Biology subjects

Monaghan, P.

Publications and source records attributed to Monaghan, P..

7 recordsLinked to original sources

bioRxiv2026

Increased stress in early life epigenetically rewires pathways related to aging and longevity

Environmental conditions experienced early in life have profound consequences for vertebrate health, yet the molecular pathways linking developmental stress to aging and reduced lifespan remain poorly understood. Through a novel highly accurate epigenetic clock, developed from RRBS-based blood DNA methylation profiles, we show that experimental lifespan-reducing early-life stress rapidly accelerates epigenetic age in zebra finch chicks (Taeniopygia guttata). Corticosterone-treated 29-day-old chicks share differentially methylated loci with non-treated aged birds and cluster with 6-month-old birds. The transcriptional repressor ZBTB16 emerges as an epigenetically top age-correlated gene and is strongest affected by corticosterone. Elevated developmental corticosterone causes rapid epigenetic remodelling of metabolic pathways well-established in aging and longevity. Our results demonstrate epigenetic rewiring of the aging trajectory through conserved stress-survival mechanisms immediately following elevated early-life stress exposure.

developmental biology↗

bioRxiv2025

Seasonal decline in mitochondrial plasticity in the three-spined stickleback

Mitochondrial plasticity enables ectothermic animals to maintain performance under changing thermal conditions, but whether this ability declines through adulthood is unknown. We explored changes in mitochondrial plasticity in the three-spined stickleback (Gasterosteus aculeatus), a temperate fish that in many populations has a single breeding season over which it produces multiple clutches and then dies. Wild-caught fish were exposed to one of three thermal regimes: remaining at 12 {degrees}C, switching to constant warm (21 {degrees}C) or diel cycling (12-21 {degrees}C) for three weeks at either the beginning or end of the season. We quantified both phosphorylating and non-ATP-producing (OXPHOS and LEAK) respiration in isolated muscle mitochondria, and oxidative control efficiency (OxCE). Early in the breeding season, young fish responded to elevated temperatures by adjusting both their capacity for ATP production and non-ATP-production respiration, but this mitochondrial plasticity declined over the season. OxCE was unaffected by time of season or temperature treatment. Changing body condition was unrelated to mitochondrial function. Our findings indicate that mitochondrial plasticity declines across adult life, potentially limiting thermal resilience in older individuals, the first time this has been reported in an ectotherm. This highlights the need to account for age-related physiological changes in capacity when predicting species responses to environmental change.

evolutionary biology↗

bioRxiv2023

The impact of chemical pollution across major life transitions: a meta-analysis on oxidative stress in amphibians

Among human actions threatening biodiversity, the release of anthropogenic chemical pollutants -which have become ubiquitous in the environment- is a major concern. Chemical pollution can induce oxidative stress and damage by causing the overproduction of reactive oxygen species (ROS), and affecting the antioxidant system. In species undergoing metamorphosis ([~]80% of all extant animal species), antioxidant responses to chemical pollution may differ between pre- and post-metamorphic stages. Here, we meta-analysed (N = 86 studies, k = 2,012 estimates) the impact of chemical pollution on the redox balance across the three major amphibian life stages (embryo, larva, adult). Before metamorphosis, embryos and larvae activate their antioxidant pathways and do not show increased oxidative damage. In contrast, post-metamorphic individuals show unnoticeable antioxidant responses, and a marked oxidative damage in lipids. Also, type of pollutant (i.e., organic vs inorganic) promotes contrasting effects across amphibian life stages. Our findings show a divergent evolution of the redox balance in response to pollutants across life transitions of metamorphosing amphibians, likely linked to the characteristics of each life stage. Further comparative mechanistic approaches to wildlife responses to global changes will improve our understanding of these eco-evo-devo processes.

evolutionary biology↗

bioRxiv2021

Experimental demonstration of prenatal programming of mitochondrial aerobic metabolism lasting until adulthood

It is increasingly being postulated that among-individual variation in mitochondrial function underlies variation in individual performance (e.g. growth rate) and state of health. It has been suggested (but not adequately tested) that environmental conditions experienced before birth have been suggested to programme postnatal mitochondrial function, with persistent effects potentially lasting into adulthood. We tested this hypothesis in an avian model by experimentally manipulating prenatal conditions (incubation temperature and stability), then measuring mitochondrial aerobic metabolism in blood cells from the same individuals during the middle of the growth period and at adulthood. Mitochondrial aerobic metabolism changed markedly across life stages, and part of these age-related changes were influenced by the prenatal temperature conditions. A high incubation temperature induced a consistent and long-lasting increase in mitochondrial aerobic metabolism. Postnatal mitochondrial aerobic metabolism was positively associated with oxidative damage on DNA but not telomere length. While we detected significant within-individual consistency in mitochondrial aerobic metabolism across life-stages, the prenatal temperature regime only accounted for a relatively small proportion (<20%) of the consistent among-individual differences we observed. Our results demonstrate that prenatal conditions can program consistent and long-lasting differences in mitochondrial function, which could potentially underlie among-individual variation in performance and health state.

