Targeted mutagenesis and functional analysis of adipokinetic hormone-encoding gene in Drosophila
Jazyk angličtina Země Anglie, Velká Británie Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
25641265
DOI
10.1016/j.ibmb.2015.01.011
PII: S0965-1748(15)00018-1
Knihovny.cz E-zdroje
- Klíčová slova
- Carbohydrate metabolism, Drome-Akh, NHEJ, Neuropeptide, Stress, Trehalose,
- MeSH
- Drosophila melanogaster genetika metabolismus MeSH
- energetický metabolismus MeSH
- hemolymfa chemie MeSH
- hmyzí hormony genetika metabolismus MeSH
- homeostáza MeSH
- kyselina pyrrolidonkarboxylová analogy a deriváty metabolismus MeSH
- molekulární sekvence - údaje MeSH
- mutageneze MeSH
- oligopeptidy genetika metabolismus MeSH
- potravinová deprivace MeSH
- sekvence aminokyselin MeSH
- sekvence nukleotidů MeSH
- tělesná hmotnost MeSH
- trehalosa metabolismus MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- adipokinetic hormone MeSH Prohlížeč
- hmyzí hormony MeSH
- kyselina pyrrolidonkarboxylová MeSH
- oligopeptidy MeSH
- trehalosa 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.
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