Les plantes sont des organismes sessiles qui présentent plusieurs caractéristiques leur permettant de s'adapter rapidement aux variations de conditions environnementales. En particulier la lumière représente une source d’information essentielle utilisée tout au long du cycle de vie pour ajuster leur développement. Cette thèse avait pour objet l’étude de l’impact des mécanismes chromatiniens dans la régulation de l’expression des gènes pouvant influencer l’adaptabilité des plantes aux variations de signaux lumineux, à travers deux types de réponses caractérisées par des échelles de temps différentes chez la plante modèle Arabidopsis thaliana. La première étude portait sur des processus chromatiniens dynamiques participant à la régulation de l’expression génique, et utilisait comme modèle le dé‐étiolement. La triméthylation de la lysine 4 de l’histone H3 (H3K4me3), une modification posttraductionnelle généralement associée à un état transcriptionnel actif a été plus particulièrement étudiée. Afin de mieux connaître cette voie, le gène SWD2‐Like b (S2Lb) a été caractérisé. Il s’agit d’un nouveau partenaire de complexes COMPASS‐like et un déterminant important du niveau global de H3K4me3. L’analyse de plantes dans lesquelles ce gène est inactivé a montré qu’un défaut d’accumulation de H3K4me3 corrélait avec une induction plus faible de gènes de réponse à la lumière au cours du dé‐étiolement. Ces résultats et les nouveaux outils obtenus constituent une base solide pour étudier l’influence de cette marque et des facteurs associés sur la modulation fine de l’expression génique en relation avec d’autres marques chromatiniennes. La seconde étude cherchait à déterminer l’impact des variations épigénétiques sur la capacité des plantes à induire un syndrome d’évitement de l’ombre, une réponse adaptative à des conditions de lumière défavorables produites par des compétiteurs. Un phénotypage à grande échelle dans deux conditions de lumière induisant des réponses opposées a été réalisé sur une population de lignées recombinantes inbred (epiRIL), dans laquelle les variations épigénétiques (méthylation de l’ADN) sont maximisées mais les variations de séquence nucléotidique sont minimes. Une plus grande variation phénotypique ainsi qu’une plus grande amplitude dans la capacité de réponse à l’ombre ont été observées dans la population epiRIL. De plus, une cartographie QTL a permis d’identifier une région au début du chromosome 3 spécifiquement associée à la réponse d’évitement de l’ombre. Bien qu’une caractérisation plus fine soit nécessaire, le locus impliqué pourrait correspondre à une première description de QTL « épigénétique » influençant la plasticité phénotypique des plantes en réponse à une variation des conditions de l’environnement. / Plants are sessile organisms that successfully face variations of the environment by taking advantage of their ability to adapt their physiology and morphology. In particular, light perception constitutes an essential source of information used throughout their life cycle to fine‐tune development. The work presented was aimed at studying the role of chromatin‐associated mechanisms on adaptive responses to light cues at two different timescales in the model plant species Arabidopsis thaliana. In a first part, the role of chromatin dynamics in the regulation of gene expression was assessed during de‐etiolation, a developmental transition of seedlings that is triggered upon the first perception of light. It focused mainly on the trimethylation of histone H3 at lysine 4 (H3K4me3), a post‐translational modification associated with transcriptionally active states. To gain new insights into this pathway, the SWD2‐Like b (S2Lb) gene was characterized and shown to represent a new partner of plant COMPASS‐like complexes and a major determinant of H3K4me3 in A.thaliana. Loss‐of‐function plant lines for the S2Lb gene revealed that a default in H3K4me3 enrichment correlates with impaired inducibility of several light‐responsive genes during de‐etiolation. The findings described here set the bases to investigating how this mark and the associated factors influence the modulation of gene expression in relation with other chromatin marks. The second part of this thesis was aimed at assessing the impact of epigenetic variation on the capacity of plants to undergo the shade‐avoidance response (SAR), an adaptive developmental response to unfavorable light conditions produced by competitors. A population of epigenetic Recombinant Inbred Lines (epiRILs), in which epigenetic variation (DNA cytosine methylation) is maximized and nucleotidic sequence variation is minimized, was used for a large‐scale phenotyping under two light conditions triggering opposite responses. The epiRIL population exhibited larger amplitude of phenotypic variation than wild‐type parents in each condition as well as a wider range of response to shade. A region at the beginning of chromosome 3 was identified by QTL mapping to specifically associate to the SAR. Though it remains to be characterized, the locus involved may represent a first “epigenetic QTL” influencing phenotypic plasticity in response to environmental changes.

