Targeted mutagenesis and functional analysis of adipokinetic hormone-encoding gene in Drosophila
Language English Country England, Great Britain Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
25641265
DOI
10.1016/j.ibmb.2015.01.011
PII: S0965-1748(15)00018-1
Knihovny.cz E-resources
- Keywords
- Carbohydrate metabolism, Drome-Akh, NHEJ, Neuropeptide, Stress, Trehalose,
- MeSH
- Drosophila melanogaster genetics metabolism MeSH
- Energy Metabolism MeSH
- Hemolymph chemistry MeSH
- Insect Hormones genetics metabolism MeSH
- Homeostasis MeSH
- Pyrrolidonecarboxylic Acid analogs & derivatives metabolism MeSH
- Molecular Sequence Data MeSH
- Mutagenesis MeSH
- Oligopeptides genetics metabolism MeSH
- Food Deprivation MeSH
- Amino Acid Sequence MeSH
- Base Sequence MeSH
- Body Weight MeSH
- Trehalose metabolism MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- adipokinetic hormone MeSH Browser
- Insect Hormones MeSH
- Pyrrolidonecarboxylic Acid MeSH
- Oligopeptides MeSH
- Trehalose MeSH
Adipokinetic hormones (Akhs) are small peptides (8-10 amino acid [aa] residues long) found in insects that regulate metabolic responses to stress by stimulating catabolic reactions and mobilizing energy stores. We employed Transcription activator-like effector nuclease (TALEN) mutagenesis and isolated an Akh(1) mutant carrying a small deletion in the gene that resulted in a truncated peptide; the second aa (Leu) was missing from the functional octapeptide. This null Dmel/Akh mutant is suitable to study Akh function without any effect on the C-terminal associated peptide encoded by the same gene. The mutant flies were fully viable and compared to the control flies, had significantly low levels of hemolymph saccharides including trehalose and were resistant to starvation. These characteristics are similar to those obtained from the flies carrying targeted ablation of Akh-expressing neurons (reported earlier). We also found that the Akh(1) mutants are slightly heavy and had a slow metabolic rate. Furthermore, we showed that the ectopic expression of Dmel∖Akh reverses the Akh(1) phenotype and restores the wild-type characteristics. Our results confirmed that Akh is an important regulator of metabolic homeostasis in Drosophila.
References provided by Crossref.org
Functional Analysis of Adipokinetic Hormone Signaling in Bombyx mori
Hormonal Regulation of Response to Oxidative Stress in Insects-An Update
