INTRODUCTION
Individual variation in fitness is usually large, and at least part of
that variation is caused by variation in phenotypic quality, as
evidenced by positive associations between reproductive success and
parental survival . The early-life environment has been suggested to
play a major role in shaping variation in phenotypic quality . Studies
of the link between early-life conditions and fitness prospects either
measure fitness components directly, by following individuals for a
significant part of their lives, or use markers of morphological,
physiological and/or molecular state as fitness proxy. Unfortunately,
fitness prospects can be difficult to infer using such proxies, because
responses to environmental perturbations typically differ between
markers . In this context, the length and dynamics of telomeres,
complexes of proteins and repetitive DNA at the end of eukaryotic
chromosomes , have emerged as relatively robust markers of past
experiences. Telomere length and dynamics have been shown to be
susceptible to early-life environmental conditions , and longer
telomeres and/or lower rates of telomere shortening predict longevity
and/or other fitness components in humans and model and non-model
organisms .
Variation in telomere length is already present early in life in humans
and non-model organisms . While the variation present at birth is mostly
maintained throughout adulthood , variation in telomere shortening in
early life is associated with morbidity and mortality . However,
developing individuals live in complex environments, and despite a
recent surge in research effort , little is known about the overall
effects of early-life conditions on telomere length (reviewed in . In
particular the outcome of the interplay between multiple stressors
during growth and their effect on telomere dynamics is poorly
understood. The combined effect of stressors on telomere shortening may
be additive, whereby the combined result is the sum of the effect of
each stressor separately, or synergistic, when multiple stressors
interact to produce an effect that is greater than the sum of the
individual effects in isolation. Understanding whether the combined
effect of multiple stressors is additive or synergistic is of
importance, because developing animals will only rarely grow up in
conditions that are optimal in every way; it is more likely that some of
the many environmental aspects that affect development are at a
sub-optimal level, and as such can be considered a stressor.
To address the question whether effects of different stressors are
additive or synergistic we examined how/whether two extrinsic stressors,
manipulated brood size and parasitic infections, interact to affect
growth and telomere shortening of nestling jackdaws Corvusmonedula . A stressful social environment (increased sibling
competition) has proven to negatively affect growth and telomere
dynamics in this and other bird populations . The effects of parasitic
infections on telomere shortening are increasingly attracting attention,
with some studies finding that parasitized individuals had shorter
telomeres or higher rates of telomere loss , while other studies did not
find a clear relationship between parasitic infections and telomere
dynamics (; ; ; . Nestling jackdaws in our population are frequently
parasitized by the carnid fly Carnus hemapterus , a
blood-sucking ectoparasite that is commonly found infecting nestlings
from various medium to big size bird species (i.e. starlings,
bee-eaters, tawny owls, raptors . Gravid females lay their eggs within
the bird’s nest material on which the larvae then feed. The imago
emerges the next year around the time the birds’ eggs hatch and
parasitize nestlings through a large part of the development period .
Due to the end replication problem during cell division and/or loss of
the single strand overhang , telomeres shorten in length as cell
division progresses. Thus, because Carnus hemapterus feeds on
blood, the parasite could increase red blood cell replacement rate,
thereby directly affecting telomere dynamics, or indirectly affect
telomere dynamics by triggering related physiological processes (i.e.
oxidative stress). Nevertheless, we anticipated that parasites would
accelerate telomere shortening in their hosts, as reported for great tit
nestlings reared in nests experimentally infested with hematophagous hen
fleas . Summarizing, we expect parasitized nestlings and nestlings
reared in enlarged brood to show reduced growth and faster rates of
telomere shortening, and we tested whether these effects were additive
or synergistic.