scholarly journals The intracellular symbiont Wolbachia enhances recombination in a dose-dependent manner

2019 ◽  
Author(s):  
Kaeli N. Bryant ◽  
Irene L.G. Newton
Keyword(s):  
Drosophila Melanogaster ◽  
Cell Biology ◽  
Horizontal Transmission ◽  
Specific Effect ◽  
Dependent Manner ◽  
X Chromosomes ◽  
Intracellular Symbiont ◽  
Host Nutrition ◽  
Infected Insect ◽  
Dose Dependent

AbstractWolbachia pipientis is an intracellular alphaproteobacterium that infects 40-60% of insect species and is well known for host reproductive manipulations. Although Wolbachia are primarily maternally transmitted, evidence of horizontal transmission can be found in incongruent host-symbiont phylogenies and recent acquisitions of the same Wolbachia strain by distantly related species. Parasitoids and predator-prey interactions may indeed facilitate the transfer of Wolbachia between insect lineages but it is likely that Wolbachia are acquired via introgression in many cases. Many hypotheses exist as to explain Wolbachia prevalence and penetrance such as nutritional supplementation, protection from parasites, protection from viruses, or straight up reproductive parasitism. Using classical genetics we show that Wolbachia increase recombination in infected lineages across two genomic intervals. This increase in recombination is titer dependent as the wMelPop variant, which infects at higher load in Drosophila melanogaster, increases recombination 5% more than the wMel variant. In addition, we also show that Spiroplasma poulsonii, the other bacterial intracellular symbiont of Drosophila melanogaster, does not induce an increase in recombination. Our results suggest that Wolbachia infection specifically alters host recombination landscape in a dose dependent manner.Article SummaryThe ubiquitous bacterial symbiont Wolbachia is known to alter host reproduction through manipulation of host cell biology, protect from pathogens, and supplement host nutrition. In this work we show that Wolbachia specifically increases host recombination in a dose dependent manner. Flies harboring Wolbachia exhibit elevated rates of recombination across the 2nd and X chromosomes and this increase is proportional to their Wolbachia load. In contrast, another intracellular symbiont, Spiroplasma, does not lead to an increase in recombination across the intervals tested. Our results point to a specific effect of Wolbachia infection that may have a significant effect on infected insect populations.

scholarly journals The Intracellular Symbiont Wolbachia pipientis Enhances Recombination in a Dose-Dependent Manner

Insects ◽  
2020 ◽  
Vol 11 (5) ◽  
pp. 284
Author(s):  
Kaeli N. Bryant ◽  
Irene L. G. Newton
Keyword(s):  
Drosophila Melanogaster ◽  
Horizontal Transmission ◽  
Wolbachia Infection ◽  
Wolbachia Strain ◽  
Dependent Manner ◽  
Predator Prey ◽  
Wolbachia Pipientis ◽  
Intracellular Symbiont ◽  
Dose Dependent ◽  
Classical Genetics

Wolbachia pipientis is an intracellular alphaproteobacterium that infects 40%–60% of insect species and is well known for host reproductive manipulations. Although Wolbachia are primarily maternally transmitted, evidence of horizontal transmission can be found in incongruent host–symbiont phylogenies and recent acquisitions of the same Wolbachia strain by distantly related species. Parasitoids and predator–prey interactions may indeed facilitate the transfer of Wolbachia between insect lineages, but it is likely that Wolbachia are acquired via introgression in many cases. Many hypotheses exist to explain Wolbachia prevalence and penetrance, such as nutritional supplementation, protection from parasites, protection from viruses, or direct reproductive parasitism. Using classical genetics, we show that Wolbachia increase recombination in infected lineages across two genomic intervals. This increase in recombination is titer-dependent as the wMelPop variant, which infects at higher load in Drosophila melanogaster, increases recombination 5% more than the wMel variant. In addition, we also show that Spiroplasma poulsonii, another bacterial intracellular symbiont of D. melanogaster, does not induce an increase in recombination. Our results suggest that Wolbachia infection specifically alters its host’s recombination landscape in a dose-dependent manner.

