Three Kinds of Niche Construction

Niche construction theory concerns how organisms can change selection pressures by altering the feature–factor relationship between themselves and their environment. These alterations are standardly understood to be brought about through two kinds of organism–environment interaction: perturbative and relocational niche construction. We argue that a reconceptualization is needed on the grounds that if a niche is understood as the feature–factor relationship, then there are three fundamental ways in which organisms can engage in niche construction: constitutive, relational, and external niche construction. We further motivate our reconceptualization by showing some examples of organismic activities which fall outside of the current categorization of niche construction, but nonetheless should be included. We end by discussing two objections to niche construction and show how our reconceptualization helps to undercut these objections

Genetic architecture and lifetime dynamics of inbreeding depression in a wild

Inbreeding depression is ubiquitous, but we still know little about its genetic architecture and precise effects in wild populations. Here, we combine long-term life-history data with 417 K imputed SNP genotypes for 5952 wild Soay sheep to explore inbreeding depression on a key fitness component, annual survival. Inbreeding manifests in long runs of homozygosity (ROH), which make up nearly half of the genome in the most inbred individuals. The ROH landscape varies widely across the genome, with islands where up to 87% and deserts where only 4% of individuals have ROH. The fitness consequences of inbreeding are severe; a 10% increase in individual inbreeding F(ROH) is associated with a 60% reduction in the odds of survival in lambs, though inbreeding depression decreases with age. Finally, a genome-wide association scan on ROH shows that many loci with small effects and five loci with larger effects contribute to inbreeding depression in survival

Deterritorializing the Future

Understanding how pasts resource presents is a fundamental first step towards building alternative futures in the Anthropocene. This collection brings together scholars from a range of disciplines to explore concepts of care, vulnerability, time, extinction, loss and inheritance across more-than-human worlds, connecting contemporary developments in the posthumanities with the field of critical heritage studies. Drawing on contributions from archaeology, anthropology, critical heritage studies, gender studies, geography, histories of science, media studies, philosophy, and science and technology studies, the book aims to place concepts of heritage at the centre of discussions of the Anthropocene and its associated climate and extinction crises – not as a nostalgic longing for how things were, but as a means of expanding collective imaginations and thinking critically and speculatively about the future and its alternatives. Contributors: Christina Fredengren, Cecilia Åsberg, Anna Bohlin, Adrian Van Allen, Esther Breithoff, Rodney Harrison, Colin Sterling, Joanna Zylinska, Denis Byrne, J. Kelechi Ugwuanyi, Caitlin DeSilvey, Anatolijs Venovcevs, Anna Storm and Claire Colebrook

Deterritorializing the Future: Heritage in, of and after the Anthropocene

Understanding how pasts resource presents is a fundamental first step towards building alternative futures in the Anthropocene. This collection brings together scholars from a range of disciplines to explore concepts of care, vulnerability, time, extinction, loss and inheritance across more-than-human worlds, connecting contemporary developments in the posthumanities with the field of critical heritage studies. Drawing on contributions from archaeology, anthropology, critical heritage studies, gender studies, geography, histories of science, media studies, philosophy, and science and technology studies, the book aims to place concepts of heritage at the centre of discussions of the Anthropocene and its associated climate and extinction crises – not as a nostalgic longing for how things were, but as a means of expanding collective imaginations and thinking critically and speculatively about the future and its alternatives

Deterritorializing the Future

Understanding how pasts resource presents is a fundamental first step towards building alternative futures in the Anthropocene. This collection brings together scholars from a range of disciplines to explore concepts of care, vulnerability, time, extinction, loss and inheritance across more-than-human worlds, connecting contemporary developments in the posthumanities with the field of critical heritage studies. Drawing on contributions from archaeology, anthropology, critical heritage studies, gender studies, geography, histories of science, media studies, philosophy, and science and technology studies, the book aims to place concepts of heritage at the centre of discussions of the Anthropocene and its associated climate and extinction crises – not as a nostalgic longing for how things were, but as a means of expanding collective imaginations and thinking critically and speculatively about the future and its alternatives. Contributors: Christina Fredengren, Cecilia Åsberg, Anna Bohlin, Adrian Van Allen, Esther Breithoff, Rodney Harrison, Colin Sterling, Joanna Zylinska, Denis Byrne, J. Kelechi Ugwuanyi, Caitlin DeSilvey, Anatolijs Venovcevs, Anna Storm and Claire Colebrook

