The synthesis of juvenile hormone in vitro by diapausing and nondiapausing Culex pipiens L. was measured by radiochemical assay. Paired corpora allata from diapausing females synthesized < 18 fmols of juvenile hormone per hour during the first 3 wk after emergence. In contrast, juvenile hormone synthesis in nondiapausing females increased rapidly reaching a peak of 87.3 +/- 21 (mean +/- SE) fmol/h 3 d after emergence. By 3 wk, juvenile hormone synthesis had decreased in both groups of females, but corpora allata from nondiapausing mosquitoes still were 3 times more active than those from diapausing mosquitoes. By 16 wk after diapause induction, females maintained at 8:16 (L:D) h and 15 degrees C produced levels of juvenile hormone similar to 3-wk-old nondiapausing females. When females were held in diapause conditions for up to 22 wk, follicles gradually grew longer and by 15 wk were significantly longer than in the previous 14 wk. Blood feeding also increased in older females, indicating that over time, juvenile hormone synthesis gradually stimulated blood-feeding behavior. When 21-d-old diapausing mosquitoes were moved to a long-day photoperiod of 16:8 (L:D) h and 26 degrees C, juvenile hormone synthesis increased rapidly and peaked 5 d later while the ovarian follicles grew to the resting stage. Allatectomy of young diapausing females prevented follicle growth and blood feeding when diapause was terminated prematurely, demonstrating that the physiological events associated with diapause termination were associated with juvenile hormone biosynthesis.
Adult cat fleas were exposed to residues of pyriproxyfen and methoprene in glass vials, then fed on a cat 24 h later to investigate the mode of action of juvenoid growth regulators on embryonic development in flea eggs. Eggs laid by pyriproxyfen-treated fleas within 70 h after exposure to this juvenoid were often devoid of yolk and frequently collapsed after oviposition. Minimal amounts of yolk were deposited in eggs laid after 70 h, and no blastoderm was formed. These results are significant because both modes of action were different than those observed earlier by investigators studying ovicidal effects in adult insects treated with juvenile hormone. In contrast to the pyriproxyfen results, eggs laid by methoprene-treated fleas showed no gross morphological effects, and these eggs remained turgid during embryogenesis. However, the eggs either did not hatch or the larvae died within hours after hatching. Histological examination of the eggs revealed that most of the eggs contained segmented embryos which had apparently died during blastokinesis. Although eggs of some insects exposed to juvenile hormone during oogenesis fail to undergo germ band formation, there was no evidence of this effect in methoprene-treated cat fleas.
In the corn earworm Helicoverpa zea yolk deposition in oocytes begins 8-10 h after adult eclosion and is controlled by juvenile hormone (JH). Hemolymph from females at the time of yolk formation, analyzed by SDS-PAGE, contains polypeptides apparently identical to polypeptides from eggs; and these have been tentatively designated as apovitellogenins (apovgs). ApoVgs were not found in male hemolymph. The hormonal control of production of the apoVg with an apparent molecular weight of 165 kDa (apoVg-I) was studied by SDS-PAGE. Decapitation of females immediately after eclosion did not prevent the appearance of apoVg-I whereas the same operation done 5-7 h prior to eclosion abolished its production. Treatment of the latter group of females with methoprene, a JH analogue, restored production of apoVg-I whereas injection of 20-hydroxyecdysone (20-HE) did not. When pharate adults were kept at 10°C from 10-12 h before the time of their anticipated eclosion, wlosion was delayed for 4-7 d. In such females, maintained at the same temperature, apoVg-I appeared only on day 3, and its appearance could be accelerated by two days with methoprene treatment immediately after eclosion. Decapitation of chilled females just after eclosion prevented the appearance of apoVg-I even after 16 d at 10°C. Likewise, Vg was absent in chilled females decapitated after eclosion and then maintained at room temperature. Methoprene induced apoVg-I production one day after treatment in chilled decapitated females maintained after eclosion either chilled or at room temperature. 20-HE had no effect on these females. Methoprene did not induce Vg in adult males. ApoVg-I of H. zea did not cross-react with Manduca sexta and Plodia interpunctella Vg antibodies. These results demonstrate that Vg synthesis in H. zea is regulated by JH.
When cat fleas, Ctenocephalides felis (Bouché), were fed concentrations of lufenuron in cattle blood ranging from 0.5 to 4 ppm, adult mortality increased in a dose-dependent manner to a maximum of approximately 24% over a period of 10 d. Fleas treated with 0.5 ppm produced abnormal endocuticle consisting of protein globules embedded in an amorphous chitin matrix. At concentrations of 1.0 ppm or greater, endocuticle formation was inhibited. Ultrastructural studies demonstrated that inhibition of chitin synthesis was associated with degeneration of the epidermal cells. The amount of epidermal cytoplasm decreased and cytoplasmic organelles including mitochondria, ribosomes, and golgi showed lytic changes. At least some mortality of treated fleas was likely the result of a weakened endocuticle and the corresponding decrease in resiliency of the cuticle to expansion during blood-feeding and egg production. An unexpected result of lufenuron treatment was the inhibition of midgut epithelial cell differentiation. At concentrations of 0.5 and 1.0 ppm, partially differentiated epithelial cells were seen in the midgut of bloodfed fleas along with fully differentiated cells.
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