The P-element-induced silencing effect of KP transposons is dose dependent in Drosophila melanogaster

Genome ◽  
2011 ◽  
Vol 54 (9) ◽  
pp. 752-762 ◽  
Author(s):  
Alireza Sameny ◽  
John Locke
Keyword(s):  
Drosophila Melanogaster ◽  
Critical Role ◽  
Mutagenic Effect ◽  
P Element ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
P Elements ◽  
Single Well ◽  
Dose Dependent

Transposable elements are found in the genomes of all eukaryotes and play a critical role in altering gene expression and genome organization. In Drosophila melanogaster, transposable P elements are responsible for the phenomenon of hybrid dysgenesis. KP elements, a deletion-derivative of the complete P element, can suppress this mutagenic effect. KP elements can also silence the expression of certain other P-element-mediated transgenes in a process called P-element-dependent silencing (PDS), which is thought to involve the recruitment of heterochromatin proteins. To explore the mechanism of this silencing, we have mobilized KP elements to create a series of strains that contain single, well-defined KP insertions that show PDS. To understand the quantitative role of KP elements in PDS, these single inserts were combined in a series of crosses to obtain genotypes with zero, one, or two KP elements, from which we could examine the effect of KP gene dose. The extent of PDS in these genotypes was shown to be dose dependent in a logarithmic rather than linear fashion. A logarithmic dose dependency is consistent with the KP products interacting with heterochromatic proteins in a concentration-dependent manner such that two molecules are needed to induce gene silencing.

Virgin Coconut (Cocos nucifera) Oil Attenuates Rotenone-Induced Toxicity in Fruit Flies (Drosophila melanogaster)

2021 ◽  
Vol 2 (1) ◽  
pp. 26-37
Author(s):  
O.O. Dosumu ◽  
◽  
E.N. Akang ◽  
O.K. Idowu ◽  
G.J. Adeyemi
Keyword(s):  
Drosophila Melanogaster ◽  
Cocos Nucifera ◽  
Coconut Oil ◽  
Redox Status ◽  
Fruit Flies ◽  
Dependent Manner ◽  
Toxicity Assay ◽  
Behavioural Test ◽  
Locomotor Deficits ◽  
Dose Dependent

Background: Parkinson's disease (PD) is a multifactorial neurodegenerative disease with pathogenic mechanisms traceable to oxidative damage and mitochondrial dysfunction. Rotenone, a chemical compound commonly found in pesticides, has been found to inhibit mitochondrial complex-I and initiate PD-like symptoms in mammals and several invertebrates. Virgin Coconut Oil (VCNO) obtained from the coconut fruit has been found to possess anti-oxidative and anti-inflammatory properties. Objectives: The present study evaluated the effect of VCNO on rotenone-induced Parkinsonism in fruit flies- Drosophila melanogaster (D. melanogaster). Methods: Canton special (CS) strains of D. melanogaster, aged between 1 to 3 days were orally exposed for 7 days to 0, 250, 500 and 750 μM rotenone diet for toxicity assay, and 0, 2.5, 5 and 10 % w/w VCNO diet for longevity assay. Thereafter, 5 % VCNO diet was selected for evaluation against 500 μM rotenone. Subsequently, behavioural test (negative geotaxis), markers for redox status and enzyme activities were evaluated. Results: The results showed that rotenone induced toxicity in the flies, while VCNO increased the lifespan of D. melanogaster in a dose-dependent manner. In addition, VCNO ameliorated rotenone-induced locomotor deficits, elevated MDA, as well as the depleted GSH levels. It also mitigated the inhibited activities of SOD, CAT and ATPase in the flies. Conclusions: VCNO protected D. melanogaster against rotenone-induced toxicity by extending longevity, preventing locomotor deficits and reducing oxidative stress.

scholarly journals Quercetin Suppresses Apoptosis and Attenuates Intervertebral Disc Degeneration via the SIRT1-Autophagy Pathway

