Effect of allatectomy on fat body lipid metabolism of the male desert locust during adult development

1971 ◽  
Vol 17 (5) ◽  
pp. 813-821 ◽  
Author(s):  
P.R. Walker ◽  
E. Bailey
Keyword(s):  
Lipid Metabolism ◽  
Adult Development ◽  
Fat Body ◽  
Desert Locust ◽  
Body Lipid

scholarly journals MicroRNA-277 targetsinsulin-like peptides 7and8to control lipid metabolism and reproduction inAedes aegyptimosquitoes

2017 ◽  
Vol 114 (38) ◽  
pp. E8017-E8024 ◽  
Author(s):  
Lin Ling ◽  
Vladimir A. Kokoza ◽  
Changyu Zhang ◽  
Emre Aksoy ◽  
Alexander S. Raikhel
Keyword(s):  
Lipid Metabolism ◽  
Molecular Mechanisms ◽  
Fat Body ◽  
Critical Role ◽  
Target Prediction ◽  
Luciferase Reporter ◽  
Ovary Development ◽  
Mrna Levels ◽  
Essential Components ◽  
Energy Store

Hematophagous female mosquitoes transmit numerous devastating human diseases, including malaria, dengue fever, Zika virus, and others. Because of their obligatory requirement of a vertebrate blood meal for reproduction, these mosquitoes need a lot of energy; therefore, understanding the molecular mechanisms linking metabolism and reproduction is of particular importance. Lipids are the major energy store providing the fuel required for host seeking and reproduction. They are essential components of the fat body, a metabolic tissue that is the insect analog of vertebrate liver and adipose tissue. In this study, we found that microRNA-277 (miR-277) plays an important role in regulating mosquito lipid metabolism. The genetic disruption of miR-277 using the CRISPR-Cas9 system led to failures in both lipid storage and ovary development. miR-277 mimic injection partially rescued these phenotypic manifestations. Examination of subcellular localization of FOXO protein via CRISPR-assisted, single-stranded oligodeoxynucleotide-mediated homology-directed repair revealed that insulin signaling is up-regulated in response to miR-277 depletion. In silico target prediction identified that insulin-like peptides 7 and 8 (ilp7andilp8) are putative targets of miR-277; RNA immunoprecipitation and a luciferase reporter assay confirmed thatilp7andilp8are direct targets of this miRNA. CRISPR-Cas9 depletion ofilp7andilp8led to metabolic and reproductive defects. These depletions identified differential actions of ILP7 and ILP8 in lipid homeostasis and ovarian development. Thus, miR-277 plays a critical role in mosquito lipid metabolism and reproduction by targetingilp7andilp8, and serves as a monitor to control ILP7 and ILP8 mRNA levels.

scholarly journals The mechanism of C-20 hydroxylation of α-ecdysone in the desert locust, Schistocerca gregaria

1977 ◽  
Vol 168 (3) ◽  
pp. 513-520 ◽  
Author(s):  
P Johnson ◽  
H H Rees
Keyword(s):  
Schistocerca Gregaria ◽  
Fat Body ◽  
Difference Spectrum ◽  
Maximum Activity ◽  
Malpighian Tubules ◽  
Desert Locust ◽  
Ph Optimum ◽  
Developmental Variation ◽  
Moulting Hormone ◽  
Cytochrome P 450

1. The C-20 hydroxylation of alpha-ecdysone to produce beta-ecdysone was investigated in the desert locust, Schistocerca gregaria. 2. alpha-Ecdysone C-20 hydroxylase activity was located primarily in the fat-body and Malpighian tubules. The properties of the hydroxylation system from Malpighian tubules investigated further. 3. The enzyme system was mitochondrial, had a pH optimum of 6.5, an apparent Km of 12.5 micron and required O2 and NADPH. 4. The activity of the hydroxylation system showed developmental variation within the fifth instar, the maximum activity corresponding to the maximum tire of endogenous moulting hormone. The significance of these results is assessed in relation to the control of the endogenous titre of beta-ecdysone. 5. The mechanism of the hydroxylation system was investigated by using known inhibitors of hydroxylation reactions such as CO, metyrapone and cyanide. 6. The CO difference spectrum of the reduced mitochondrial preparation indicated the presence of cytochrome P-450 in the preparation. 7. It concluded that the alpha-ecdysone C-20 hydroxylase system is a cytochrome P-450-deendent mono-oxygenase.

