Genetic divergence in the kinetics of ovarian activity and brain control in virgin Drosophila melanogaster females

ABSTRACT rDNA magnification in Drosophila melanogaster is defined experimentally as the ability of bb/Ybb - males to produce exceptional progeny that are wild type with respect to rDNA associated phenotypes. Here, we show that some of these bobbed-plus progeny result not from genetic reversion at the bb locus but rather from variants at two or more autosomal loci that ameliorate the bobbed phenotype of rDNA deficient males in Drosophila. In doing so we resolve several aspects of a long-standing paradox concerning the phenomenon of rDNA magnification. This problem arose from the use of two genetic assays, which were presumed to be identical, but paradoxically, produced conflicting data on both the kinetics of reversion and the stability of magnified bb + chromosomes. We resolve this problem by demonstrating that in one assay bobbed-plus progeny arise primarily by genetic reversion at the bobbed locus, whereas in the other assay bobbed-plus progeny arise both by reversion and by an epistatic effect of autosomal modifiers on the bobbed phenotype. We further show that such modifiers can facilitate the appearance of phenotypically bobbed-plus progeny even under conditions where genetic reversion is blocked by magnification defective mutants. Finally, we present a speculative model relating the action of these modifiers to the large increases in rDNA content observed in males undergoing magnification.

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The kinetics of X-ray-induced somatic crossing-over in Drosophila melanogaster and the effects of dose fractionation

Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis ◽

10.1016/0027-5107(72)90017-6 ◽

1972 ◽

Vol 14 (3) ◽

pp. 309-314 ◽

Cited By ~ 13

Author(s):

J.R. Merriam ◽

W.E. Fyffe

Keyword(s):

Drosophila Melanogaster ◽

Dose Fractionation ◽

Crossing Over ◽

X Ray ◽

Kinetics Of

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Genetic Divergence Under Uniform Selection. I. Similarity Among Populations of Drosophila melanogaster in Their Responses to Artificial Selection for Modifiers of ci D

Evolution ◽

10.2307/2408547 ◽

1984 ◽

Vol 38 (1) ◽

pp. 55 ◽

Cited By ~ 10

Author(s):

Frederick M. Cohan

Keyword(s):

Drosophila Melanogaster ◽

Artificial Selection ◽

Genetic Divergence ◽

Selection For

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Lifespan extension by dietary restriction in female Drosophila melanogaster is not caused by a reduction in vitellogenesis or ovarian activity

Experimental Gerontology ◽

10.1016/j.exger.2004.03.018 ◽

2004 ◽

Vol 39 (7) ◽

pp. 1011-1019 ◽

Cited By ~ 71

Author(s):

William Mair ◽

Carla M Sgrò ◽

Alice P Johnson ◽

Tracey Chapman ◽

Linda Partridge

Keyword(s):

Drosophila Melanogaster ◽

Dietary Restriction ◽

Lifespan Extension ◽

Ovarian Activity

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Serotonergic modulation of visual neurons in Drosophila melanogaster

10.1101/619759 ◽

2019 ◽

Cited By ~ 1

Author(s):

Maureen M Sampson ◽

Katherine M Myers Gschweng ◽

Ben J Hardcastle ◽

Shivan L Bonanno ◽

Tyler R Sizemore ◽

...

Keyword(s):

