作者: Laura Wedd , Regan Ashby , Sylvain Foret , Ryszard Maleszka
DOI: 10.7717/PEERJ.3109
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摘要: BACKGROUND Deficiencies in lysosomal a-mannosidase (LAM) activity animals, caused either by mutations or consuming toxic alkaloids, lead to severe phenotypic and behavioural consequences. Yet, epialleles adversely affecting LAM expression exist the honey bee population suggesting that they might be beneficial certain contexts cannot eliminated natural selection. METHODS We have used a combination of enzymology, molecular biology metabolomics characterise catalytic properties (AmLAM) then an indolizidine alkaloid swainsonine inhibit its vitro vivo. RESULTS show AmLAM is inhibited albeit at slightly higher concentrations than other animals. Dietary exposure growing larvae leads pronounced metabolic changes not only saccharides, but also amino acids, polyols polyamines. Interestingly, abundance two fatty acids implicated epigenetic regulation significantly reduced treated individuals. Additionally, swainsonie causes loco-like symptoms, increased mortality subtle decrease rate larval growth resulting subsequent developmental delay pupal metamorphosis. DISCUSSION consider our findings context cellular function, development, environmental toxicity colony-level impacts. The observed heterochrony swainsonine-treated with lower offer plausible explanation for existence impaired expression. Individuals carrying such provide additional level diversity could functioning colony whereby more flexibility timing adult emergence useful task allocation.