摘要:

AbstractWe have examined the effects of RH 5849, a non‐steroidal ecdysteroid mimic, on the growth and development ofPlodia interpunctella. When RH 5849 was administered in the diet, larval growth was inhibited in a dose‐dependent manner, while concentrations of 15 ppm and greater were highly toxic. However, the deleterious effects of RH 5849 could be prevented, except at very high concentrations of RH 5849, by the simultaneous administration of the juvenile hormone mimic methoprene. Larvae simultaneously treated with both hormone mimics continued to grow until they attained a size about three times normal. This growth was accompanied by at least one and sometimes two supernumerary molts, whereas, only an occasional supernumerary molt occurred in larvae treated with methoprene alone. In larvae undergoing super numerary molts, wing imaginal discs produced a tanned pupal cuticle, but did not evaginate. When wing discs were cultured in vitro, RH 5849 stimulated evagination and chitin synthesis at concentrations of 10 and 1 μM, respectively. Likewise, RH 5849 stimulated GlcNAc uptake and inhibited cellular proliferation in IAL‐PID2 cells at similar concentrations. These in vitro effects of RH 5849 also were produced by 20‐hydroxyecdysone, but at lower concentrations. We conclude that RH 5849 exhibits molting hormone activity in vivo as well as in vitro. However, the toxicological effects inP. interpuncetellaresult from action on feeding and growth, rather than molting. Thus, RH 5849 represents a new class of IGR, which will have impact on our understanding of endocrine regulation and open up new avenues for pest

ISSN:0739-4462    

DOI:10.1002/arch.940150402

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1990

数据来源: WILEY

摘要:

AbstractBinding sites for vitellogenin were solubilized and analyzed either with a filter assay or with ligand blotting. We tested sodium dodecylsulfate (SDS), Chaps, octyl‐β‐D‐glucoside, and sodium dexocycholate and found SDS and sodium deoxycholate to be most effective in solubilizing both high and low molecular weight binding sites. In the filter assay the sodium deoxycholate extracts but not the SDS extracts, maintained binding activity after dilution of the solubilizer below its critical micellar concentration. In ligand blotting we consistently observed, in vitellogenic folicles, binding sites with an apparent Mrof approximately 200,000, 35,000, and three closely spaced bands between 14,000 and 20,000. Binding of vitellogenin to all binding sites was suppressed in the presence of the drug suramin. Analysis of corpora lutea and oothecae as well as of ovariole sheath, follicle cell/basal lamina, and oocyte plasma membrne preparations showed that the 35 and 14–20 kDa binding sites are located in the outer follicle compartments, and the 200 kDa binding site in the oocyte plasma membrane. In the latter we occasionally also observed binding sites with an apparent Mrof approximately 150,000, 95,000, 67,000 and 30,000, particularly at stages after ovulation. The 35 and 14–20 kDa binding sites, as visualized in stained gels and in ligand blotting, are rather abundant and were also seen in several other male and female tissues ofNauphoetaand even in other species. They also bound other14C‐labeled hemolymph proteins and thus appear to be rather unsepcfic. As binding analysis with nonsolubilized and sodium deoxycholate‐solubilized membranes revealed that the quantity of vitellogenin bound by binding sites of the outer follicle compartments was low, it is conceivable that teh abundance of the 14–20 kDa and 35 kDa binding sites in ligand blotting is merely an effect of SDS and does not reflect the in vivo situation. We suppose that the 200 kDa binding site of the oocyte plasma membrane represents the vitellogenin receptor involve

ISSN:0739-4462    

DOI:10.1002/arch.940150403

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1990

数据来源: WILEY

摘要:

AbstractA few queens of the honeybee,Apis mellifera scutellata, were imported from Africa and released in Brazil in 1957. Progeny of these bees have now largely colonized the American tropics. Their imminent arrival in the United States poses a serious threat to the beekeeping industry and to agriculture dependent on honeybee pollination. African and European bees are morphologically very similar. DNA restriction fragment length polymorphisms are proving successful in distinguishing between the two. Several DNA markers specific to European honeybees have been described previously. Reported here are three cloned honeybee DNA probes that reveal polymorphisms that appear to be either African or European specific. Of fourteen alleles or haplotypes identified, five were present only in African and neotropical (Venezuelan and Mexican) African bees but absent in European‐derived bees, two were present only in European‐derived bees but absent in samples from South Africa. Another allele showed apparent frequency differences among populations. Such markers are useful in studying the genetics of neotropical African bee populations. Venezuelan and Mexican honeybee colonies show a preponderance of the African alleles with low levels of the European alleles. These observations of nuclear DNA, revealing limited paternal European introgression, together with previous mitochondrial DNA findings showing negligible European maternal gene flow into feral African populations, indicate that neotropical African bees are primarily Afri

ISSN:0739-4462    

DOI:10.1002/arch.940150404

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1990

数据来源: WILEY

摘要:

AbstractThe enzymes involved in the side chain hydroxylation and side chain desaturation of the sclerotizing precursor N‐acetyldopamine (NADA) were obtained in the soluble form from the larval cuticle ofSarcophaga bullataand the mechanism of the reaction was investigated. Phenylthiourea, a well‐known inhibitor of phenoloxidases, drastically inhibited both the reactions, indicating the requirement of a phenoloxidase component. N‐acetylcysteine, a powerful quinone trap, trapped the transiently formed NADA quinone and prevented the production of both N‐acetylnorepinephrine and dehydro NADA. Exogenously added NADA quinone was readily converted by these enzyme preparations to N‐acetylnorepinephrine and dehydro NADA. 4‐Alkyl‐o‐quinone:2‐hydroxy‐p‐quinone methide isomerase obtained from the cuticular preparations converted chemically synthesized NADA quinone to its quinone methide. The quinone methide formed reacted rapidly and nonezymatically with water to form N‐acetylnorepinephrine as the stable product. Similarly 4‐(2‐hydroxyethl)‐o‐benzoquinone was converted to 3,4‐dihydroxyphenyl glycol. When the NADA quinone‐quinone isomerase reaction was performed in buffer containing 10% methanol, β‐methoxy NADA was obtained as an additional product. Furthermore, the quinones of N‐acetylnorepinephrine and 3,4‐dihydroxyphenyl glycol were converted to N‐acetylarterenone and 2‐hydroxy‐3′,4′‐dihydroxyacetophenone, respectively, by the enzyme. Comparison of nonenzymatic versus enzymatic transformation of NADA to N‐acetylnorepinephrine revealed that the enzymatic reaction is at least 100 times faster than the nonezymatic rate. Resolution of the NADA desaturase system on Benzamidine Sepharose and Sephacryl S‐200 columns yielded the above‐mentioned quinone isomerase and NADA quinone methide:dehydro NADA isomerase. The latter, on reconstitution with mushroom tyrosinase and hemolymph quinone isomerase, catalyzed the biosynthesis of dehydro NADA from NADA with the intermediary formation of NADA quinone and NADA quinone methide.The results are interpreted in terms of the quinone methide model elabrated by our group [Sugumaran:Adv. Insect Physiol.21 :179–231, 1988; Sugumaran et al.: Arch. Insect Biochem. Physiol. 11 :109,1989] and it i s concluded that the two enzyme p‐sclerotization model [Andersen:Insect Biochem.19:59–67,375–382,1989] is i

ISSN:0739-4462    

DOI:10.1002/arch.940150405

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1990

数据来源: WILEY

摘要:

AbstractThe metabolism of N‐β‐alanyldopamine (NBAD) bySarcophaga bullatawas investigated. Incubation of NBAD with larval cuticular preparations resulted in the covalent bindings of NBAD to the cuticle and generation of N‐β‐alanylnorepinephrine (NBANE) as the soluble product. When the reaction was carried out in presence of a powerful quinone trap viz., N‐acetylcysteine, NBANE formation was totally abolished; but a new compound characterized as NBAD‐quinone‐N‐acetylcysteine adduct was generated. These results indicate that NBAD quinone is an obligatory intermediate for the biosynthesis of NBANE in sarcophagid cuticle. Accordingly, phenylthiourea—a well‐known phenoloxidase inhibitor—completely inhibited the NBANE production even at 5 μM level. A soluble enzyme isolated from cuticle converted exogenously supplied NBAD quinone to NBANE. Chemical considerations indicated that the enzyme is an isomerase and is converting NBAD quinone to its quinone methide which was rapidly and nonenzymatically hydrated to form NBANE. Consistent with this hypothesis is the finding that NBAD quinone methide can be trapped as β‐methoxy NBAD by performing the enzymatic reaction in 10% methanol. Moreover, when the reaction was carried out in presence of kynurenine, two diastereoisomeric structures of papiliochrome II‐{Nar‐[α‐3‐aminopropionyl amino methyl‐3,4‐dihydroxybenzyl]‐L‐kynurenine} could be isolated as byproducts, indicating that the further reactions of NBAD quinone methide with exogenously added nucleophiles are nonenzymatic and nonstereoselective. Based on these results, it is concluded that NBAD is metabolized via NBAD quinone and NBAD quinone methide by the action of phenoloxidase and quinone isomerase respectively. The resultant NBAD quinone methide, being highly reactive, undergoes nonenzymatic and nonstereoselective Michael‐1,6‐addition reaction with either water (to form NBANE) or other nucleophiles in cuticle to account

ISSN:0739-4462    

DOI:10.1002/arch.940150406

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1990

数据来源: WILEY

ISSN:0739-4462    

DOI:10.1002/arch.940150407

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1990

数据来源: WILEY

ISSN:0739-4462    

DOI:10.1002/arch.940150408

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1990

数据来源: WILEY

ISSN:0739-4462    

DOI:10.1002/arch.940150409

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1990

数据来源: WILEY

ISSN:0739-4462    

DOI:10.1002/arch.940150410

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1990

数据来源: WILEY

ISSN:0739-4462    

DOI:10.1002/arch.940150401

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1990

数据来源: WILEY