In light of human-mediated environmental change, a fundamental goal for biologists is to determine which phenotypic characteristics enable some individuals, populations or species to be more adept at coping with such change, while rendering others more vulnerable. Studying ongoing range expansions provide a unique opportunity to address this question by allowing documentation of how novel environments shape phenotypic variation on ecological timescales. At range-edges, individuals are exposed to strong selective pressures and population genetic challenges (e.g. bottlenecks and/or founder effects), which make genetic adaptation difficult. Nevertheless, certain species, such as the house sparrow (Passer domesticus), seem to thrive in their introduced ranges, despite genetic challenges, resulting in a genetic paradox. Increasing evidence suggests that rapid phenotypic differentiation at range-edges may be facilitated by phenotypic plasticity among individuals. Further, a role for epigenetic mechanisms as molecular drivers of such plasticity—particularly in genetically depauperate populations—has recently garnered empirical support across a broad range of taxa. For my dissertation, I investigated the role of epigenetic mechanisms (i.e. DNA methylation) as a potential mediator of range expansion success in vertebrates. Specifically, I proposed that success or failure at range-edges may be underlain by variation in the capacity for epigenetically-mediated plasticity (i.e. epigenetic potential) and used extant literature on an inherently plastic and highly integrated physiological system (i.e. the HPA-axis) to support this hypothesis (Chapter I). I then tested these ideas empirically by examining the relative contribution of genetic and epigenetic variation to immunological variation in Kenyan house sparrows (Chapter II) and explored whether mediators of neural plasticity (i.e. BDNF) and epigenetic potential (i.e. DNA methyltransferases; DNMTs) varied among populations of Senegalese house sparrows, including the potential for covariation among BDNF, DNMTs and corticosterone (CORT) within individuals (Chapter III). Flexibility in the regulation of glucocorticoids (GCs) via the HPA-axis is crucial for survival at range-edges because (i) GCs act as integrators capable of coordinating diverse physiological and/or behavioral responses and (ii) the HPA-axis contains multiple regulatory checkpoints which may help to buffer organisms from maladaptive responses (via redundancy) while simultaneously allowing for the fine-tuning of phenotypic responses to future stressors contingent on current and past experiences. GC regulatory flexibility can be influenced by (and in some cases have an effect on) variation in the capacity for epigenetic mechanisms to regulate environmentally-induced phenotypic changes (i.e. epigenetic potential). DNMTs are capacitators of epigenetic change, thus provide one such example of how variation in epigenetic potential could arise via genetic (e.g. variation in coding regions of DNMT genes) and/or environmental (e.g. developmental programming of DNMT expression) factors. For my first chapter, I conducted a literature review to explore where within the HPA-axis epigenetic potential was most likely to occur and to demonstrate how such variation could promote/constrain range expansion success via its impact on GC regulatory flexibility. Results from the literature search revealed that within the HPA-axis, evidence for epigenetic regulation was highest for receptors, suggesting that variation in epigenetic potential of these targets may be most impactful for variation in GC regulatory flexibility. Using a physiological regulatory network (PRN) framework, I showed how variation in epigenetic potential can modify plasticity of PRN states by altering the regulatory relationships (e.g. connectivity) between HPA elements (e.g. GCs as central hubs) and other physiological/behavioral traits (e.g. subnetworks). As such, I portrayed how genetic forms of epigenetic potential can dictate the upper/lower limits of an individual’s homeostatic range, while environmental forms can act to further titrate GC regulatory flexibility through plasticity of PRN states or stabilization of PRN states. The concept of epigenetic potential in the HPA-axis demonstrates how plasticity at the molecular level can influence plasticity at the whole-organism level, which is likely to be important when coping with novel challenges at range-edges. Among the strongest of selective pressures faced by range-edge populations is exposure to parasites, particularly those with which individuals have little to no evolutionary history. Previous work from our lab on house sparrows in Kenya—site of an ongoing range expansion—revealed that range-edge birds had higher expression of Toll-like receptor 4 (TLR4—a microbial surveillance gene) than birds from the range-core. Moreover, extensive inter-individual variation in genome-wide DNA methylation