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1.
J Exp Biol ; 227(Suppl_1)2024 Mar 07.
Artículo en Inglés | MEDLINE | ID: mdl-38449325

RESUMEN

Although the long-lasting effects of variation in early-life environment have been well documented across organisms, the underlying causal mechanisms are only recently starting to be unraveled. Yet understanding the underlying mechanisms of long-lasting effects can help us predict how organisms will respond to changing environments. Birds offer a great system in which to study developmental plasticity and its underlying mechanisms owing to the production of large external eggs and variation in developmental trajectories, combined with a long tradition of applied, physiological, ecological and evolutionary research. Epigenetic changes (such as DNA methylation) have been suggested to be a key mechanism mediating long-lasting effects of the early-life environment across taxa. More recently, changes in the early-life gut microbiome have been identified as another potential mediator of developmental plasticity. As a first step in understanding whether these mechanisms contribute to developmental plasticity in birds, this Review summarizes how changes in early-life environment (both prenatal and postnatal) influence epigenetic markers and the gut microbiome. The literature shows how both early-life biotic (such as resources and social environment) and abiotic (thermal environment and various anthropogenic stressors) factors modify epigenetic markers and the gut microbiome in birds, yet data concerning many other environmental factors are limited. The causal links of these modifications to lasting phenotypic changes are still scarce, but changes in the hypothalamic-pituitary-adrenal axis have been identified as one putative pathway. This Review identifies several knowledge gaps, including data on the long-term effects, stability of the molecular changes, and lack of diversity in the systems studied, and provides directions for future research.


Asunto(s)
Aves , Epigénesis Genética , Microbiota , Animales , Aves/genética , Aves/crecimiento & desarrollo , Sistema Hipotálamo-Hipofisario , Sistema Hipófiso-Suprarrenal
2.
Biol Open ; 13(3)2024 Mar 01.
Artículo en Inglés | MEDLINE | ID: mdl-38385271

RESUMEN

Although mitochondrial respiration is believed to explain a substantial part of the variation in resting metabolic rate (RMR), few studies have empirically studied the relationship between organismal and cellular metabolism. We therefore investigated the relationship between RMR and mitochondrial respiration of permeabilized blood cells in wild great tits (Parus major L.). We also studied the correlation between mitochondrial respiration traits and blood cell count, as normalizing mitochondrial respiration by the cell count is a method commonly used to study blood metabolism. In contrast to previous studies, our results show that there was no relationship between RMR and mitochondrial respiration in intact blood cells (i.e. with the ROUTINE respiration). However, when cells were permeabilized and interrelation re-assessed under saturating substrate availability, we found that RMR was positively related to phosphorylating respiration rates through complexes I and II (i.e. OXPHOS respiration) and to the mitochondrial efficiency to produce energy (i.e. net phosphorylation efficiency), though variation explained by the models was low (i.e. linear model: R2=0.14 to 0.21). However, unlike studies in mammals, LEAK respiration without [i.e. L(n)] and with [i.e. L(Omy)] adenylates was not significantly related to RMR. These results suggest that phosphorylating respiration in blood cells can potentially be used to predict RMR in wild birds, but that this relationship may have to be addressed in standardized conditions (permeabilized cells) and that the prediction risks being imprecise. We also showed that, in our conditions, there was no relationship between any mitochondrial respiration trait and blood cell count. Hence, we caution against normalising respiration rates using this parameter as is sometimes done. Future work should address the functional explanations for the observed relationships, and determine why these appear labile across space, time, taxon, and physiological state.


Asunto(s)
Metabolismo Basal , Metabolismo Energético , Animales , Metabolismo Basal/fisiología , Mitocondrias , Respiración , Recuento de Células Sanguíneas , Mamíferos
3.
Evol Appl ; 16(10): 1753-1769, 2023 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-38020869

