Antidiuretic effects of a factor in brain/corpora cardiaca/corpora allata extract on fluid reabsorption across the cryptonephric complex of Manduca sexta. (1/39)

Extracts of the brain/corpora cardiaca/corpora allata (Br/CC/CA) complex of Manduca sexta larvae elicit an antidiuretic effect, measured by an increase in fluid reabsorption across the cryptonephric complex of larval M. sexta. Separation of the extract by reversed-phase liquid chromatography gave two fractions with antidiuretic effects. The more potent of these two factors was further characterized for its effects on the cryptonephric complex. Its antidiuretic effect is not inhibited by bumetanide, a drug that inhibits M. sexta diuretic hormone (Mas-DH)-stimulated fluid reabsorption. These data indicate that the mechanism of the antidiuretic effect of the factor is different from that of Mas-DH on the cryptonephric complex. The basal reabsorption of the cryptonephric complex is blocked when treated on the lumen side with bafilomycin A(1), an inhibitor of the H(+)-ATPase, or with amiloride, an inhibitor of the H(+)/K(+) antiporter. However, the antidiuretic-factor-stimulated fluid reabsorption is not affected by either bafilomycin A(1) or amiloride. The increase in reabsorption triggered by the semi-purified factor can be inhibited by Cl(-) channel blockers or by removing Cl(-) from the lumen side of the cryptonephric complex. It appears that this factor activates a Cl(-) pump associated with the cryptonephric complex. Forskolin mimics the effect of this factor on fluid reabsorption, and the effect of forskolin is not inhibited by bumetanide. A selective and potent inhibitor of protein kinase A, H-89, also inhibits antidiuretic-factor-stimulated fluid reabsorption. Addition of the factor to cryptonephric complexes maintained in vitro caused a significant increase in cyclic AMP levels extracted from these tissues compared with values for controls. These data suggest that the antidiuretic effect of the factor in Br/CC/CA extract is mediated by cyclic AMP.  (+info)

A mutant Drosophila insulin receptor homolog that extends life-span and impairs neuroendocrine function. (2/39)

The Drosophila melanogaster gene insulin-like receptor (InR) is homologous to mammalian insulin receptors as well as to Caenorhabditis elegans daf-2, a signal transducer regulating worm dauer formation and adult longevity. We describe a heteroallelic, hypomorphic genotype of mutant InR, which yields dwarf females with up to an 85% extension of adult longevity and dwarf males with reduced late age-specific mortality. Treatment of the long-lived InR dwarfs with a juvenile hormone analog restores life expectancy toward that of wild-type controls. We conclude that juvenile hormone deficiency, which results from InR signal pathway mutation, is sufficient to extend life-span, and that in flies, insulin-like ligands nonautonomously mediate aging through retardation of growth or activation of specific endocrine tissue.  (+info)

Juvenile hormone regulation of longevity in the migratory monarch butterfly. (3/39)

Monarch butterflies (Danaus plexippus) of eastern North America are well known for their long-range migration to overwintering roosts in south-central Mexico. An essential feature of this migration involves the exceptional longevity of the migrant adults; individuals persist from August/September to March while their summer counterparts are likely to live less than two months as adults. Migrant adults persist during a state of reproductive diapause in which both male and female reproductive development is arrested as a consequence of suppressed synthesis of juvenile hormone. Here, we describe survival in monarch butterflies as a function of the migrant syndrome. We show that migrant adults are longer lived than summer adults when each are maintained under standard laboratory conditions, that the longevity of migrant adults is curtailed by treatment with juvenile hormone and that the longevity of summer adults is increased by 100% when juvenile hormone synthesis is prevented by surgical removal of its source, the corpora allatum. Thus, monarch butterfly persistence through a long winter season is ensured in part by reduced ageing that is under endocrine regulation, as well as by the unique environmental properties of their winter roost sites. Phenotypic plasticity for ageing is an integral component of the monarch butterflies' migration-diapause syndrome.  (+info)

Insect NMDA receptors mediate juvenile hormone biosynthesis. (4/39)