was found among Kenyan house sparrows, including an inverse relationship between epigenetic diversity and genetic diversity across populations. For my second chapter, I investigated whether these two observations were related, asking whether and how DNA methylation and/or genetic variation within the putative promoter of the TLR4 gene contributed to variation in TLR4 expression. I found that DNA methylation status at CpG1, which varied from only ~73-100%, was a strong predictor of TLR4 expression within individuals. Interestingly, other studies have shown that similar magnitudes of variation in DNA methylation of TLR4 can result in differences in the susceptibility/resistance to bacterial pathogens, thus, it’s plausible that the variation we observed could have functional implications for host defense. I also discovered four genetically linked polymorphisms within the TLR4 promoter that grouped into two general genotypes. We revealed a trend that suggests that genotype differences may influence TLR4 expression, confirmation of which may be possible with increased representation from individuals with the rare genotype. Given that DNA methylation did not vary systematically among populations and evidence for extensive genetic admixture at the Kenyan range-edge, it seems likely that individual-level factors (e.g. genotype, early-life experience, infection history, etc.) may be more predictive of variation in DNA methylation of TLR4 than population-level processes. Coping with novel challenges often requires coordinated adjustments to environmentally-sensitive (i.e. plastic) traits. Findings from my first dissertation chapter, as well as previous research from the Martin lab, revealed that CORT regulation, exploratory behavior and epigenetic mechanisms likely contribute to range expansion success in house sparrows. Within the hippocampus, mediators of neural plasticity such as brain-derived neurotrophic factor (BDNF), play a unique role in the bidirectional regulation of CORT and exploratory behavior, with important implications for hippocampal-dependent learning and memory. Moreover, evidence suggests that the regulatory capacity of CORT and BDNF to influence learning and memory relies heavily on the catalytic capacity of epigenetic modification enzymes—including DNA methyltransferases (DNMTs). For my third chapter, I explored whether previous CORT/behavioral/epigenetic patterns contributed to population-level differences in hippocampal BDNF expression and/or hippocampal expression of DNMTs (mediators of epigenetic potential), including potential covariation among CORT, BDNF and DNMTs within individuals. I collected house sparrows from three populations in Senegal—site of an ongoing range expansion—and measured stressor-induced CORT, hippocampal BDNF, DNMT1 and DNMT3a expression. Given the potential importance of neural plasticity and epigenetic potential for coping with novel challenges, I hypothesized that BDNF and DNMT expression would be highest at the range-edge, while positive covariation would occur between CORT, BDNF and/or DNMT expression within individuals. I found that intermediate levels of CORT resulted in the highest BDNF expression within individuals, suggesting that interactions between CORT and BDNF are likely important for balancing homeostatic and progressive (e.g. cognitive) changes within the hippocampus in response to environmental challenges. I also found that CORT positively covaried with DNMT1 expression in one, but not both, range-edge populations, while the reverse was true at the range-core. These findings suggest that in newly established population, CORT may promote epigenetic potential, allowing for rapid and fine-tuned organism-wide responses to novel stressors, while at the range-core, where stressors are presumably less novel, CORT may inhibit epigenetic potential as a means of diverting resources away from cognitive processes and towards maintaining homeostasis. Altogether, my dissertation has demonstrated how inherently plastic sub-organismal level traits (i.e. molecular, physiological, and neurological) may interact and contribute to range expansion success in an introduced bird. Specifically, my research has not only shown that epigenetic variation can influence an ecologically-relevant trait, but also that variation in the regulatory potential of epigenetic mechanisms can be mediated by intrinsic and extrinsic factors. These studies have expanded our understanding about how epigenetic mechanisms act as regulatory mediators of plasticity at the molecular level and can influence (and be influenced by) variation at multiple phenotypic levels, with implications for whole-organism performance in natural populations. I hope that my work contributes to the field of ecological epigenetics by providing the framework for epigenetic potential as an additional tool for assessing how epigenetic processes contribute to phenotypic outcomes in the face of rapid environmental change.