RESUMEN

Offspring phenotype at birth is determined by its genotype and the prenatal environment including exposure to maternal hormones. Variation in both maternal glucocorticoids and thyroid hormones can affect offspring phenotype, but the underlying molecular mechanisms, especially those contributing to long-lasting effects, remain unclear. Epigenetic changes (such as DNA methylation) have been postulated as mediators of long-lasting effects of early-life environment. In this study, we determined the effects of elevated prenatal glucocorticoid and thyroid hormones on handling stress response (breath rate) as well as DNA methylation and gene expression of glucocorticoid receptor (GR) and thyroid hormone receptor (THR) in great tits (Parus major). Eggs were injected before incubation onset with corticosterone (the main avian glucocorticoid) and/or thyroid hormones (thyroxine and triiodothyronine) to simulate variation in maternal hormone deposition. Breath rate during handling and gene expression of GR and THR were evaluated 14 days after hatching. Methylation status of GR and THR genes was analyzed from the longitudinal blood cells sampled 7 and 14 days after hatching, as well as the following autumn. Elevated prenatal corticosterone level significantly increased the breath rate during handling, indicating an enhanced metabolic stress response. Prenatal corticosterone manipulation had CpG-site-specific effects on DNA methylation at the GR putative promoter region, while it did not significantly affect GR gene expression. GR expression was negatively associated with earlier hatching date and chick size. THR methylation or expression did not exhibit any significant relationship with the hormonal treatments or the examined covariates, suggesting that TH signaling may be more robust due to its crucial role in development. This study provides some support to the hypothesis suggesting that maternal corticosterone may influence offspring metabolic stress response via epigenetic alterations, yet their possible adaptive role in optimizing offspring phenotype to the prevailing conditions, context-dependency, and the underlying molecular interplay needs further research.

4.
J Exp Biol ; 226(21)2023 11 01.
Artículo en Inglés | MEDLINE | ID: mdl-37815441

RESUMEN

In avian species, the number of chicks in the nest and subsequent sibling competition for food are major components of the offspring's early-life environment. A large brood size is known to affect chick growth, leading in some cases to long-lasting effects for the offspring, such as a decrease in size at fledgling and in survival after fledging. An important pathway underlying different growth patterns could be the variation in offspring mitochondrial metabolism through its central role in converting energy. Here, we performed a brood size manipulation in great tits (Parus major) to unravel its impact on offspring mitochondrial metabolism and reactive oxygen species (ROS) production in red blood cells. We investigated the effects of brood size on chick growth and survival, and tested for long-lasting effects on juvenile mitochondrial metabolism and phenotype. As expected, chicks raised in reduced broods had a higher body mass compared with enlarged and control groups. However, mitochondrial metabolism and ROS production were not significantly affected by the treatment at either chick or juvenile stages. Interestingly, chicks raised in very small broods were smaller in size and had higher mitochondrial metabolic rates. The nest of rearing had a significant effect on nestling mitochondrial metabolism. The contribution of the rearing environment in determining offspring mitochondrial metabolism emphasizes the plasticity of mitochondrial metabolism in relation to the nest environment. This study opens new avenues regarding the effect of postnatal environmental conditions in shaping offspring early-life mitochondrial metabolism.


Asunto(s)
Passeriformes , Animales , Especies Reactivas de Oxígeno , Clima
5.
J Exp Biol ; 226(15)2023 08 01.
Artículo en Inglés | MEDLINE | ID: mdl-37529973

RESUMEN

The social environment is one of the primary sources of challenging stimuli that can induce a stress response in animals. It comprises both short-term and stable interactions among conspecifics (including unrelated individuals, mates, potential mates and kin). Social stress is of unique interest in the field of stress research because (1) the social domain is arguably the most complex and fluctuating component of an animal's environment; (2) stress is socially transmissible; and (3) stress can be buffered by social partners. Thus, social interactions can be both the cause and cure of stress. Here, we review the history of social stress research, and discuss social stressors and their effects on organisms across early life and adulthood. We also consider cross-generational effects. We discuss the physiological mechanisms underpinning social stressors and stress responses, as well as the potential adaptive value of responses to social stressors. Finally, we identify outstanding challenges in social stress research, and propose a framework for addressing these in future work.