2020 ◽  
Vol 8 ◽  
Author(s):  
Dong Wang ◽  
Xin He ◽  
Di Wang ◽  
Pandi Peng ◽  
Xiaolong Xu ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Protective Effect ◽  
Disc Degeneration ◽  
Intervertebral Disc Degeneration ◽  
Specific Effect ◽  
Therapeutic Effects ◽  
Dependent Manner ◽  
Autophagy Pathway ◽  
Dose Dependent

Intervertebral disc degeneration (IDD) has been generally accepted as the major cause of low back pain (LBP), which causes an enormous socioeconomic burden. Previous studies demonstrated that the apoptosis of nucleus pulposus (NP) cells and the dyshomeostasis of extracellular matrix (ECM) contributed to the pathogenesis of IDD, and effective therapies were still lacking. Quercetin, a natural flavonoid possessing a specific effect of autophagy stimulation and SIRT1 activation, showed some protective effect on a series of degenerative diseases. Based on previous studies, we hypothesized that quercetin might have therapeutic effects on IDD by inhibiting the apoptosis of NP cells and dyshomeostasis of ECM via the SIRT1-autophagy pathway. In this study, we revealed that quercetin treatment inhibited the apoptosis of NP cells and ECM degeneration induced by oxidative stress. We also found that quercetin promoted the expression of SIRT1 and autophagy in NP cells in a dose-dependent manner. Autophagy inhibitor 3-methyladenine (3-MA) reversed the protective effect of quercetin on apoptosis and ECM degeneration. Moreover, SIRT1 enzymatic activity inhibitor EX-527, suppressed quercetin-induced autophagy and the protective effect on NP cells, indicating that quercetin protected NP cells against apoptosis and prevented ECM degeneration via SIRT1-autophagy pathway. In vivo, quercetin was also demonstrated to alleviate the progression of IDD in rats. Taken together, our results suggest that quercetin prevents IDD by promoting SIRT1-dependent autophagy, indicating one novel and effective therapeutic method for IDD.

Interaction between perchlorate and nifedipine on insulin secretion from mouse pancreastic islets

1993 ◽  
Vol 13 (2) ◽  
pp. 107-117 ◽  
Author(s):  
Gerd Larsson-Nyrén ◽  
Janove Sehlin
Keyword(s):  
Insulin Secretion ◽  
Insulin Release ◽  
Specific Effect ◽  
Maximum Effect ◽  
Dependent Manner ◽  
Inhibitory Effects ◽  
Maximum Inhibition ◽  
Second Phases ◽  
Dose Dependent ◽  
Higher Sensitivity

In order to elucidate the mechanisms responsible for the stimulatory effect of perchlorate (ClO4−) on insulin secretion, we have investigated the interaction between this chaotropic anion and the organic calcium antagonist nifedipine. This drug, known as a blocker of L-type calcium channels, was chosen as a tool to test the idea that ClO4− acts on insulin secretion by stimulating the gating of voltage-controlled Ca2+ channels. ClO4− amplified the stimulatory effect of D-glucose on insulin release from perfused pancreas (first and second phases) as well as from isolated islets incubated in static incubations for 60 min. This indicates that ClO4− amplifies physiologically regulated insulin secretion. Nifedipine reduced D-glucose-induced (20 mM) insulin release in a dose-dependent manner with half-maximum effect at about 0.8 μM and apparent maximum effect at 5 μM nifedipine. In the presence of 20 mM D-glucose, the inhibitory effects of 0.5, 1 or 5 μM nifedipine were only slightly, if at all, counteracted by perchlorate. When 12 mM ClO4− and 20 mM D-glucose were combined, calculation of the specific effect of ClO4− revealed that nifedipine produced almost maximum inhibition already at 0.05 μM. Thus, the perchlorate-induced amplification of D-glucose-stimulated insulin release shows higher sensitivity to nifedipine than the D-glucose-effect as such. This supports the hypothesis that perchlorate primarily affects the voltage-sensitive L-type calcium channel in the β-cell.

scholarly journals Amaranth Leaf Extract Protects Against Hydrogen Peroxide Induced Oxidative Stress in Drosophila Melanogaster