In vertebrates, the N-methyl-D-aspartate subtype of glutamate receptors (NMDAR) appears to play a role in neuronal development, synaptic plasticity, memory formation, and pituitary activity. However, functional NMDAR have not yet been characterized in insects. We have now demonstrated immunohistochemically glutamatergic nerve terminals in the corpora allata of an adult female cockroach, Diploptera punctata. Cockroach corpus allatum (CA) cells, exposed to NMDA in vitro, exhibited elevated cytosolic [Ca(2+)], but not in culture medium nominally free of calcium or containing NMDAR-specific channel blockers: MK-801 and Mg(2+). Sensitivity of cockroach corpora allata to NMDA changed cyclically during the ovarian cycle. Highly active glands of 4-day-old mated females, exposed to 3 microM NMDA, produced 70% more juvenile hormone (JH) in vitro, but the relatively inactive glands of 8-day-old mated females showed little response to the agonist. The stimulatory effect of NMDA was eliminated by augmenting the culture medium with MK-801, conantokin, or high Mg(2+). Having obtained substantive evidence of functioning NMDAR in insect corpora allata, we used reverse transcription PCR to demonstrate two mRNA transcripts, DNMDAR1 and DNMDAR2, in the ring gland and brain of last-instar Drosophila melanogaster. Immunohistochemical labeling, using mouse monoclonal antibody against rat NMDAR1, showed that only one of the three types of endocrine cells in the ring gland, CA cells, expressed rat NMDAR1-like immunoreactive protein. This antibody also labeled two brain neurons in the lateral protocerebrum, one neuron per brain hemisphere. Finally, we used the same primers for DNMDAR1 to demonstrate a fragment of putative NMDA receptor in the corpora allata of Diploptera punctata. Our results suggest that the NMDAR has a role in regulating JH synthesis and that ionotropic-subtype glutamate receptors became specialized early in animal evolution.  (+info)

In vivo membrane trafficking role for an insect N-ethylmaleimide-sensitive factor which is developmentally regulated in endocrine cells. (5/39)

The hexameric ATPase, N-ethylmaleimide-sensitive factor (NSF) is implicated in the release of neurotransmitters and in mediating fusion between intracellular membranes. Due to the conservation of proteins in constitutive and regulated membrane fusion reactions, NSF and its downstream targets have been predicted also to participate in fusion reactions underlying endocrine function, but there is little experimental evidence to support such a role for NSF in insect neuroendocrine secretion. Here we have characterized the NSF orthologue (MsNSF) from the endocrine model for development Manduca sexta. MsNSF is developmentally regulated in endocrine organs of the protocerebral complex. Enrichment of MsNSF in corpora cardiaca (CC) and not in corpora allata (CA) indicates that it might play a preferential role in releasing hormones produced in CC. Endocrine/paracrine cells of the enteric system in M. sexta exhibit selective MsNSF enrichment. Together the data point to a more selective participation of MsNSF in development of M. sexta by its involvement in a subset of factors, whereas other as-yet-unidentified homolog(s) might regulate secretion from CA and a large set of endocrine/paracrine cells. We further characterized the in vivo role of MsNSF by heterologous expression. In contrast to vertebrate NSF, MsNSF is functional in yeast membrane fusion in vivo. MsNSF rectifies defects in SEC18 (yeast NSF homologue) at nearly all discernible steps where Sec18p has been implicated in the biosynthetic route. This underscores the utility of our approach to delineate functional roles for proteins from systems that are not currently amenable to in vitro reconstitution.  (+info)

The retinoic-like juvenile hormone controls the looping of left-right asymmetric organs in Drosophila. (6/39)