Asunto(s)
Evolución Biológica , Estrés Psicológico , Animales , Medio Social
6.
Anim Microbiome ; 5(1): 19, 2023 Mar 22.
Artículo en Inglés | MEDLINE | ID: mdl-36949549

RESUMEN

BACKGROUND: The gut microbiome forms at an early stage, yet data on the environmental factors influencing the development of wild avian microbiomes is limited. As the gut microbiome is a vital part of organismal health, it is important to understand how it may connect to host performance. The early studies with wild gut microbiome have shown that the rearing environment may be of importance in gut microbiome formation, yet the results vary across taxa, and the effects of specific environmental factors have not been characterized. Here, wild great tit (Parus major) broods were manipulated to either reduce or enlarge the original brood soon after hatching. We investigated if brood size was associated with nestling bacterial gut microbiome, and whether gut microbiome diversity predicted survival. Fecal samples were collected at mid-nestling stage and sequenced with the 16S rRNA gene amplicon sequencing, and nestling growth and survival were measured. RESULTS: Gut microbiome diversity showed high variation between individuals, but this variation was not significantly explained by brood size or body mass. Additionally, we did not find a significant effect of brood size on body mass or gut microbiome composition. We also demonstrated that early handling had no impact on nestling performance or gut microbiome. Furthermore, we found no significant association between gut microbiome diversity and short-term (survival to fledging) or mid-term (apparent juvenile) survival. CONCLUSIONS: We found no clear association between early-life environment, offspring condition and gut microbiome. This suggests that brood size is not a significantly contributing factor to great tit nestling condition, and that other environmental and genetic factors may be more strongly linked to offspring condition and gut microbiome. Future studies should expand into other early-life environmental factors e.g., diet composition and quality, and parental influences.

7.
J Exp Biol ; 226(6)2023 03 15.
Artículo en Inglés | MEDLINE | ID: mdl-36714994

RESUMEN

The early-life environment is known to affect later-life health and disease, which could be mediated by the early-life programming of telomere length, a key hallmark of ageing. According to the fetal programming of telomere biology hypothesis, variation in prenatal exposure to hormones is likely to influence telomere length. Yet, the contribution of key metabolic hormones, i.e. thyroid hormones (THs), has been largely ignored. We recently showed that in contrast to predictions, exposure to elevated prenatal THs increased postnatal telomere length in wild collared flycatchers, but the generality of such effect, the underlying proximate mechanisms and consequences for survival have not been investigated. We therefore conducted a comprehensive study evaluating the impact of THs on potential drivers of telomere dynamics (growth, post-natal THs, mitochondria and oxidative stress), telomere length and medium-term survival using wild great tits as a model system. While prenatal THs did not significantly affect telomere length a week after hatching (i.e. day 7), they influenced postnatal telomere shortening (i.e. shorter telomeres at day 14 and the following winter) but not apparent survival. Circulating THs, mitochondrial density or oxidative stress biomarkers were not significantly influenced, whereas the TH-supplemented group showed accelerated growth, which may explain the observed delayed effect on telomeres. We discuss several alternative hypotheses that may explain the contrast with our previous findings in flycatchers. Given that shorter telomeres in early life tend to be carried until adulthood and are often associated with decreased survival prospects, the effects of prenatal THs on telomeres may have long-lasting effects on senescence.


Asunto(s)
Passeriformes , Pájaros Cantores , Embarazo , Animales , Femenino , Acortamiento del Telómero , Envejecimiento , Desarrollo Fetal , Vitaminas , Telómero , Hormonas Tiroideas , Hormonas
8.
Mol Ecol Resour ; 23(7): 1488-1508, 2023 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-35466564

RESUMEN

The field of molecular biology is advancing fast with new powerful technologies, sequencing methods and analysis software being developed constantly. Commonly used tools originally developed for research on humans and model species are now regularly used in ecological and evolutionary research. There is also a growing interest in the causes and consequences of epigenetic variation in natural populations. Studying ecological epigenetics is currently challenging, especially for vertebrate systems, because of the required technical expertise, complications with analyses and interpretation, and limitations in acquiring sufficiently high sample sizes. Importantly, neglecting the limitations of the experimental setup, technology and analyses may affect the reliability and reproducibility, and the extent to which unbiased conclusions can be drawn from these studies. Here, we provide a practical guide for researchers aiming to study DNA methylation variation in wild vertebrates. We review the technical aspects of epigenetic research, concentrating on DNA methylation using bisulfite sequencing, discuss the limitations and possible pitfalls, and how to overcome them through rigid and reproducible data analysis. This review provides a solid foundation for the proper design of epigenetic studies, a clear roadmap on the best practices for correct data analysis and a realistic view on the limitations for studying ecological epigenetics in vertebrates. This review will help researchers studying the ecological and evolutionary implications of epigenetic variation in wild populations.


