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- All Subjects: Evolution
- Creators: Arizona State University. School of Life Sciences. Center for Biology and Society. Embryo Project Encyclopedia.
- Creators: School of Molecular Sciences
One of the largest problems facing modern medicine is drug resistance. Many classes of drugs can be rendered ineffective if their target is able to acquire beneficial mutations. While this is an excellent showcase of the power of evolution, it necessitates the development of increasingly stronger drugs to combat resistant pathogens. Not only is this strategy costly and time consuming, it is also unsustainable. To contend with this problem, many multi-drug treatment strategies are being explored. Previous studies have shown that resistance to some drug combinations is not possible, for example, resistance to a common antifungal drug, fluconazole, seems impossible in the presence of radicicol. We believe that in order to understand the viability of multi-drug strategies in combating drug resistance, we must understand the full spectrum of resistance mutations that an organism can develop, not just the most common ones. It is possible that rare mutations exist that are resistant to both drugs. Knowing the frequency of such mutations is important for making predictions about how problematic they will be when multi-drug strategies are used to treat human disease. This experiment aims to expand on previous research on the evolution of drug resistance in S. cerevisiae by using molecular barcodes to track ~100,000 evolving lineages simultaneously. The barcoded cells were evolved with serial transfers for seven weeks (200 generations) in three concentrations of the antifungal Fluconazole, three concentrations of the Hsp90 inhibitor Radicicol, and in four combinations of Fluconazole and Radicicol. Sequencing data was used to track barcode frequencies over the course of the evolution, allowing us to observe resistant lineages as they rise and quantify differences in resistance evolution across the different conditions. We were able to successfully observe over 100,000 replicates simultaneously, revealing many adaptive lineages in all conditions. Our results also show clear differences across drug concentrations and combinations, with the highest drug concentrations exhibiting distinct behaviors.
Cancer rates vary between people, between cultures, and between tissue types, driven by clinically relevant distinctions in the risk factors that lead to different cancer types. Despite the importance of cancer location in human health, little is known about tissue-specific cancers in non-human animals. We can gain significant insight into how evolutionary history has shaped mechanisms of cancer suppression by examining how life history traits impact cancer susceptibility across species. Here, we perform multi-level analysis to test how species-level life history strategies are associated with differences in neoplasia prevalence, and apply this to mammary neoplasia within mammals. We propose that the same patterns of cancer prevalence that have been reported across species will be maintained at the tissue-specific level. We used a combination of factor analysis and phylogenetic regression on 13 life history traits across 90 mammalian species to determine the correlation between a life history trait and how it relates to mammary neoplasia prevalence. The factor analysis presented ways to calculate quantifiable underlying factors that contribute to covariance of entangled life history variables. A greater risk of mammary neoplasia was found to be correlated most significantly with shorter gestation length. With this analysis, a framework is provided for how different life history modalities can influence cancer vulnerability. Additionally, statistical methods developed for this project present a framework for future comparative oncology studies and have the potential for many diverse applications.
The sex of a reptile embryo partly results from the production of sex hormones during development, and one process to produce those hormones depends on the temperature of the embryo's environment. The production of sex hormones can result solely from genetics or from genetics in combination with the influence of environmental factors. In genotypic sex determination, also called genetic or chromosomal sex determination, an organism's genes determine which hormones are produced. Non-genetic sex determination occurs when the sex of an organism can be altered during a sensitive period of development due to external factors such as temperature, humidity, or social interactions. Temperature-dependent sex determination (TSD), where the temperature of the embryo's environment influences its sex development, is a widespread non-genetic process of sex determination among vertebrates, including reptiles. All crocodilians, most turtles, many fish, and some lizards exhibit TSD.
Wilhelm Johannsen in Denmark first proposed the distinction between genotype and phenotype in the study of heredity in 1909. This distinction is between the hereditary dispositions of organisms (their genotypes) and the ways in which those dispositions manifest themselves in the physical characteristics of those organisms (their phenotypes). This distinction was an outgrowth of Johannsen's experiments concerning heritable variation in plants, and it influenced his pure line theory of heredity. While the meaning and significance of the genotype-phenotype distinction has been a topic of debate-among Johannsen's contemporaries, later biological theorists, and historians of science-many consider the distinction one of the conceptual pillars of twentieth century genetics. Moreover some have used it to characterize the relationships between studies of development, genetics, and evolution.
Tooth enamel contains relics of its formation process, in the form of microstructures, which indicate the incremental way in which it forms. These microstructures, called cross-striations and striae of Retzius, develop as enamel-forming cells called ameloblasts, whcih cyclically deposit enamel on developing teeth in accordance with two different biological clocks. Cross-striations result from a twenty-four hour cycle, called a Circadian rhythm, in the enamel deposition process, while striae of Retzius have a longer periodicity. Unlike other tissues, enamel does not remodel after it forms, leaving those microstructures intact after deposition. Cross-striations and striae of Retzius thus provide evidence of the timing and processes of tooth development, and they indicate how organisms in a lineage differently grow and develop across generations. Researchers have examined those microstructures to investigate human evolution.