Female sexual receptivity is defective in juvenile hormone-deficient mutants of theapterous gene ofDrosophila melanogaster

Ringo, John; Werczberger, Ruth; Altaratz, Michal; Segal, Daniel

doi:10.1007/bf01066724

Cited by 59 publications

(32 citation statements)

References 34 publications

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“…Earlier sexual receptiveness was also achieved by topical application of JH, or a synthetic JH analog, methoprene [125]. The topical application of JH or methoprene restored sexual receptiveness when the latter was reduced by mutations such as apterous [126] and icebox (ibx) [127]. These results are compatible with the hypothesis that JH plays a role in the development of female sexual receptiveness.…”

Section: Central Mechanismssupporting

confidence: 75%

Sexual behavior mutants revisited: molecular and cellular basis of Drosophila mating

Yamamoto¹,

Nakano²

1999

Cellular and Molecular Life Sciences (CMLS)

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The study of Drosophila melanogaster by a combination of forward genetics with specific mutants, and reverse genetics, in which a given gene is expressed in an appropriate brain area to test its effect on behavior, provides a unique opportunity to explore the causal relationship between a particular gene, its function in the cell and the behavioral outcome at the organismic level. Enhanced male-to-male courtship has been shown to occur as a result of mutations in several different genes. For example, the Voila mutant exhibits intense GAL4 reporter expression in the tarsal gustatory sensilla, suggesting the importance of tapping by a male on the female abdomen with his forelegs. Feminization of parts of the antennal lobe and mushroom body by targeted expression of a female-determining gene transformer+ (tra+) drives the male to court other males. Mutations in the tra target gene fruitless (fru), which is expressed in the antennal lobe as well as the suboesophageal ganglion (the gustatory inputs are processed here), also induce homosexual courtship in males. These results suggest that sensory inputs mediated and/or processed by the tarsal receptors, suboesophageal ganglion, antennal lobe and mushroom body contribute to the regulation of male-female courtship. Mosaic analysis localized the neural center for male courtship behavior to the posterior dorsal brain, in which the sensory information processed by the aforementioned neural structures may be integrated. Another mosaic study mapped the neural center for female sexual behavior, as measured by her receptiveness to copulation, to the anterior dorsal brain. The issue as to how the mutations that reduce female sexual receptiveness, e.g. dissatisfaction (dsf), spinster (spin) and chaste (cht), affect the structure and/or function of this neural center deserves to be addressed urgently.

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Section: Central Mechanismssupporting

confidence: 75%

Sexual behavior mutants revisited: molecular and cellular basis of Drosophila mating

Yamamoto¹,

Nakano²

1999

Cellular and Molecular Life Sciences (CMLS)

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“…JH has been implicated in vitellogenin biosynthesis in ovarian follicle cells (Jowett and Postlethwait, 1980;Bownes, 1989;Soller et al, 1999) and in endocytic uptake by the oocyte (Postlethwait and Weiser, 1973;Postlethwait and Handler, 1978;Giorgi, 1979;Saunders et al, 1990). Additionally, JH has been implicated in female receptivity (Manning, 1966;Bouletreau-Merle, 1973;Ringo et al, 1991), and this hormone plays a role in the histolysis of larval fat body following eclosion (Postlethwait and Jones, 1978;Wilson et al, 1983).…”

Section: Introductionmentioning

confidence: 97%

“…One mutant that is deficient in JH, apparently due to an indirect effect on JH titer, is the apterous (ap) mutant (Bownes, 1989;Altaratz et al, 1991). Adults homozygous for severe alleles of ap, such as ap 4 , are nonvitellogenic, defective in female receptivity, and have retarded histolysis of larval fat body (Butterworth and King, 1965;Postlethwait and Weiser, 1973;Gavin and Williamson, 1976;Postlethwait and Jones, 1978;Wilson, 1981;Redfern and Bownes, 1982;Wilson, 1982;Ringo et al, 1991). Some of these phenotypic characteristics are similar to those shown by D. melanogaster females rendered JH deficient by either surgery or with precocene.…”

Section: Introductionmentioning

confidence: 98%

Juvenile hormone involvement in Drosophila melanogaster male reproduction as suggested by the Methoprene-tolerant27 mutant phenotype

Wilson

DeMoor

Lei

2003

Insect Biochemistry and Molecular Biology

102

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“…Implantation of JH-secreting corpora allata (CA) (6) just before eclosion or application of methoprene (8), a JH mimic (JHM), caused females to mate precociously. Decreased JH in the apterous mutant (9) or after treatment of females with precocene, a compound cytotoxic for the CA (10), reduced female mating. These findings suggest that JH may play a role in the maturation of female receptivity in D. melanogaster.…”

mentioning

confidence: 99%

Regulation of onset of female mating and sex pheromone production by juvenile hormone in Drosophila melanogaster

Bilen

Atallah

Azanchi

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Juvenile hormone (JH) coordinates timing of female reproductive maturation in most insects. In Drosophila melanogaster, JH plays roles in both mating and egg maturation. However, very little is known about the molecular pathways associated with mating. Our behavioral analysis of females genetically lacking the corpora allata, the glands that produce JH, showed that they were courted less by males and mated later than control females. Application of the JH mimic, methoprene, to the allatectomized females just after eclosion rescued both the male courtship and the mating delay. Our studies of the null mutants of the JH receptors, Methoprene tolerant (Met) and germ cell-expressed (gce), showed that lack of Met in Met 27 females delayed the onset of mating, whereas lack of Gce had little effect. The Met 27 females were shown to be more attractive but less behaviorally receptive to copulation attempts. The behavioral but not the attractiveness phenotype was rescued by the Met genomic transgene. Analysis of the female cuticular hydrocarbon profiles showed that corpora allata ablation caused a delay in production of the major female-specific sex pheromones (the 7,11-C27 and -C29 dienes) and a change in the cuticular hydrocarbon blend. In the Met 27 null mutant, by 48 h, the major C27 diene was greatly increased relative to wild type. In contrast, the gce 2.5k null mutant females were courted similarly to control females despite changes in certain cuticular hydrocarbons. Our findings indicate that JH acts primarily via Met to modulate the timing of onset of female sex pheromone production and mating.

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Female sexual receptivity is defective in juvenile hormone-deficient mutants of theapterous gene ofDrosophila melanogaster

Cited by 59 publications

References 34 publications

Sexual behavior mutants revisited: molecular and cellular basis of Drosophila mating

Sexual behavior mutants revisited: molecular and cellular basis of Drosophila mating

Juvenile hormone involvement in Drosophila melanogaster male reproduction as suggested by the Methoprene-tolerant27 mutant phenotype

Regulation of onset of female mating and sex pheromone production by juvenile hormone in Drosophila melanogaster

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