Asunto(s)
Metilación de ADN , Epigénesis Genética , Animales , Humanos , Reproducibilidad de los Resultados , Vertebrados/genética , Ecología
9.
Trends Ecol Evol ; 38(1): 35-43, 2023 01.
Artículo en Inglés | MEDLINE | ID: mdl-36243622

RESUMEN

Non-target organisms are globally exposed to herbicides. While many herbicides - for example, glyphosate - were initially considered safe, increasing evidence demonstrates that they have profound effects on ecosystem functions via altered microbial communities. We provide a comprehensive framework on how herbicide residues may modulate ecosystem-level outcomes via alteration of microbiomes. The changes in soil microbiome are likely to influence key nutrient cycling and plant-soil processes. Herbicide-altered microbiome affects plant and animal performance and can influence trophic interactions such as herbivory and pollination. These changes are expected to lead to ecosystem and even evolutionary consequences for both microbes and hosts. Tackling the threats caused by agrochemicals to ecosystem functions and services requires tools and solutions based on a comprehensive understanding of microbe-mediated risks.


Asunto(s)
Herbicidas , Microbiota , Animales , Herbicidas/farmacología , Herbicidas/química , Ecosistema , Plantas , Suelo/química , Evolución Biológica
10.
Physiol Biochem Zool ; 95(6): 544-550, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-36240021

RESUMEN

AbstractMaternal hormones, such as thyroid hormones (THs) transferred to embryos and eggs, are key signaling pathways for mediating maternal effects. To be able to respond to maternal cues, embryos must express the key molecular "machinery" of hormone pathways, such as enzymes and receptors. While altricial birds begin TH production only at or after hatching, experimental evidence suggests that their phenotype can be influenced by maternal THs deposited into the egg. However, it is not understood how or when altricial birds express genes in the TH pathway. For the first time, we measured the expression of key TH-pathway genes in altricial embryos by using two common altricial ecological model species, pied flycatcher (Ficedula hypoleuca) and blue tit (Cyanistes caeruleus). Deiodinase DIO1 gene expression could not be reliably confirmed in either species, but deiodinase enzyme genes DIO2 and DIO3 were expressed in both species. Given that DIO2 converts thyroxine to biologically active triiodothyronine and that DIO3 mostly converts triiodothyronine to inactive forms of THs, our results suggest that embryos may modulate maternal signals. TH receptors (THRA and THRB) and a monocarboxylate membrane transporter gene (SLC16A2) were also expressed, enabling TH responses. Our results suggest that altricial embryos may be able to respond to and potentially modulate maternal signals conveyed by THs in early development.


Asunto(s)
Tiroxina , Triyodotironina , Animales , Aves , Señales (Psicología) , Yoduro Peroxidasa/genética , Yoduro Peroxidasa/metabolismo , Proteínas de Transporte de Membrana , Hormonas Tiroideas
11.
Horm Behav ; 142: 105180, 2022 06.
Artículo en Inglés | MEDLINE | ID: mdl-35569424

RESUMEN

Variation in stress responses has been investigated in relation to environmental factors, species ecology, life history and fitness. Moreover, mechanistic studies have unravelled molecular mechanisms of how acute and chronic stress responses cause physiological impacts ('damage'), and how this damage can be repaired. However, it is not yet understood how the fitness effects of damage and repair influence stress response evolution. Here we study the evolution of hormone levels as a function of stressor occurrence, damage and the efficiency of repair. We hypothesise that the evolution of stress responses depends on the fitness consequences of damage and the ability to repair that damage. To obtain some general insights, we model a simplified scenario in which an organism repeatedly encounters a stressor with a certain frequency and predictability (temporal autocorrelation). The organism can defend itself by mounting a stress response (elevated hormone level), but this causes damage that takes time to repair. We identify optimal strategies in this scenario and then investigate how those strategies respond to acute and chronic exposures to the stressor. We find that for higher repair rates, baseline and peak hormone levels are higher. This typically means that the organism experiences higher levels of damage, which it can afford because that damage is repaired more quickly, but for very high repair rates the damage does not build up. With increasing predictability of the stressor, stress responses are sustained for longer, because the animal expects the stressor to persist, and thus damage builds up. This can result in very high (and potentially fatal) levels of damage when organisms are exposed to chronic stressors to which they are not evolutionarily adapted. Overall, our results highlight that at least three factors need to be considered jointly to advance our understanding of how stress physiology has evolved: (i) temporal dynamics of stressor occurrence; (ii) relative mortality risk imposed by the stressor itself versus damage caused by the stress response; and (iii) the efficiency of repair mechanisms.