physiology↗

bioRxiv2019

Ageing before birth: pace and stability of prenatal growth affect telomere dynamics

Pre-natal effects on telomere length are increasingly recognized as a potential contributor to the developmental origin of health and adult diseases. While it is becoming clear that telomere length is strongly influenced by pre-natal conditions, the factors affecting telomere dynamics during embryogenesis remain poorly understood. We manipulated both the pace and stability of prenatal growth using incubation temperature in Japanese quail and investigated the impact on telomere dynamics from embryogenesis to adulthood, along with potential drivers of telomere shortening such as oxidative damage and prenatal glucocorticoid levels. Telomere length was not affected by these manipulations for the first 75% of prenatal development, but was reduced at hatching in response to both experimentally induced fast embryo growth and growth instability. These early-life effects on telomere length persisted until adulthood. The effect of developmental instability on telomere length at hatching was potentially mediated by an increased secretion of glucocorticoid hormones during development. Both the pace and the stability of prenatal growth appear as key factors determining telomere length and dynamics up to adulthood, with fast and unstable embryo growth leading to short telomeres with the potential for adverse associated outcomes in terms of reduced longevity and greater risk of disease.

physiology↗

bioRxiv2019

Inter-specific variation of maternal thyroid hormones associate with migration, mode of development, and captivity: a phylogenetic comparative analysis

Life-history traits vary largely across species and several physiological parameters have been proposed to be associated with life-history variation, such as metabolic rates, glucocorticoids, and oxidative stress. Interestingly, the association between thyroid hormones (THs) and life history variation has never been considered, despite a close interaction between THs and these physiological traits. Because of the crucial effects on embryonic development, THs can also induce transgenerational plasticity when transferred to developing offspring, for instance, via egg yolks in birds. In this study, we compiled a unique data set of maternal yolk THs in 34 bird species across 17 families and 6 orders, and tested for associations with various life-history traits. Our phylogenetic mixed models indicated that both concentrations and total amounts of the two most important forms of THs (T3 and T4) were higher in the eggs of migratory species than in those of resident species, and that there were higher total amounts of T3 in the eggs of precocial species than in those of altricial species. However, maternal THs did not show clear associations with any traits of the pace-of-life syndrome, such as developmental duration, growth rate, or lifespan. When taking environmental factors into account, we found that captive species deposited higher TH concentrations and larger amounts in the egg yolks than wild species. These findings suggest that maternal THs are likely involved in the evolution of life-history variation, or vice versa.

evolutionary biology↗

bioRxiv2019

Maternal stress promotes offspring growth without oxidative costs in wild red squirrels

Elevations in glucocorticoid levels (GCs) in breeding females may induce adaptive shifts in offspring life histories. Offspring produced by mothers with elevated GCs may be better prepared to face harsh environments where a faster pace of life is beneficial. We examined how experimentally elevated GCs in pregnant or lactating North American red squirrels (Tamiasciurus hudsonicus) affected offspring postnatal growth, structural size, oxidative stress levels (two antioxidants and oxidative protein damage) in three different tissues (blood, heart, liver), and liver telomere lengths. We predicted that offspring from mothers treated with GCs would grow faster but would also have higher levels of oxidative stress and shorter telomeres, which may predict reduced longevity. Offspring from mothers treated with GCs during pregnancy were 8.3% lighter around birth but grew (in body mass) 17.0% faster than those from controls, whereas offspring from mothers treated with GCs during lactation grew 34.8% slower than those from controls and did not differ in body mass around birth. Treating mothers with GCs during pregnancy or lactation did not alter the oxidative stress levels or telomere lengths of their offspring. Fast-growing offspring from any of the treatment groups did not have higher oxidative stress levels or shorter telomere lengths, indicating that offspring that grew faster early in life did not exhibit oxidative costs after this period of growth. Our results indicate that elevations in maternal GCs may induce plasticity in offspring growth without long-term oxidative costs to the offspring that might result in a shortened lifespan. Summary StatementWe show that experimental increases in glucocorticoids in breeding female North American red squirrels affects offspring postnatal growth but not levels of oxidative damage and antioxidants or telomere lengths.

evolutionary biology↗