<p>This thesis deals with the evolution of individuals within a species adapted to utilize specific resources, i.e. resource polymorphism. Although a well-known phenomenon, the understanding of the mechanisms behind is not complete. Considering the ruling theories, resource polymorphism is suggested to depend on severe competition for resources, the presence of open niches to be occupied leading to a reduction in competition, and disruptive selection where generalist are out-competed due trade-offs in foraging efficiency for different prey. In order to study resource polymorphism, I have used fish as the animal group in focus and the methods I have used range over laboratory experiments, field experiments, literature surveys and theoretical modelling.</p><p>In my work, I have showed that different resource use induces different body shapes and that the rate of change is dependent of the encounter rate of different resources. The induced body changes partly led to increased foraging efficiency but surprisingly I did not find any trade-offs due to specialization. However, when studying predation risk in relation to resource polymorphism, my studies point towards that resource use and predation risk may act as balancing factors in such a way that disruptive selection can take place.</p><p>My work also shows that population feedbacks have to be explored when considering the evolution of resource polymorphism. In pond and field experiments, I found that changes in resource densities affected the actual resource use despite previous adaptations to certain resources. By performing a literature survey, I found that cannibalism indirectly by its effect on population dynamics seems to facilitate the evolution of resource polymorphism. Modelling a size-structured population, I found that resource dynamics were stabilized, and the relative availability of different resources was levelled out due to cannibalism.</p><p>Taken together, my studies strongly suggest that to understand the development of resource polymorphism in consumer populations, future studies have to include the effect of a dynamic environment both with respect to resources and predators.</p>

<p>A central goal of evolutionary biology is to understand the processes responsible for morphological, genetic and behavioural differentiation between sexes and among geographically distinct populations. Perhaps the most significant processes are genetic drift, natural selection, phenotypic plasticity and sexual selection. The main aim of this thesis was to investigate differentiation among individuals and populations of the sex-role reversed pipefish (<i>Syngnathus typhle</i>) and, consequently, determine which processes may be responsible for emerging patterns. This unique species is characterised by males predominately choosing amongst displaying females.</p><p>In this thesis I revealed, on a microgeographic scale, morphological differentiation without genetic divergence among populations. Interestingly, females differed in size whereas the males did not. For females in this sex-role reversed species, the costs of expressing a plastic phenotype may be outweighed by the potential gains from greater survivorship, higher fecundity or increased mating success. Thus, females gain the ability to make themselves as conspicuous and attractive to males as possible in the specific environment they are living. Moreover, behavioural experiments, which focussed on describing “personalities”, reproductive investment strategies, and mate-sampling tactics, also indicated that males as well as females had the behavioural plasticity required to adjust to the environment in which they live. To this end, using video playbacks as experimental stimuli may be especially rewarding in this species.</p><p>Overall, the studies in this thesis acknowledge the ability of species to fine-tune their phenotype to maximise fitness and, therefore, highlight the importance of considering patterns of differentiation in an environment-specific context. </p>

Whether microevolutionary processes can explain macroevolutionary patterns has long been a matter of contentious debate. The debate has persisted largely because of the challenging task of connecting microevolutionary theory, which examines population-level phenomena on the generation scale, to data collected across larger spatial and temporal scales. My dissertation research broadly examines phenotypic evolution across multiple scales by connecting microevolutionary theory to macroevolutionary phenomena such as speciation and large-scale phenotypic change. In particular, I focus on the so-called "paradox of stasis"; which wrestles with the apparent conflict between frequently-observed cases of rapid evolution on short timescales and the frequent appearance of stasis in the fossil record. I attempt to link micro and macroevolution by using the theoretical framework of evolutionary quantitative genetics for modeling the effects of drift and selection. My four dissertation chapters examine four different systems (1) connecting quantitative genetic models of sexual selection to speciation (2) connecting microevolutionary and macroevolutionary body size data across scales of time (3) using phylogenetic comparative methods and quantitative