2021 ◽  
Author(s):  
Johnmark Ndinawe ◽  
Hellen W. Kinyi
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Antioxidant Activity ◽  
Ascorbic Acid ◽  
Drosophila Melanogaster ◽  
Leaf Extract ◽  
Dependent Manner ◽  
Polyphenol Compounds ◽  
Dose Dependent

Abstract ObjectiveAmaranths leaves are rich in ascorbic acid and polyphenol compounds which have antioxidant activity. The aim of this study was to evaluate their in vivo antioxidant activity. The effect of consumption of Amaranth leaf extract on in vivo antioxidant activity, catalase enzyme activity and H2O2 induced oxidative stress in Drosophila melanogaster flies was assessed.ResultsConsumption of Amaranth leaf extract was associated with increased survival on exposure to H202 in a dose dependent manner in Drosophila melanogaster flies.

scholarly journals Evidence for a lipid specific effect in nutrient induced human proximal gastric relaxation

Gut ◽  
1998 ◽  
Vol 43 (2) ◽  
pp. 248-251 ◽  
Author(s):  
J T McLaughlin ◽  
L E A Troncon ◽  
J Barlow ◽  
L J Heggie ◽  
D G Thompson
Keyword(s):  
Motor Performance ◽  
Energy Content ◽  
Specific Effect ◽  
Dependent Manner ◽  
Specific Mechanism ◽  
Proximal Stomach ◽  
Gastric Tone ◽  
Before And After ◽  
Gastrointestinal Motor ◽  
Dose Dependent

Background/Aim—The presence of lipid in the upper gut is able to modify gastrointestinal motor performance, but its influence on the relaxation of the human stomach, which is known to modify gastric emptying, remains incompletely understood. The relaxation of the proximal stomach in response to various lipid concentrations was therefore studied in healthy volunteers. Since the observed effects could be mediated through osmolality or energy sensitive pathways, the effects of equicaloric and equiosmolar non-lipid solutions were also determined.Methods—The tone of the proximal stomach was measured during stepwise inflation of a non-compliant bag sited in the proximal stomach, both before and after a test meal was delivered intragastrically. Iso-osmolar lipid emulsions were diluted in iso-osmolar saline at concentrations of 1.25, 2.5, 5, 10, and 20%. NaCl solutions at osmolalities of 300, 600, 1200 and 2400 mmol/kg and glucose solutions of 836 and 3344 kJ/l were also given.Results—All lipid meals of 2.5% or greater concentration induced a reduction in gastric tone in a non-dose-dependent manner, responses to 5% lipid (median (range) 74 (62–92)%) being similar to those to 20% lipid (80 (55–83)%; p>0.05). No relaxation was elicited by isocaloric glucose. NaCl only consistently caused relaxation at 2400 mmol/kg.Conclusion—Lipid meals reduce human proximal gastric tone by a lipid specific mechanism, independently of their energy content or osmolality.

The GLP-1 agonist exendin-4 reduces food intake in nonhuman primates through changes in meal size

2007 ◽  
Vol 293 (3) ◽  
pp. R983-R987 ◽  
Author(s):  
Karen A. Scott ◽  
Timothy H. Moran
Keyword(s):  
Food Intake ◽  
Rhesus Macaques ◽  
Specific Effect ◽  
Meal Size ◽  
Reduce Food Intake ◽  
Dependent Manner ◽  
Primate Model ◽  
Glucagon Like Peptide 1 ◽  
Long Acting ◽  
Dose Dependent