Asunto(s)
Adaptación Fisiológica , Hormonas , Adaptación Fisiológica/fisiología , Animales , Estrés Fisiológico/fisiología
12.
J Anim Ecol ; 91(7): 1489-1506, 2022 07.
Artículo en Inglés | MEDLINE | ID: mdl-35470435

RESUMEN

In vertebrates, thyroid hormones (THs) play an important role in the regulation of growth, development, metabolism, photoperiodic responses and migration. Maternally transferred THs are important for normal early phase embryonic development when embryos are not able to produce endogenous THs. Previous studies have shown that variation in maternal THs within the physiological range can influence offspring phenotype. Given the essential functions of maternal THs in development and metabolism, THs may be a mediator of life-history variation across species. We tested the hypothesis that differences in life histories are associated with differences in maternal TH transfer across species. Using birds as a model, we specifically tested whether maternally transferred yolk THs covary with migratory status, developmental mode and traits related to pace-of-life (e.g. basal metabolic rate, maximum life span). We collected un-incubated eggs (n = 1-21 eggs per species, median = 7) from 34 wild and captive bird species across 17 families and six orders to measure yolk THs [both triiodothyronine (T3) and thyroxine (T4)], compiled life-history trait data from the literature and used Bayesian phylogenetic mixed models to test our hypotheses. Our models indicated that both concentrations and total amounts of the two main forms of THs (T3 and T4) were higher in the eggs of migratory species compared to resident species, and total amounts were higher in the eggs of precocial species, which have longer prenatal developmental periods, than in those of altricial species. However, maternal yolk THs did not show clear associations with pace-of-life-related traits, such as fecundity, basal metabolic rate or maximum life span. We quantified interspecific variation in maternal yolk THs in birds, and our findings suggest higher maternal TH transfer is associated with the precocial mode of development and migratory status. Whether maternal THs represent a part of the mechanism underlying the evolution of precocial development and migration or a consequence of such life histories is currently unclear. We therefore encourage further studies to explore the physiological mechanisms and evolutionary processes underlying these patterns.


Asunto(s)
Hormonas Tiroideas , Triyodotironina , Animales , Teorema de Bayes , Aves , Filogenia , Hormonas Tiroideas/metabolismo , Triyodotironina/metabolismo
13.
J Exp Biol ; 225(9)2022 05 01.
Artículo en Inglés | MEDLINE | ID: mdl-35420125

RESUMEN

Developmental plasticity is partly mediated by transgenerational effects, including those mediated by the maternal endocrine system. Glucocorticoid and thyroid hormones may play central roles in developmental programming through their action on metabolism and growth. However, the mechanisms by which they affect growth and development remain understudied. One hypothesis is that maternal hormones directly affect the production and availability of energy-carrying molecules (e.g. ATP) by their action on mitochondrial function. To test this hypothesis, we experimentally increased glucocorticoid and thyroid hormones in wild great tit eggs (Parus major) to investigate their impact on offspring mitochondrial aerobic metabolism (measured in blood cells), and subsequent growth and survival. We show that prenatal glucocorticoid supplementation affected offspring cellular aerobic metabolism by decreasing mitochondrial density, maximal mitochondrial respiration and oxidative phosphorylation, while increasing the proportion of the maximum capacity being used under endogenous conditions. Prenatal glucocorticoid supplementation only had mild effects on offspring body mass, size and condition during the rearing period, but led to a sex-specific (females only) decrease in body mass a few months after fledging. Contrary to our expectations, thyroid hormone supplementation did not affect offspring growth or mitochondrial metabolism. Recapture probability as juveniles or adults was not significantly affected by prenatal hormonal treatment. Our results demonstrate that prenatal glucocorticoids can affect post-natal mitochondrial density and aerobic metabolism. The weak effects on growth and apparent survival suggest that nestlings were mostly able to compensate for the transient decrease in mitochondrial aerobic metabolism induced by prenatal glucocorticoids.