genetic models to examine the evolution of a classic example of stasis, mammalian body temperature and (4) finally, using multi-locus phylogeography to understand the evolutionary processes that contribute to the diversification of a widespread snake across broad spatial scales. In chapter 2, I demonstrate that genetic drift combined with sexual selection can promotes speciation and diversification of male ornaments. Furthermore, I demonstrate that drift promotes the evolution of elaborate ornaments even when preferences are costly. In chapter 3, I combine data from microevolutionary field studies, the fossil record, and phylogenetic comparative data into a single analytical framework to resolve apparent conflicts between micro and macroevolutionary patterns. To do so, I compiled and analyzed the largest database of phenotypic divergence data in existence. I demonstrate that patterns of stasis persist until a million-year threshold, after which divergence begins to accumulate in a time-dependent manner. This pattern is best fit with a hierarchical model that describes evolution as occurring in bursts on the million-year timescale, but that allows for rapid, but bounded, evolution on short timescales. In chapter 4, I demonstrate that mammalian body temperature -- which has been previously presented as a classic example of stasis -- does in fact evolve extensively across the mammalian radiation (albeit slowly). Furthermore, I show that mammalian body temperature evolves in response to changing environmental conditions. Finally, I evaluate the role that genetic constraints play in the apparent slowness of body temperature evolution. In chapter 5, I examine a well-studied empirical system of garter snakes in which a strong signature of stabilizing selection has been found for phenotypic traits. Using multiple mitochondrial and nuclear loci, I show that introgression is rampant between species, and dynamic patterns of range expansion, contraction, and introgression among clades have led to a complex pattern of genetic variation. This structure of genetic variation underscores the need to examine range-wide processes for generating phenotypic divergence across clades. Overall, these chapters suggest that apparent disconnects between microevolutionary processes and macroevolutionary patterns could be explained by the scaling of population-level theory over large spatial and temporal scales. / Graduation date: 2013 / Access restricted to the OSU Community at author's request from Oct. 25, 2012 - Oct. 25, 2013

Thesis (M.S.)--Oregon State University, 2007. / Printout. Includes bibliographical references (leaves 81-84). Also available on the World Wide Web.

Thesis (Ph. D.)--Ohio State University, 2006. / Title from first page of PDF file. Includes bibliographical references (p. 413-447).

Marine mammals comprise a paraphyletic group of species whose current abundance and distribution has been greatly shaped by past environmental changes and anthropogenic impacts. This thesis describes molecular ecological approaches to answer questions regarding habitat requirements, genetic differentiation, and life-history trade-offs in three species of marine mammals.  The annual sea-ice dynamics of the Arctic may have large effects on the abundance and distribution of Arctic species such as the pagophilic ringed seal (Pusa hispida). Paper I describes and applies a simple molecular method for isolating and characterizing a relatively large set of single nucleotide polymorphisms (SNPs) in the ringed seal. These SNPs have been genotyped in a yet-to-be-analysed dataset which will form the basis in an assessment of the micro-evolutionary effects of annual sea-ice dynamics on ringed seal.  Current management efforts directed towards the North Atlantic fin whale (Balaenoptera physalus) are hampered by an unclear understanding of population structure. Paper II investigates the DNA basis for the high levels of genetic differentiation that have been reported in allozyme studies of the North Atlantic fin whale. We find that additional processes (at the organismal level) may have contributed to shaping the phenotype of the underlying allozyme variation. Telomeres may potentially serve as markers for determining the chronological and biological age of animals where other means of inference is difficult. Paper III describes the application and evaluation of four qPCR assays for telomere length estimation in humpback whales (Megaptera novaeangliae), finding that reliable telomere length estimates require extensive quality control. Paper IV applies the best performing qPCR assay to test whether telomeres may provide a method for genetic determination of chronological age in whales and concludes that the biological and experimental variation in telomere length estimates is too large to determine age with sufficient resolution. Finally, because telomere length and rate of telomere loss also may be affected by other cellular and organismal processes, such as resource allocation among self-maintenance mechanisms, growth and reproduction, Paper V describes the correlations between individual telomere length and rate of telomere loss, and sex, maturity status and female reproductive output. We found that the costs of reproduction in terms of telomere loss are higher in mature humpback whales than in juveniles; that reproductive costs are higher in males than females; and that differences among females tend to correlate with reproductive output. / At the time of doctoral defence the following papers were unpublished and had a status as follows: Paper 2: Submitted; Paper 3:Submitted; Paper 4: Manuscript; Paper 5:Manuscript

