Diss. (sammanfattning) Uppsala : Uppsala universitet, 2009. / Härtill 5 uppsatser.

Thesis (M.S.)--Michigan State University. Interdepartmental Biological Sciences, 2008. / Title from PDF t.p. (viewed on Aug. 3, 2009) Includes bibliographical references (p.166-168). Also issued in print.

Thesis (Doctoral)--Ruprecht-Karls-Universität in Heidelberg, 1982.

Thesis (M.A.)--Bowling Green State University, 2006. / Document formatted into pages; contains v, 45 p. Includes bibliographical references.

Thesis (Ph. D.)--University of Texas at Austin, 2007. / Vita. Includes bibliographical references.

abstract: Skeletal diseases related to reduced bone strength, like osteoporosis, vary in frequency and severity among human populations due in part to underlying genetic differentiation. With >600 disease-associated mutations (DAMs), COL1a1, which encodes the primary subunit of type I collagen, the main structural protein in bone, is most commonly associated with this phenotypic variation. Although numerous studies have explored genotype-phenotype relationships with COL1a1, surprisingly, no study has undertaken an evolutionary approach to determine how changes in constraint over time can be modeled to help predict bone-related disease factors. Here, molecular population and comparative species genetic analyses were conducted to characterize the evolutionary history of COL1a1. First, nucleotide and protein sequences of COL1a1 in 14 taxa representing ~450 million years of vertebrate evolution were used to investigate constraint across gene regions. Protein residues of historically high conservation are significantly correlated with disease severity today, providing a highly accurate model for disease prediction, yet interestingly, intron composition also exhibits high conservation suggesting strong historical purifying selection. Second, a human population genetic analysis of 192 COL1a1 nucleotide sequences representing 10 ethnically and geographically diverse samples was conducted. This random sample of the population shows surprisingly high numbers of amino acid polymorphisms (albeit rare in frequency), suggesting that not all protein variants today are highly deleterious. Further, an unusual haplotype structure was identified across populations, but which is only associated with noncoding variation in the 5' region of COL1a1 where gene expression alteration is most likely. Finally, a population genetic analysis of 40 chimpanzee COL1a1 sequences shows no amino acid polymorphism, yet does reveal an unusual haplotype structure with significantly extended linkage disequilibrium >30 kilobases away, as well as a surprisingly common exon duplication that is generally highly deleterious in humans. Altogether, these analyses indicate a history of temporally and spatially varying purifying selection on not only coding, but noncoding COL1a1 regions that is also reflected in population differentiation. In contrast to clinical studies, this approach reveals potentially functional variation, which in future analyses could explain the observed bone strength variation not only seen within humans, but other closely related primates. / Dissertation/Thesis / Ph.D. Biology 2010

'Culture' is defined as information, such as knowledge, beliefs, skills, attitudes or values, that is passed from individual to individual via social (or cultural) transmission and expressed in behaviour or artifacts. 'Cultural evolution' holds that this cultural inheritance system is governed by the same Darwinian processes as gene-based biological evolution. In Part A of this thesis it is argued that as compelling a case can now be made for a Darwinian theory of cultural evolution as Darwin himself presented in The Origin Of Species for biological evolution, If culture does indeed evolve, then it follows that the structure of a science of cultural evolution should broadly resemble that of the science of biological evolution. Hence Part A concludes by outlining a unified science of cultural evolution based on the sub-disciplines of evolutionary biology. Parts B and C comprise original empirical and theoretical work constituting two branches of this science of cultural evolution. Part B describes a series of experiments testing for a number of hypothesised biases in cultural transmission. Evidence was found for a 'social bias' that acts to promote information concerning third-party social relationships over equivalent non-social information, and a 'hierarchical bias' that acts to transform knowledge of everyday events from low-level actions into higher-level goals. Three other hypothesised biases concerning status, anthropomorphism and neoteny were not supported, although each gave rise to potential, future work using this methodology. Part C presents a theoretical investigation into the coevolution of the genetic bases of human mating behaviour and culturally inherited folk beliefs regarding paternity. Gene-culture coevolution and agent-based models suggested that beliefs in 'partible paternity' (that more than one man can father a child) create a new more polygamous form of society compared with beliefs in singular paternity (that only one man can father a child).

The frequency with which individuals do not develop their third molars, or wisdom teeth, is increasing worldwide. This current topic of human evolution is relevant to the research of anthropologists, geneticists, dentists, and other researchers involved in the study of human dentition. Many explanations have been offered to account for the prevalence of molar agenesis including, evolutionary, environmental, and genetic theories. The purpose of this research project is to determine the frequency of third molar agenesis and investigate the relationship between third molar agenesis and maxillomandibular jaw dimensions in a sample of orthodontic patients. This research tests the hypotheses that: H1: Individuals with agenesis of third molars will be significantly different in maxillomandibular dimensions than individuals without agenesis, H2: The agenesis of maxillary third molars is associated with the anteroposterior dimensions of the maxilla, and H3: The agenesis of mandibular third molars is not associated with the anteroposterior dimensions of the mandible. Therefore, the null hypothesis for this research is H0: An individual’s sex and the presence/absence of the third molar are independent. The sample for this research project includes 543 individuals from the University of New Mexico’s Maxwell Museum of Anthropology Orthodontics Case File System. This study examines panoramic radiographs of the dentition for each individual to ascertain whether any of the third molars was congenitally absent, and records the cephalometric measurements for each case for statistical analysis. This study uses descriptive statistics, crosstabulation analysis, chi-square tests, non-parametric Kruskal-Wallis tests, and logistic regression analysis to investigate any associations between third molar agenesis and maxillomandibular jaw dimensions. The results show that Native Americans (9.2%), Hispanics (8.46%), and European Americans (8.37%) have a higher frequency of third molar agenesis than African Americans (0.17%) and Asians (0.17%). This finding is consistent with the published body of work on third molar agenesis, in spite of the small sample sizes for diverse populations. There is a significant difference in the number of molars missing among groups. For the present study, based on crosstabulation analysis, most individuals are missing two molars (34.9%), followed by one absent (31.7%), a lack of four molars (25.3%), and finally a lack of 3 molars (7.9%). Individuals with third molar agenesis are nearly twice as likely to be missing a molar from the mandible (62.8%) than the maxilla (36.9%). This study uses crosstabulation analysis, chi-square analysis, non-parametric Kruskal-Wallis tests, and logistic regression analysis to assess the association between third molar agenesis and measurements of the dental arcade. This study did not find an association between an individual’s maxillomandibular dimensions and third molar agenesis. Therefore, this study did not find support for the hypothesis that individuals with third molar agenesis would have smaller maxillomandibular dimensions than individuals without agenesis. Based on the findings of this study, an association between the size of an individual’s mouth and third molar agenesis does not exist in the sample analyzed. Third molar agenesis is not occurring due to a lack of room in the mouth, but possibly results from heredity. Therefore, it may be more likely that genetic variation influences third molar agenesis, rather than an evolutionary change in diet.