Exendin-4 (Ex4), a long-acting glucagon-like peptide-1 (GLP-1) receptor agonist, has been shown to reduce food intake and suppress gastric emptying in rodents and humans. In this study we investigated the effects of peripheral administration of Ex4 on food intake and meal patterns in adult male rhesus macaques. Rhesus macaques ( n = 4) that had been trained to lever press for food pellets were injected intramuscularly 15 min before the start of their 6-h daily feeding period. Ex4 was given at doses of 0.10, 0.32, 0.56, 1.0, and 3.0 μg/kg. Ex4 suppressed food intake in a dose-dependent manner, with the 3.0 μg/kg dose completely preventing feeding during the 6-h period and the 0.10 μg/kg dose suppressing intake by 17%. Doses of 0.32, 0.56, 1.0, and 3.0 μg/kg caused significant reductions in cumulative intake at all six hourly time points. Ex4 inhibited food intake through a specific effect on meal size. Meal size was significantly reduced in a dose-dependent manner with significant reductions at the 0.32 and 1.0 μg/kg doses ( P < 0.05). Day 2 and 3intakes returned to baseline levels with no compensation for Ex4-induced feeding suppression. Administration of doses of 0.32 and 0.56 μg/kg Ex4 over 5 consecutive days led to sustained reductions in intake with no evidence of compensation. Again, these reductions were due to specific effects on meal size. These results demonstrate that activation of GLP-1 pathways has potent effects on the controls of meal size and overall food intake in a nonhuman primate model.

Effect of the Suppressor of Underreplication (SuUR) Gene on Position-Effect Variegation Silencing in Drosophila melanogaster

Genetics ◽  
2003 ◽  
Vol 165 (3) ◽  
pp. 1209-1220
Author(s):  
E S Belyaeva ◽  
L V Boldyreva ◽  
E I Volkova ◽  
R A Nanayev ◽  
A A Alekseyenko ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Position Effect ◽  
Polytene Chromosomes ◽  
Morphological Characters ◽  
Position Effect Variegation ◽  
Dependent Manner ◽  
Dose Dependent ◽  
Suur Protein ◽  
Chromosome Regions ◽  
Suur Gene

Abstract It has been previously shown that the SuUR gene encodes a protein located in intercalary and pericentromeric heterochromatin in Drosophila melanogaster polytene chromosomes. The SuUR mutation suppresses the formation of ectopic contacts and DNA underreplication in polytene chromosomes; SuUR+ in extra doses enhances the expression of these characters. This study demonstrates that heterochromatin-dependent PEV silencing is also influenced by SuUR. The SuUR protein localizes to chromosome regions compacted as a result of PEV; the SuUR mutation suppresses DNA underreplication arising in regions of polytene chromosomes undergoing PEV. The SuUR mutation also suppresses variegation of both adult morphological characters and chromatin compaction observed in rearranged chromosomes. In contrast, SuUR+ in extra doses and its overexpression enhance variegation. Thus, SuUR affects PEV silencing in a dose-dependent manner. However, its effect is expressed weaker than that of the strong modifier Su(var)2-5.

scholarly journals Porphyromonas gingivalisVirulence in aDrosophila melanogasterModel

2010 ◽  
Vol 79 (1) ◽  
pp. 439-448 ◽  
Author(s):  
Christina O. Igboin ◽  
Melvin L. Moeschberger ◽  
Ann L. Griffen ◽  
Eugene J. Leys
Keyword(s):  
Drosophila Melanogaster ◽  
Porphyromonas Gingivalis ◽  
Systemic Infection ◽  
Epidemiologic Studies ◽  
Dependent Manner ◽  
New Model ◽  
Host Interactions ◽  
Infection Models ◽  
Mammalian Infection ◽  
Dose Dependent

ABSTRACTPorphyromonas gingivalishas been implicated in the etiology of adult periodontitis. In this study, we examined the viability ofDrosophila melanogasteras a new model for examiningP. gingivalis-host interactions.P. gingivalis(W83) infection ofDrosophilaresulted in a systemic infection that killed in a dose-dependent manner. Differences in the virulence of several clinically prevalentP. gingivalisstrains were observed in theDrosophilakilling model, and the results correlated well with studies in mammalian infection models and human epidemiologic studies.P. gingivalispathobiology inDrosophiladid not result from uncontrolled growth of the bacterium in theDrosophilahemolymph (blood) or overt damage toDrosophilatissues.P. gingivaliskilling ofDrosophilawas multifactorial, involving several bacterial factors that are also involved in virulence in mammals. The results from this study suggest that many aspects ofP. gingivalispathogenesis in mammals are conserved inDrosophila, and thus theDrosophilakilling model should be useful for characterizingP. gingivalis-host interactions and, potentially, polymicrobe-host interactions.

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