Akihiro Fukunaga

Induction of Oogenesis in Mosquitoes (Diptera: Culicidae) by Infusion of the Hemocoel with Amino Acids

Abstract As done previously with adult females of Culex pipiens pallens Coquillett, a mixture of 17 amino acids was infused into the hemocoel of females of seven anautogenous and one autogenous mosquito species belonging to three genera. In Culex. p. quinquefasciatus Say, Cx. tritaeniorhynchus Giles, Cx. kyotoensis Yamaguti & LaCasse, Aedes albopictus (Skuse), Armigeres subalbatus (Coquillett), and Cx. p. molestus Forskal, which previously had laid autogenously matured first batch of eggs, ovarian development was stimulated and frequently continued to maturity. In most mosquitoes, the number of mature follicles nearly doubled when the period of infusion was extended from 24 to 48 h. Therefore, the two previously indicated roles of amino acids, one to initiate ovarian development and the other to regulate the number of maturing oocytes, were confirmed in these species. In Cx. halifaxii Theobald and Ae. japonicus (Theobald), however, the frequency of activation and maturation of ovaries was low compared with the other species, indicating that those species may require some factors other than an increase in amino acids for normal ovarian development after a blood meal.

Ovarian development induced in decapitated female Culex pipiens pallens mosquitoes by infusion of physiological quantities of 20-hydroxyecdysone together with amino acids.

Infusion of 20-hydroxyecdysone into the hemocoel of unfed decapitated female Culex pipiens pallens mosquitoes, at a very low rate of 500-2000pg per day, often stimulated oögenesis of this species, when the hormone was infused together with amino acids. The hormone alone or amino acids alone showed no such stimulatory effect. Previous reports that using an abdomen ligated immediately after a blood meal for hormone injection reduced the quantity of 20-hydroxyecdysone needed to activate unfed female Aedes aegypti by a few thousand times, are therefore due mainly to a sufficient supply of amino acids from the midgut in the isolated abdomen.

Evidence for cell-replacement repair of X-ray-induced teratogenic damage in male genital imaginal discs of Drosophila melanogaster.

Male genital imaginal discs from old (late-third-instar) larvae of Drosophila that had been X-irradiated with appropriate doses developed into severely damaged adult genitalia when implanted into old larvae, but they developed into completely normal adult genitalia when transplanted into 2-day-younger larvae. The major cause of X-ray-initiated teratogenesis in the genital disc was DNA damage because development of the genital discs of strain mei-9a with defective DNA repair was twice as sensitive as that of the wild-type strain to impairment by X-irradiation, just as larvae of this strain were twice as sensitive to killing by X-irradiation as those of the wild-type strain. Complete repair of X-ray-induced teratogenic damage in the genital discs on transplantation into young host larvae was similar in the wild-type and mei-9a strains. These results are discussed in relation to the hypothesis that repair of X-ray-induced teratogenic damage depends not on DNA repair but on replacement of damage-bearing primordial cells by healthy ones after suicidal elimination of the former.

Cloning of a novel homeobox (NK-7.1) containing gene, DmHboxNK-7.1, from Drosophila melanogaster.

We have cloned a novel Drosophila melanogaster homeobox (Hbox) containing gene, NK-7.1 (Dm.HboxNK-7.1), which is located at 88B3 on the chromosome map, and is 1.5 kb downstream of the spn-B gene. The newly identified gene is expressed at high levels in the embryo, is switched off during larval and pupal stages, and is expressed again in the adult. The Hbox is highly similar to NK-1/S59 (Drosophila) and NK-3/bap (Drosophila). The amino acid (aa) identity ratios (%) were 58 between NK-7.1 and NK-1/S59, and between NK-7.1 and NK-3/bap. The other characteristic structures are the presence of homopolymeric aa stretches consisting of Q, N, and E.