The continuing rise of antibiotic resistance is threatening a return to the world of pre-antibiotic medicine. Multi-drug resistant pathogens are already claiming lives and causing economic losses in developing and developed countries alike. We need, therefore, to understand what allows resistant strains to spread; what makes them evolutionarily competitive in and amongst other strains and species. The majority of laboratory studies of antibiotic resistance focus on simple growth in liquid culture. By contrast, microbes commonly grow as surface-associated communities, in which interactions between neighbouring cells have strong consequences for competition and evolution. My first goal was to understand how growth in such environments affects the success of a resistant strain. By competing an antibiotic resistant and susceptible strain of the pathogenic bacterium Pseudomonas aeruginosa, I found that growth in dense colonies on agar allowed a resistant strain to protect susceptible strains, to the extent that the susceptible strain may even prevail under antibiotic treatment. This effect was specific to a cooperative mechanism of antibiotic resistance, however; a β-lactamase enzyme that digests the antibiotics surrounding a resistant cell. A further, unexpected reason that susceptible cells could prevail was that they elongate under antibiotic treatment, allowing them to push shorter resistant cells aside in the competition for the growing edge of a colony. My work suggests that the rise of cooperative resistance mechanisms should be more easily suppressed than for non-social mechanisms. However, one major strategy to overcome antibiotic resistance is the use of antibiotic-adjuvants, drugs which inhibit a mechanism of antibiotic resistance. It is not clear if these adjuvants will tend to suppress or promote cooperative resistance mechanisms. I performed experiments to test the effects of inhibitory adjuvants on cooperative resistance. These revealed that the effects of adjuvants are varied. In liquid culture, an adjuvant inhibited resistance evolution, while, in colony experiments, it promoted resistance evolution by removing the cross protection of susceptible strains. Given the complexity and importance of antibiotic adjuvants, I developed an eco-evolutionary model to dissect these complexities associated with the combination of interacting microbial and molecular species. As in my experiments, the models identified conditions where an inhibitory adjuvant can increase selection for resistance. However, the theory also identifies scenarios for which adjuvants will delay resistance evolution by shutting down the associated evolutionary pathway. Broadening the modelling framework to include the stochastic effects of rare mutation, I found that early administration of adjuvant inhibitors can be a powerful way to suppress the emergence of antibiotic resistance. Microbial interactions are complex and affected by the growth environment. My thesis underlines that the study of antibiotic resistance will benefit from greater consideration of how bacteria interact and, more broadly, how their ecology and evolution determine the rise, or fall, of resistance.

In this thesis, I investigated the role of parental care in evolution. Parents provide the environment in which offspring develop and therefore have a large influence on their offspring's phenotypes, and so are in prime position to influence evolutionary processes. I used an experimental approach, and focused on the burying beetle, Nicrophorus vespilloides. The burying beetle is a perfect system for this question: they exhibit elaborate biparental care which is correlated with rapid speciation in the Nicrophorus genus. I started with a thorough exploration of burying beetle ecology and how the guild structure and interspecific competition in local populations can shape phenotypic evolution of my focal species, N. vespilloides. Interspecific competition shapes how the carrion niche is partitioned, which feeds back onto the evolution of body size within Nicrophorus reducing competition. The evolution of parental care in this genus likely facilitated its adaptive radiation, as parental care is linked with body size, both within and across species. But to what extent does the ecology shape the production and maintenance of phenotypic and genetic variation? I then use a quantitative genetic approach to show that body size and development time of N. vespilloides shows no additive genetic variation. Evolution of these fitness related traits can only occur through maternal effects or sibling effects. I tested this prediction by mimicking the radiation of the burying beetles by imposing my own selection on body size when parents could care for their offspring and when they could not. The presence of post-hatching parental care dramatically changed how populations responded to selection, through a combination of cooperation between parents and offspring, and cooperation between offspring. As well as shaping the evolutionary potential of populations, an experimental change in parental care can induce new selective forces, favouring adaptive novelties for the new social environment. Larvae evolving without parental care evolved disproportionately larger mandibles when small to better adapt them to a life without care. Much is known about the evolution of parental care across the animal kingdom, but what happens next: are the burying beetles a "one-off"? I compiled data across the arthropods comparing clades that exhibit post-hatching parental care with their sister clades and show that clades with care are more species rich. While the mechanism may not be the same as with Nicrophorus, I discussed other potential mechanisms that may be at play in the role of parents in evolution.