Genetic and environmental constraints causing species’ range limits

Human-caused global change has led to shifts in the geographic distribution of many wild species. This has renewed the interest of understanding the factors that shape species’ contemporary range limits from both an ecological and evolutionary perspective. Recent evolutionary theory particularly emphasized the role of past demographic processes and neutral evolution in contributing to range limits. The aim of my thesis was to study these factors and their interaction with the environment experienced at range edges in an empirical system, the North American plant Arabidopsis lyrata. By crossing populations of varying range position and demographic history, and raising their offspring in gardens distributed across and beyond the species range, I found that populations with a history of small size due to past range expansion or rear-edge isolation suffered from increased expression of mutational load driven by genetic drift. This latter effect was even stronger under environmental stress, particularly under a warmer climate. Furthermore, populations at range edges with heightened past exposure to genetic drift had a reduced signature of climate adaptation. Finally, I compared A. lyrata and a novel species it gave rise to, A. arenicola, with a more northern distribution, in a climate chamber experiment. This new taxon diverged from A. lyrata in coping with a cool climate and strong reproductive isolation, most likely allowing it to to colonize subarctic regions and escape maladaptive gene flow. Results generally support the newer evolutionary theory about a predominant role of neutral evolution in contributing to geographic range limits, via genetic drift opposing purifying and directional selection. The study of sister taxa however shows that these constraints to evolution at range limits are not absolute, and can be broken

Epigenetic Mechanisms as Drivers of Environmental Responses in Stony Corals

The current pace of anthropogenic global change is imposing unprecedented conditions to biological systems. Coral reef ecosystems are particularly sensitive to the rapid increase in thermal anomalies and the changes in water chemistry caused by global change. However, although their decline has been documented worldwide, there are signs suggesting that stony corals harbor greater phenotypic plasticity than previously expected, sparking the interest in the study acquired non-genetic modifications (e.g., epigenome, microbiome) potentially increasing their resilience to global change, and constituting one of the main targets for intervention. Epigenetics constitutes an exciting frontier to understand how the environment influences the regulation of the expression of genetic information and modulates phenotypic variation. This has the potential to change the way we understand short-term acclimation and adaptation to a changing environment, aiding to improve predictive models of ecosystemic persistence under current and future climatic scenarios. However, while there is evidence supporting the idea of epigenetic mechanisms participating in rapid-response acclimatization, specific details about how this process is influenced by specific environmental conditions are lacking. In non-model organisms, we often lack information about the presence and functionality of some of these mechanisms, limiting the application of epigenetics in the study of ecosystem resilience in response to global change. This dissertation aims to elucidate how epigenetic mechanisms contribute to coral phenotypic responses to the effects of global change in the oceans. For that purpose, hypotheses about the presence and responsiveness of different epigenetic mechanisms in corals, its interaction with the genome and microbial communities, as well as its role modulating gene expression and phenotypic responses to diverse stressors were explored. Histone repertoires and/or full methylomes were characterized for the first time in the corals Acropora cervicornis and Montastraea cavernosa. The participation of these epigenetic mechanisms modulating responses to nutrient contamination, seasonal environmental change, thermal stress and acidification was demonstrated, providing evidence supporting its participation in intragenerational plasticity. A conserved seasonal methylation program was observed in A. cervicornis. This together with the strong influence of the genome over DNA methylation evidence its heritability and its potential to participate in intergenerational plasticit

Vectors of transmission: An early nicotine puff triggers a long-lasting microRNA molecular “memory� in C. elegans.

The prevalence of passive and active nicotine exposure among neonates, children and adolescents remains relatively high and varies among cultures and countries. Currently, there is ample evidence that a safe nicotine dose or level does not exist. For that, early exposure to any nicotine product is considered "catastrophic" to the children's future and wellbeing. The cycle of nicotine addiction, relapse, and enduring health disparities remains unpreventable. This is majorly due to the incomplete understanding of nicotine-induced molecular signaling and mechanisms. Recently, the role of epigenetics in the developmental origin of diseases has been highlighted. With this in mind, this study aims to identify and validate the roles of particular epigenetics factors known as microRNAs in nicotine-induced early and late-onset diseases. Our workflow started with post-embryonic exposure to nicotine and was followed by global microRNA profiling across three generations. Based on the transcriptomic findings, we identified 14 transgenerational miRNAs that can serve as biomarkers for early parental nicotine exposure. Bioinformatics analysis coupled with a literature review allowed us to focus on three factors: mpk-1, sir-2.1, miR-80 for further validation. We were intrigued in finding a potential relationship among these factors (MS80) in mediating nicotine induced early and late-onset diseases. For that, we performed reverse genetics assays and tested their contribution to nicotine-induced larval developmental delay, larval pharyngeal pumping inhibition, adult reproduction, adult mean lifespan, and adult germ line apoptosis. Our results showed that nicotine delayed development in an MS80 independent manner. Meanwhile, MS80 had a role in mediating nicotine-induced pharyngeal pumping inhibition. As for nicotine enduring effects, our data showed that post-embryonic nicotine exposure delayed the onset of reproduction without impacting fertility. This early exposure also had a negative effect on mean worm lifespan which was promoted by nicotine-induced upregulation of miR-80. In addition, our data also allowed us to infer that early nicotine exposure increases the ROS levels which trigger an organism level response that is mediated by MS80 to induce adult germ line apoptosis. Our study is the first to show the role of MS80 in intra and transgenerational inheritance of nicotine-induced effects. We also identified functional human homologs for cel-miR-80 in nicotine addiction and discussed the promising potential of manipulating MS80 to counteract nicotine-induced cellular and organismal damage during the early stages. Therefore, MS80 could be used as a prevention approach for nicotine-induced late-onset diseases