Asunto(s)
Glucocorticoides , Passeriformes , Animales , Respiración de la Célula , Femenino , Masculino , Mitocondrias , Hormonas Tiroideas
14.
Epigenetics ; 17(6): 625-641, 2022 06.
Artículo en Inglés | MEDLINE | ID: mdl-34369261

RESUMEN

Anthropogenic pollution is known to negatively influence an organism's physiology, behaviour, and fitness. Epigenetic regulation, such as DNA methylation, has been hypothesized as a potential mechanism to mediate such effects, yet studies in wild species are lacking. We first investigated the effects of early-life exposure to the heavy metal lead (Pb) on DNA methylation levels in a wild population of great tits (Parus major), by experimentally exposing nestlings to Pb at environmentally relevant levels. Secondly, we compared nestling DNA methylation from a population exposed to long-term heavy metal pollution (close to a copper smelter), where birds suffer from pollution-related decrease in food quality, and a control population. For both comparisons, the analysis of about one million CpGs covering most of the annotated genes revealed that pollution-related changes in DNA methylation were not genome wide, but enriched for genes underlying developmental processes. However, the results were not consistent when using binomial or beta binomial regression highlighting the difficulty of modelling variance in CpGs. Our study indicates that post-natal anthropogenic heavy metal exposure can affect methylation levels of development related genes in a wild bird population.


Asunto(s)
Contaminantes Ambientales , Metales Pesados , Passeriformes , Animales , Metilación de ADN , Contaminantes Ambientales/toxicidad , Epigénesis Genética , Plomo/toxicidad , Metales Pesados/toxicidad , Passeriformes/genética
15.
J Exp Biol ; 224(20)2021 10 15.
Artículo en Inglés | MEDLINE | ID: mdl-34605889

RESUMEN

Maternal hormones constitute a key signalling pathway for mothers to shape offspring phenotype and fitness. Thyroid hormones (THs; triiodothyronine, T3; and thyroxine, T4) are metabolic hormones known to play crucial roles in embryonic development and survival in all vertebrates. During early developmental stages, embryos exclusively rely on exposure to maternal THs, and maternal hypothyroidism can cause severe embryonic maldevelopment. The TH molecule includes iodine, an element that cannot be synthesised by the organism. Therefore, TH production may become costly when environmental iodine availability is low. This may yield a trade-off for breeding females between allocating the hormones to self or to their eggs, potentially to the extent that it even influences the number of laid eggs. In this study, we investigated whether low dietary iodine may limit TH production and transfer to the eggs in a captive population of rock pigeons (Columba livia). We provided breeding females with an iodine-restricted (I-) diet or iodine-supplemented (I+) diet and measured the resulting circulating and yolk iodine and TH concentrations and the number of eggs laid. Our iodine-restricted diet successfully decreased both circulating and yolk iodine concentrations compared with the supplemented diet, but not circulating or yolk THs. This indicates that mothers may not be able to independently regulate hormone exposure for self and their embryos. However, egg production was clearly reduced in the I- group, with fewer females laying eggs. This result shows that restricted availability of iodine does induce a cost in terms of egg production. Whether females reduced egg production to preserve THs for themselves or to prevent embryos from exposure to low iodine and/or THs is as yet unclear.


Asunto(s)
Columbidae , Yodo , Animales , Yema de Huevo , Femenino , Hormonas Tiroideas , Tiroxina , Triyodotironina
16.
Environ Sci Technol ; 55(13): 8947-8954, 2021 07 06.
Artículo en Inglés | MEDLINE | ID: mdl-34110128

RESUMEN

Pollutants, such as toxic metals, negatively influence organismal health and performance, even leading to population collapses. Studies in model organisms have shown that epigenetic marks, such as DNA methylation, can be modulated by various environmental factors, including pollutants, influencing gene expression, and various organismal traits. Yet experimental data on the effects of pollution on DNA methylation from wild animal populations are largely lacking. We here experimentally investigated for the first time the effects of early-life exposure to environmentally relevant levels of a key pollutant, arsenic (As), on genome-wide DNA methylation in a wild bird population. We experimentally exposed nestlings of great tits (Parus major) to arsenic during their postnatal developmental period (3 to 14 days post-hatching) and compared their erythrocyte DNA methylation levels to those of respective controls. In contrast to predictions, we found no overall hypomethylation in the arsenic group. We found evidence for loci to be differentially methylated between the treatment groups, but for five CpG sites only. Three of the sites were located in gene bodies of zinc finger and BTB domain containing 47 (ZBTB47), HIVEP zinc finger 3 (HIVEP3), and insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1). Further studies are needed to evaluate whether epigenetic dysregulation is a commonly observed phenomenon in polluted populations and what are the consequences for organism functioning and for population dynamics.