Some effects of the nematode Mermis nigrescens upon carbohydrate metabolism in the fat body of its host, the desert locust Schistocerca gregaria

1971 ◽  
Vol 49 (4) ◽  
pp. 431-434 ◽  
Author(s):  
Roger Gordon ◽  
John M. Webster ◽  
David E. Mead
Keyword(s):  
Carbohydrate Metabolism ◽  
Glycogen Phosphorylase ◽  
Schistocerca Gregaria ◽  
Fat Body ◽  
Constant Level ◽  
Desert Locust ◽  
Carbohydrate Levels ◽  
Fat Bodies

Adult desert locusts were experimentally infected with 50 Mermis nigrescens ova and changes in the fat body carbohydrate levels and glycogen phosphorylase activities recorded. At both 2 and 3 weeks after infection, the parasitism caused a significant reduction in the level of glycogen and non-glycogen carbohydrates in the host fat body, together with a progressive depletion of active and inactive glycogen phosphorylases. By feeding extensively upon the blood carbohydrates of the host, the developing nematode deprives the fat body of carbohydrates and thereby effects a reduction in glycogenesis by the host fat body. Increased catabolism (and (or) decreased anabolism) of the fat body phosphorylases, together with a possible suppression of the host "hyperglycaemic factor" by the nematode, prevent further glycogenolysis by the fat bodies of mermithid-infected locusts and allow a low, constant level of fat body glycogen to be maintained in these insects.

scholarly journals Snazarus and its human ortholog SNX25 modulate autophagic flux

2021 ◽  
Author(s):  
Annie Lauzier ◽  
Marie-France Bossanyi ◽  
Raphaëlle Larcher ◽  
Sonya Nassari ◽  
Rupali Ugrankar ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Fat Body ◽  
Cellular Mechanism ◽  
Vesicular Trafficking ◽  
Autophagic Flux ◽  
Large Array ◽  
Sorting Nexin ◽  
Human Ortholog ◽  
Differential Isoform Expression

Macroautophagy, the degradation and recycling of cytosolic components in the lysosome, is an important cellular mechanism. It is a membrane-mediated process that is linked to vesicular trafficking events. The sorting nexin (SNX) protein family controls the sorting of a large array of cargoes, and various SNXs impact autophagy. To improve our understanding of their functions in vivo, we screened all Drosophila SNXs using inducible RNA interference in the fat body. Significantly, depletion of snazarus (snz) led to decreased autophagic flux. Interestingly, we observed altered distribution of Vamp7-positive vesicles with snz depletion, and snz's roles were conserved in human cells. SNX25, the closest human ortholog to snz, regulates both VAMP8 endocytosis and lipid metabolism. Through knockout-rescue experiments, we demonstrate that these activities are dependent on specific SNX25 domains and that the autophagic defects upon SNX25 loss can be rescued by ethanolamine addition. We also demonstrate the presence of differentially spliced forms of SNX14 and SNX25 in cancer cells. This work identifies a conserved role for snz/SNX25 as regulators of autophagic flux and reveals differential isoform expression between paralogs.

scholarly journals Examination of Interaction between the SR Proteins 9G8 and Repressor Splicing Factor 1 in the Alternative Splicing of Carnitine Palmitoyltransferase I in lipid Metabolism

2019 ◽  
Vol 1 (2) ◽  
Keyword(s):  
Lipid Metabolism ◽  
Alternative Splicing ◽  
Fat Body ◽  
Search Algorithm ◽  
Carnitine Palmitoyltransferase ◽  
Starvation Resistance ◽  
Beta Oxidation ◽  
Sr Protein ◽  
Carnitine Palmitoyltransferase I ◽  
Cooperative Relationship

The method of gene regulation underlying lipid metabolism related to obesity is poorly understood, yet alternative splicing (AS) appears to be an important mechanism for proper lipid storage. CPT1 (carnitine palmitoyltransferase I) is a beta-oxidation enzyme required for the breakdown of fatty acids. The gene coding for CPT1 is alternatively spliced to produce two different products that vary in their activity. When the splicing SR protein 9G8 is knocked down in the fat body of Drosophila, the CPT1 splicing pattern is altered. A linear search algorithm was developed that parsed through FASTA files of the CPT1 gene region and sought out sequences that matched known binding sequences of 9G8. We expected a result in exon 6A that would signal its inclusion but unexpectedly found a match in exon 5 of the CPT1 transcript. We theorized that 9G8 and the SR protein competitor RSF1, interact with one another for binding sites on the CPT1 gene to result in different isoforms. Additionally, TG data indicated that 9G8 and RSF1 KD flies displayed statistically significant higher TG levels than their control suggesting a potential cooperative relationship. We next performed a starvation resistance experiment and found that 9G8 and RSF1 KD flies phenocopied starvation resistance suggesting that both proteins interact to result in the same CPT1 product. We are using qPCR to determine if there is a difference in the AS of CPT1 among flies with decreased expression of 9G8, the SR protein antagonist RSF1 and the SR protein shuttle TRN-SR.

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