Data from: Causal link between insulin-like growth factor 1 and growth in nestlings of a wild passerine bird
Cite this dataset
Lodjak, Jaanis; Mägi, Marko; Sild, Elin; Mänd, Raivo (2017). Data from: Causal link between insulin-like growth factor 1 and growth in nestlings of a wild passerine bird [Dataset]. Dryad. https://doi.org/10.5061/dryad.rd01s
Life history of animals is strongly linked with the variability in postnatal growth rates, because the ability to achieve necessary body mass early in life is directly connected with the ability to survive and reproduce later in life. Surprisingly, little is known about the physiological mechanisms connecting food availability with the variability of growth in wild animals. We used a hormonal injection treatment in free-living nestlings of the pied flycatcher (Ficedula hypoleuca). In doing this, we aimed to see how their plasma insulin-like growth factor 1 (IGF-1) levels and its mediation of growth rate vary in response to administration of exogenous IGF-1 during the early period of postnatal development. We showed that the levels of IGF-1 as well as growth rate and body size, in terms of body mass and tarsus length, were significantly higher in IGF-1-injected nestlings, compared with those in the control group. These differences became especially pronounced from day 7 post-hatch onwards during the 13-day nestling period. Additionally, the proportional investment into growth was more profoundly downregulated in IGF-1-injected nestlings at the end of the nestling period, which achieved fledging size earlier, compared with control nestlings. Our results are the first to highlight IGF-1 as the causal link between growth conditions and variability of growth rate and body size in wild vertebrates. Interestingly, the change in IGF-1 levels also showed a plausible, distinct adaptive age- and physical maturity-dependent pattern in nestlings to match the benefits gained by them when investing in growth, with the cost endured during the early days of postnatal development to maximize their fitness. Therefore, this mechanism might be among those mediating the maintenance of genetic variability in growth rates in populations, presumably regardless of the presence of strong directional selection acting upon them.