Asunto(s)
Arsénico , Contaminantes Ambientales , Animales , Animales Salvajes , Arsénico/toxicidad , Aves/genética , Metilación de ADN , Contaminantes Ambientales/toxicidad
18.
Environ Microbiol Rep ; 13(3): 309-316, 2021 06.
Artículo en Inglés | MEDLINE | ID: mdl-33530134

RESUMEN

Glyphosate is the leading herbicide worldwide, but it also affects prokaryotes because it targets the central enzyme (5-enolpyruvylshikimate-3-phosphate, EPSP) of the shikimate pathway in the synthesis of the three essential aromatic amino acids in bacteria, fungi and plants. Our results reveal that bacteria may easily become resistant to glyphosate through changes in the 5-enolpyruvylshikimate-3-phosphate synthase active site. This indicates the importance of examining how glyphosate affects microbe-mediated ecosystem functions and human microbiomes.


Asunto(s)
3-Fosfoshikimato 1-Carboxiviniltransferasa , Fosfatos , 3-Fosfoshikimato 1-Carboxiviniltransferasa/química , 3-Fosfoshikimato 1-Carboxiviniltransferasa/genética , 3-Fosfoshikimato 1-Carboxiviniltransferasa/metabolismo , Bacterias/genética , Bacterias/metabolismo , Ecosistema , Glicina/análogos & derivados
19.
Trends Ecol Evol ; 36(1): 39-48, 2021 01.
Artículo en Inglés | MEDLINE | ID: mdl-33032863

RESUMEN

All organisms have a stress response system to cope with environmental threats, yet its precise form varies hugely within and across individuals, populations, and species. While the physiological mechanisms are increasingly understood, how stress responses have evolved remains elusive. Here, we show that important insights can be gained from models that incorporate physiological mechanisms within an evolutionary optimality analysis (the 'evo-mecho' approach). Our approach reveals environmental predictability and physiological constraints as key factors shaping stress response evolution, generating testable predictions about variation across species and contexts. We call for an integrated research programme combining theory, experimental evolution, and comparative analysis to advance scientific understanding of how this core physiological system has evolved.


Asunto(s)
Evolución Biológica , Humanos
20.
Sci Total Environ ; 750: 141422, 2021 Jan 01.
Artículo en Inglés | MEDLINE | ID: mdl-32858290

RESUMEN

Glyphosate-based herbicides (GBHs) are the most frequently used herbicides globally. They were launched as a safe solution for weed control, but recently, an increasing number of studies have shown the existence of GBH residues and highlighted the associated risks they pose throughout ecosystems. Conventional agricultural practices often include the use of GBHs, and the use of glyphosate-resistant genetically modified crops is largely based on the application of glyphosate, which increases the likelihood of its residues ending up in animal feed. These residues persist throughout the digestive process of production animals and accumulate in their excretion products. The poultry industry, in particular, is rapidly growing, and excreted products are used as plant fertilizers in line with circular food economy practices. We studied the potential effects of unintentional glyphosate contamination on an agronomically important forage grass, meadow fescue (Festuca pratensis) and a horticulturally important strawberry (Fragaria x vescana) using glyphosate residues containing poultry manure as a plant fertilizer in a common garden experiment. Glyphosate in the manure decreased plant growth in both species and vegetative reproduction in F. x vescana. Furthermore, our results indicate that glyphosate residues in organic fertilizers might have indirect effects on sexual reproduction in F. pratensis and herbivory in F. x vescana because they positively correlate with plant size. Our results highlight that glyphosate can be unintentionally spread via organic fertilizer, counteracting its ability to promote plant growth.


Asunto(s)
Fertilizantes , Herbicidas , Animales , Productos Agrícolas/genética , Ecosistema , Glicina/análogos & derivados , Herbicidas/toxicidad , Estiércol , Plantas Modificadas Genéticamente
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