pseudaletia separata larvae after parasitization by Cotesia kariyai
  • 作者: Tanaka, T.; Tagashira, E. and Sakurai, S
  • literature id: 44544
  • catalog nub: TPL_TANAKA1994ROTGO11101220
  • 文献库: Taxapad收录文献
  • type: article
  • publication name: Archives of Insect Biochemistry and Physiology
  • publish date: 1994-01-01
  • pages: 111-122
  • volume: 26
  • issue: 2-3
  • 创建时间: 2021-03-02 15:00:32
  • create by: zxmlmq (admin)
  • comment:

    none Pseudaletia separata; SEXUAL-MATURATION; TESTIS-; LARVAL-DEVELOPMENT; Testis growth; GROWTH-; Testis development, inhibition by hymenopteran parasite; HYMENOPTERAN-PARASITES; Cotesia kariyai; Parasite inhibition of host testis growth, mechanisms Cotesia kariyai; TOXINS-AND-VENOMS; Venom inhibitory effect on lepidopteran host testis growth; ASSOCIATIONS-; Polydnavirus; Virus inhibitory effect on lepidopteran host testis growth; LEPIDOPTERAN-HOSTS; Pseudaletia separata; Parasite inhibition of host testis growth, mechanisms The braconid endoparasitoid, Cotesia (=Apanteles) kariyai physiologically influences its host, Pseudaletia separata, through three factors: polydnavirus, venom, and teratocytes. Inhibiting testis development of the host seems to be one factor that is important for successful development of the parasitoid. CkPV (polydnavirus of Cotesia kariyai) plus venom depressed testis development. Testes from unparasitized day 0 last instar transplanted into isolated abdomens increased in volume after stimulation with 20-hydroxyecdysone (20HE). However, day 0 testis preincubated with CkPV plus venom for 6 h and then transplanted into an isolated abdomen did not respond to 20HE. Southern blot analysis indicated CkPV-DNA hybridized to testes-DNA from parasitized hosts, suggesting the possibility that CkPV is involved in suppression of testes growth. Binding assays using PNA indicated a 2-fold increase in ecdysteroid receptor binding activity during the late stage of parasitism. The increase in receptor activity might be related to the maintenance of a low ecdysteroid titer in parasitized hosts due to a feedback response.

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