Phenotypic plasticity is the ability of a genotype to express different phenotypes in different environments. Despite its common occurrence, few have investigated differences in plasticity between populations, the selection pressures responsible for it, and costs and constraints associated with it. In this thesis, I investigated this by studying local adaptation and phenotypic plasticity in populations of the common frog Rana temporaria, inhibiting islands with different pool types (temporary, permanent or both). The tadpoles develop in these pools, and have to finish metamorphosis before the pool dries out. I found that the tadpoles were locally adapted both in development time and in phenotypic plasticity of development time. Tadpoles from islands with temporary pools had a genetically shorter development time than tadpoles from islands with permanent pools. The population differentiation in development time, estimated as QST, was larger than the population differentiation in neutral molecular markers (FST), which suggest that divergent selection among the populations is responsible for the differentiation. Moreover, tadpoles from islands with more variation in pool drying regimes had higher phenotypic plasticity in development time than tadpoles from islands with only one pool type present. Interestingly, increased migration among populations did not select for increased plasticity, rather it was the local environmental variation that was important. This adaptation has occurred over a short time scale, as the islands are less than 300 generations old. In temporary pools, it is adaptive to finish development before the pool dries out. This could be achieved by entering the metamorphosis at a smaller size, as a smaller size takes shorter time to reach. However, I found that there is a minimum threshold size below which tadpoles’ cannot enter metamorphosis, and that there had been no evolution of this threshold size in populations living in temporary environments. That suggests that this developmental threshold is tightly linked to physiological constraints in the developmental process. Despite their expected importance as constrains on the evolution of plasticity, costs of plasticity are often not found in nature.  However, theories of why they are absent have not been tested empirically. In this thesis, I show that fitness costs of phenotypic plasticity are only found in populations with genotypes expressing high levels of phenotypic plasticity, while in populations with low-plastic genotypes, I find costs of not being plastic. This suggests that costs of plasticity increase with increased level of plasticity in the population, and that might be a reason why costs of plasticity are hard to detect.

This thesis deals with the evolution of individuals within a species adapted to utilize specific resources, i.e. resource polymorphism. Although a well-known phenomenon, the understanding of the mechanisms behind is not complete. Considering the ruling theories, resource polymorphism is suggested to depend on severe competition for resources, the presence of open niches to be occupied leading to a reduction in competition, and disruptive selection where generalist are out-competed due trade-offs in foraging efficiency for different prey. In order to study resource polymorphism, I have used fish as the animal group in focus and the methods I have used range over laboratory experiments, field experiments, literature surveys and theoretical modelling. In my work, I have showed that different resource use induces different body shapes and that the rate of change is dependent of the encounter rate of different resources. The induced body changes partly led to increased foraging efficiency but surprisingly I did not find any trade-offs due to specialization. However, when studying predation risk in relation to resource polymorphism, my studies point towards that resource use and predation risk may act as balancing factors in such a way that disruptive selection can take place. My work also shows that population feedbacks have to be explored when considering the evolution of resource polymorphism. In pond and field experiments, I found that changes in resource densities affected the actual resource use despite previous adaptations to certain resources. By performing a literature survey, I found that cannibalism indirectly by its effect on population dynamics seems to facilitate the evolution of resource polymorphism. Modelling a size-structured population, I found that resource dynamics were stabilized, and the relative availability of different resources was levelled out due to cannibalism. Taken together, my studies strongly suggest that to understand the development of resource polymorphism in consumer populations, future studies have to include the effect of a dynamic environment both with respect to resources and predators.