Drosophila Melanogaster ◽

Information Processing ◽

Visual Processing ◽

Serotonin Receptors ◽

Visual Information ◽

Optic Lobe ◽

Receptor Expression ◽

Serotonergic Neurons ◽

Visual Neurons ◽

Kinetics Of

AbstractSensory systems rely on neuromodulators, such as serotonin, to provide flexibility for information processing in the face of a highly variable stimulus space. Serotonergic neurons broadly innervate the optic ganglia of Drosophila melanogaster, a widely used model for studying vision. The role for serotonergic signaling in the Drosophila optic lobe and the mechanisms by which serotonin regulates visual neurons remain unclear. Here we map the expression patterns of serotonin receptors in the visual system, focusing on a subset of cells with processes in the first optic ganglion, the lamina, and show that serotonin can modulate visual responses. Serotonin receptors are expressed in several types of columnar cells in the lamina including 5-HT2B in lamina monopolar cell L2, required for the initial steps of visual processing, and both 5-HT1A and 5-HT1B in T1 cells, whose function is unknown. Subcellular mapping with GFP-tagged 5-HT2B and 5-HT1A constructs indicates that these receptors localize to layer M2 of the medulla, proximal to serotonergic boutons, suggesting that the medulla is the primary site of serotonergic regulation for these neurons. Serotonin increases intracellular calcium in L2 terminals in layer M2 and alters the kinetics of visually induced calcium transients in L2 neurons following dark flashes. These effects were not observed in flies without a functional 5-HT2B, which displayed severe differences in the amplitude and kinetics of their calcium response to both dark and light flashes. While we did not detect serotonin receptor expression in L1 neurons, they also undergo serotonin-induced calcium changes, presumably via cell non-autonomous signaling pathways. We provide the first functional data showing a role for serotonergic neuromodulation of neurons required for initiating visual processing in Drosophila and establish a new platform for investigating the serotonergic neuromodulation of sensory networks.Author SummarySerotonergic neurons innervate the Drosophila melanogaster eye, but the function of serotonergic signaling is not known. We found that serotonin receptors are expressed in all neuropils of the optic lobe and identify specific neurons involved in visual information processing that express serotonin receptors. We then demonstrate that activation of these receptors can alter how visual information is processed. These are the first data suggesting a functional role for serotonergic signaling in Drosophila vision. This study contributes to the understanding of serotonin biology and modulation of sensory circuits.

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Metabolic Characterization and Consequences of Mitochondrial Pyruvate Carrier Deficiency in Drosophila melanogaster

Metabolites ◽

10.3390/metabo10090363 ◽

2020 ◽

Vol 10 (9) ◽

pp. 363 ◽

Cited By ~ 2

Author(s):

Chloé Simard ◽

Andréa Lebel ◽

Eric Pierre Allain ◽

Mohamed Touaibia ◽

Etienne Hebert-Chatelain ◽

...

Keyword(s):

Drosophila Melanogaster ◽

Oxygen Consumption ◽

Citrate Synthase ◽

Control Point ◽

Substrate Oxidation ◽

Metabolic Reprogramming ◽

Wild Type ◽

Mitochondrial Oxygen Consumption ◽

Mitochondrial Pyruvate Carrier ◽

Kinetics Of

In insect, pyruvate is generally the predominant oxidative substrate for mitochondria. This metabolite is transported inside mitochondria via the mitochondrial pyruvate carrier (MPC), but whether and how this transporter controls mitochondrial oxidative capacities in insects is still relatively unknown. Here, we characterize the importance of pyruvate transport as a metabolic control point for mitochondrial substrate oxidation in two genotypes of an insect model, Drosophila melanogaster, differently expressing MPC1, an essential protein for the MPC function. We evaluated the kinetics of pyruvate oxidation, mitochondrial oxygen consumption, metabolic profile, activities of metabolic enzymes, and climbing abilities of wild-type (WT) flies and flies harboring a deficiency in MPC1 (MPC1def). We hypothesized that MPC1 deficiency would cause a metabolic reprogramming that would favor the oxidation of alternative substrates. Our results show that the MPC1def flies display significantly reduced climbing capacity, pyruvate-induced oxygen consumption, and enzymatic activities of pyruvate kinase, alanine aminotransferase, and citrate synthase. Moreover, increased proline oxidation capacity was detected in MPC1def flies, which was associated with generally lower levels of several metabolites, and particularly those involved in amino acid catabolism such as ornithine, citrulline, and arginosuccinate. This study therefore reveals the flexibility of mitochondrial substrate oxidation allowing Drosophila to maintain cellular homeostasis.

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