Biology subjects

Tangili, M.

Publications and source records attributed to Tangili, M..

7 recordsLinked to original sources

bioRxiv2026

DNA methylation correlates with lifespan and predicts remaining lifespan in the zebra finch

Biomarkers that correlate with age are essential tools for understanding aging and lifespan variation. DNA methylation (DNAm) changes predictably with age in parts of the genome. In humans, epigenetically 'old' individuals relative to their chronological age also have a reduced life expectancy but whether the link between epigenetic age and lifespan is a general feature remains an open question. We explored age-related changes in DNAm in the zebra finch (Taeniopygia castanotis), a key avian model species, using 100 longitudinal whole genome methylomes from 50 captive adults monitored until their natural death. We found genome-wide hypomethylation with age, with DNAm decreasing faster in individuals with shorter lifespans and identified 29 CpG sites where DNAm changed significantly with age. We developed an epigenetic aging clock based on 119 CpG sites, that predicted chronological age with high accuracy (median absolute deviation=0.68 years, 8.2% of maximum lifespan in our dataset). Females raised in large broods, which have shorter lifespans, showed increased epigenetic age acceleration, consistent with faster biological aging. However, epigenetic age acceleration did not predict lifespan or remaining lifespan. In contrast, the within-individual rate of change in epigenetic age significantly predicted lifespan: faster epigenetic aging was associated with a shorter lifespan. Moreover, a 'doom' clock, trained to predict post-sampling lifespan, successfully predicted remaining lifespan. Our findings provide the first evidence that DNAm provides a window into biological aging in birds, showing how early-life environments shape the aging trajectory via the epigenome and underscore the value of longitudinal data in aging studies.

molecular biology↗

bioRxiv2025

Inferences from epigenetic information in an ecological context: a case study of early-life environmental effects on DNA methylation in zebra finches

DNA methylation (DNAm) plays a key role in mediating phenotypic responses to environmental variation. Various approaches exist to link DNAm variation to phenotypes, ranging from single nucleotide resolution to the development of composite indexes ( epigenetic clocks). We here discuss the conceptual differences between these approaches through a case study using whole genome, longitudinal DNAm data from adult zebra finches raised in experimentally created small or large broods. Specifically, we (i) identified sex and age-specific CpG sites where DNAm was affected by brood size, and (ii) developed two DNAm-based indexes of the early-life environment (DMSi: based on differentially methylated sites with respect to rearing brood size; SMLmi: supervised machine learning-derived index optimized to predict brood size). We also compared results obtained by either merging or analyzing longitudinal DNAm samples separately and discussed how the permanence or transience of DNAm changes shapes responses to environmental variation through life. Our findings confirm that early-life environment leaves lasting DNAm signatures detectible in adulthood, and this effect is stronger later in life. Importantly, both indexes predicted early-life growth rates, demonstrating that DNAm-based indexes can be leveraged to retroactively quantify aspects of early-life conditions, providing a powerful novel tool in the study of wild populations.

evolutionary biology↗

bioRxiv2025

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↗

bioRxiv2025

Begging costs rather than food received cause brood size effect on growth in zebra finches

Altricial species rely on parental provisioning for early-life sustenance, and a larger brood size leads to higher levels of competition between siblings for parental resources. Early-life stress can have severe and lifelong effects on Darwinian fitness. Indeed, it is well established that being reared in a larger brood impairs growth and fitness prospects of birds, but the mechanistic underpinnings of this effect are still largely unknown. Specifically, it is not well known to what extent the reduced growth and fitness prospects of nestlings reared in large broods is due to increased resource allocation to competition versus a per capita reduction in parental provisioning rate, or a combination of the two. We cross-fostered zebra finch (Taeniopygia castanotis) chicks into small and large broods, and recorded their growth as well as the behavior of parents and offspring throughout the nestling period. As in previous experiments, growth rate was higher in small broods. In large broods, chicks begged more and parents invested more time feeding which more than compensated for the difference in brood size. We therefore conclude that the lower growth rate for nestlings raised in large broods must be atleast in part-attributed to increased energy expenditure on begging rather than a reduction in the amount of food received. These results suggest significant energetic costs associated with begging and raise the interesting possibility that brood size would not have negatively affected growth in large broods if chicks had not increased their begging effort due to increased levels of competition in nest.

animal behavior and cognition↗

bioRxiv2024

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↗

bioRxiv2024

Dosage compensation and sexual conflict in female heterogametic methylomes

DNA methylation (DNAm) suppresses gene expression and contributes to dosage compensation in mammals but whether DNAm plays a similar role in female ZW chromosome heterogametic species remains unresolved. We assessed chromosome-level DNAm using whole genome bisulphite sequencing in two avian species, zebra finches and jackdaws. Dosage compensation by DNAm would result in higher and more variable DNAm level in males relative to females on the Z chromosome. However, we found that the level of DNAm and its variance on the Z chromosome was lower in males. Moreover, male Z chromosome-based gene promoters were more frequently hypomethylated compared to females, indicating absence of upregulation on a gene-by-gene basis across the female Z chromosome. We suggest our findings reveal mitigation of an intra-genomic sexual conflict, with females suppressing expression of Z chromosome-based genes that benefit male but not female fitness. W was the most methylated chromosome, but hypermethylation on the W chromosome was mostly confined to intergenic regions, presumably resulting in the downregulation of transposable elements known to comprise a large part of the W chromosome. Thus, DNAm is involved in the development of sex-dependent phenotypes, but dosage compensation is achieved through other mechanisms.

evolutionary biology↗

bioRxiv2024

Sex-chromosome-dependent aging in female heterogametic methylomes

Recent research in humans and both model and non-model animals has shown that DNA methylation (DNAm), an epigenetic modification, is one of the mechanisms underlying the aging process. DNAm-based indices predict mortality and provide valuable insights into biological aging mechanisms. Although sex-dependent differences in lifespan are ubiquitous and sex chromosomes are thought to play an important role in sex-specific aging, they have been largely ignored in epigenetic aging studies. We characterized the genome-wide distribution of age-related CpG sites from longitudinal samples in two avian species (zebra finch and jackdaw), including for the first time the avian sex chromosomes (Z and the female-specific, haploid W). In both species, we find a small fraction of the CpG sites to show age-related changes in DNAm with the majority of them being located on the haploid, female-specific W chromosome where DNAm levels predominantly decrease with age. Age-related CpG sites were overrepresented on the zebra finch but underrepresented on the jackdaw Z chromosome. Our results highlight distinct age-related changes in sex chromosome DNAm compared to the rest of the genome in two avian species, suggesting this previously understudied feature of sex chromosomes may be instrumental in sex-dependent aging. Moreover, studying the DNAm of sex chromosomes might be particularly useful in aging research, facilitating the identification of shared (sex-dependent) age-related pathways and processes between phylogenetically diverse organisms.

evolutionary biology↗