In vertebrate development, the establishment of left-right asymmetry is essential for sidedness and the directional looping of organs like the heart. Both the nodal pathway and retinoic acid play major and conserved regulatory roles in these processes. We carried out a novel screen in Drosophila to identify mutants that specifically affect the looping of left-right asymmetric organs. We report the isolation of spin, a novel mutant in which the looping of the genitalia and spermiduct are incomplete; under-rotation of the genitalia indicates that spin controls looping morphogenesis but not direction, thus uncoupling left-right asymmetry and looping morphogenesis. spin is a novel, rotation-specific allele of the fasciclin2 (Fas2) gene, which encodes a cell-adhesion protein involved in several aspects of neurogenesis. In spin mutants, the synapses connecting specific neurosecretory cells to the corpora allata are affected. The corpus allatum is part of the ring gland and is involved in the control of juvenile hormone titers during development. Our genetic and pharmacological results indicate that Fas2(spin) rotation defects are linked to an abnormal endocrine function and an elevated level of juvenile hormone. As juvenile hormone is an insect sesquiterpenoid related to retinoic acid, these results establish a new genetic model for studying organ looping and demonstrate an evolutionarily conserved role for terpenoids in this process.  (+info)

Stimulation of JH biosynthesis by the corpora allata of adult female Aedes aegypti in vitro: effect of farnesoic acid and Aedes allatotropin. (7/39)

Previous studies have demonstrated that the synthesis of juvenile hormone (JH) by the isolated corpora allata (CA) complex in vitro as well as the JH titer in the yellow fever mosquito Aedes aegypti are elevated before feeding and low after a blood meal. In the present study, we used an in vitro radiochemical assay to analyze the effect of farnesoic acid (FA) and Aedes allatotropin (Aedes-AT) on the biosynthesis of JH and methyl farnesoate (MF) by the isolated CA complex of A. aegypti adult female. CA complex from day-0 females (0-1 h after emergence) exhibited a low basal juvenile hormone III (JH III) biosynthetic activity and did not respond to either allatotropic or FA stimulation. However, incubation of CA complexes from newly emerged females with Aedes-AT plus FA resulted in very high production of JH III. This is the first report suggesting that allatotropin makes corpora allata in newly emerged females capable for JH biosynthesis. When we studied CA complexes dissected from females 1 day after emergence, the stimulatory action of Aedes-AT was strong and dose-dependent, with maximum stimulation in the range of 10(-8)-10(-9) mol l(-1), suggesting that Aedes-AT is indeed a true allatotropin (a molecule with allatotropic activity) in A. aegypti. The addition to the culture medium of 40 micro mol l(-1) FA, a JH precursor, resulted in a 9-fold increase in JH III biosynthesis in 2-, 4- and 6-day-old sugar-fed females. The two major labeled products synthesized by the stimulated CA complex were identified as JH III and MF by RP-HPLC and GC-MS. Treatment of CA complexes with FA, but not Aedes-AT, resulted in an increase in MF. Application of both Aedes-AT and FA to the CA complexes of 2-, 4- and 6-day-old females resulted in the same effects as FA alone. These data suggest that in sugar-fed females, FA and Aedes-AT exert different effects on the terminal steps in JH biosynthesis.  (+info)

Juvenile hormone and division of labor in honey bee colonies: effects of allatectomy on flight behavior and metabolism. (8/39)

Three experiments were performed to determine why removal of the corpora allata (the glands that produce juvenile hormone) causes honey bees to fail to return to their hive upon initiating flight. In Experiment 1, the naturally occurring flights of allatectomized bees were tracked with radar to determine whether the deficit is physical or cognitive. The results indicated a physical impairment: allatectomized bees had a significantly slower ground speed than sham and untreated bees during orientation flights, but otherwise attributes such as flight range and area were normal. Flight impairment was confirmed in Experiment 2, based on observations of takeoff made in the field at the hive entrance. The allatectomized group had a significantly smaller percentage of flightworthy bees than did the sham and untreated groups. Experiment 3 confirmed the flight impairment in laboratory tests and showed that allatectomy causes a decrease in metabolic rate. Allatectomized bees had significantly lower metabolic rates than untreated and sham bees, while allatectomized bees receiving hormone replacement had intermediate values. These results indicate that allatectomy causes flight impairment, probably partly due to effects on metabolic rate. They also suggest that juvenile hormone plays an additional, previously unknown, role in coordinating the physiological underpinning of division of labor in honey bee colonies.  (+info)

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