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Jimeno, B.

Publications and source records attributed to Jimeno, B..

4 recordsLinked to original sources

Long-term effects of early-life adversity on DNA methylation in zebra finches

Early-life experiences can have profound and long-lasting effects on adult phenotype and thereby Darwinian fitness, though the mechanisms driving these effects remain poorly understood. Epigenetic alterations, especially DNA methylation which affects gene expression, potentially mediate developmental condition effects on adult phenotype. We tested for such effects using captive zebra finches that were reared in either small or large broods, a manipulation that is known to have pleiotropic phenotypic effects. Analyzing whole genome DNA methylation patterns in erythrocytes from 50 individuals sampled in adulthood, we found 0.8% of all CpG sites after filtering to be differentially methylated after correction for multiple testing. We identified 149 non-transiently differentially methylated sites (DMSs) where the DNA methylation difference between treatments was larger than 25%. These DMSs were located in 19 autosomal chromosomes, in or near genes involved in critical biological processes such as cell growth, division, and differentiation, regulation of immune response, muscle contraction, and neuronal signaling. These findings suggest that epigenetic modifications such as DNA methylation potentially mediate long-term effects of early-life adversity via differential gene expression, but follow-up studies are needed to identify the extent to which the observed DMSs are functionally related to the previously observed phenotypic effects.

ecology↗

Epigenetic potential and dispersal propensity in a free-living songbird: a spatial and temporal approach

Natal dispersal is a key life-history trait determining fitness and driving population dynamics, genetic structure and species distributions. Despite existing evidence that not all phenotypes are equally likely to successfully establish in new areas, the mechanistic underpinnings of natal dispersal remain poorly understood. The propensity to disperse into a new environment can be favored by a high degree of phenotypic plasticity which facilitates local adaptation and may be achieved via epigenetic mechanisms, which modify gene expression and enable rapid phenotypic changes. Epigenetic processes occur in particular genomic regions - DNA methylation on CpG sites in vertebrates -, and thus individual genomes may differ in their capacity to be modified epigenetically. This "Epigenetic potential" (EP) may represent the range of phenotypic plasticity attainable by an individual, and be a key determinant of successful settlement in novel areas. We investigated the association between EP - quantified as the number of genome-wide CpG variants - and natal dispersal propensity in a long-term study population of Pied flycatchers (Ficedula hypoleuca) monitored since colonization of a new habitat 35 years ago. We tested this association at three levels, comparing EP between: i) individuals dispersing between and within habitat patches; ii) immigrants to the population and locally-born individuals; and iii) individuals from first (comprising colonizers or their direct descendants) and later generations of the population (consisting of locally-born individuals, which did not show natal dispersal). Results show a significant, positive association between EP and dispersal propensity in comparisons i) and iii), but not ii). Furthermore, CpG variants were non-randomly distributed across the genome, suggesting species- and/or population-specific CpGs being more frequent in promoters and exons. Our findings point to EP playing a role in dispersal propensity at spatial and temporal scales, supporting the idea that epigenetically-driven phenotypic plasticity facilitates dispersal and environmental coping in free-living birds.

ecology↗

Do glucocorticoids indicate stress? Meta-analysis reveals a tight association between glucocorticoids and metabolic rate

Glucocorticoid (GC) variation has long been thought to reflect variation in organismal stress, but associations between GCs and Darwinian fitness components are diverse in magnitude, direction, and highly context-dependent. This paradox reveals our poor understanding of the causes of GC variation, contrasting with the detailed knowledge of the functional consequences of GC variation. Amongst an array of effects in many physiological systems, GCs orchestrate energy availability to anticipate and recover from predictable and unpredictable environmental fluctuations and challenges. Although this is mechanistically well-known, the extent to which GC levels are quantitatively explained by energy metabolism is unresolved. We investigated this association through meta-analysis, selecting studies of endotherms in which (1) an experiment was performed that affected metabolic rate and (2) metabolic rate and GC-levels were measured simultaneously. We found that an increase in metabolic rate was associated with an increase in GC levels in 20 out of 21 studies (32 out of 35 effect sizes). More importantly, there was a strong positive correlation between the increases in metabolic rate and GCs (p=0.003). This pattern was similar in birds and mammals, and independent of the nature of the experimental treatment. We conclude that metabolic rate is a major driver of GC variation within individuals. Stressors often affect metabolic rate, leading us to question whether GC levels provide information on stress beyond the stressors effect on metabolic rate.

ecology↗

Body mass aging trajectory is modulated by environmental conditions but independent of lifespan

How lifespan associates with aging trajectories of health and disease is an urgent question in societies with increasing lifespan. Body mass declines with age are associated with decreased organismal functioning in many species. We tested whether two factors that decreased lifespan in zebra finches, sex and manipulated environmental quality, accelerated the onset and/or rate of within-individual body mass declines. We subjected 597 birds for nine years to experimentally manipulated foraging costs (harsh = H, benign = B) during development and in adulthood in a 2x2 design. This yielded four treatment combinations (HH, HB, BH, BB). Harsh environments during development and in adulthood decreased average body mass additively. In males, the aging trajectory was quadratic, with a maximum between 3.5 and 4 years, and independent of the environment (HH=HB=BH=BB). In females, the shape of the aging trajectory differed between environments: a quadratic trajectory as in males in the benign adult environment (HB=BB), a linear decline when benign development was followed by harsh adulthood (BH) and a linear increase when in a lifelong harsh environment (HH). We found no evidence for an association between lifespan and body mass aging trajectories either between or within experimental groups. However, females lived shorter than males, and their body mass decline started earlier for most treatment combinations. Thus, we conclude that foraging conditions can affect the shape of body mass aging trajectories, but these are independent of lifespan.

ecology↗