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- All Subjects: Evolution
Description
Resource transfers can confer many adaptive benefits such as specialization, helping genetically related individuals, future compensation, and risk-pooling. Need-based transfers are a risk-pooling mechanism in which partners mitigate unpredictable losses by transferring resources based on need. Need-based transfers are likely to be most useful for resources that are necessary and unpredictable because being unable to reliably obtain essential resources would be devastating. However, need-based transfers make people vulnerable to two types of exploitation: a person can be greedy by asking when not in need and a person with a surplus of resources can be stingy by not giving to someone in need. Previous research suggests that people might have cognitive mechanisms for detecting greediness and stinginess, which would serve to protect against exploitation by cheaters. This study investigated whether resources that are necessary and unpredictable are most likely to trigger greediness and stinginess detection mechanisms. Participants saw four types of rules. One rule could be violated through greedy behavior, another through stingy behavior, another by not paying a debt, and another was a descriptive rule that could be violated by not finding one type of resource near another type of resource. Then, participants saw information about events relating to one of the rules and indicated whether the rule in question could have been violated. Consistent with past research, participants were better at detecting greediness, stinginess, and debts not paid than at detecting violations of a descriptive rule. However, contrary to my predictions, the necessity and unpredictability of resources did not impact people’s ability to detect greediness and stinginess. The lack of support for my hypothesis might be because the benefits of detecting greediness and stinginess might outweigh the costs even for situations in which need-based transfer rules are unlikely to apply, because people might be able to consciously activate their greediness and stinginess mechanisms even for resources that would not naturally trigger them, or because of methodological limitations.
ContributorsMunoz Castro, Andres (Author) / Aktipis, Athena (Thesis advisor) / Hruschka, Daniel (Committee member) / Neuberg, Steven (Committee member) / Arizona State University (Publisher)
Created2019
Description
Cooperative cellular phenotypes are universal across multicellular life. Division of labor, regulated proliferation, and controlled cell death are essential in the maintenance of a multicellular body. Breakdowns in these cooperative phenotypes are foundational in understanding the initiation and progression of neoplastic diseases, such as cancer. Cooperative cellular phenotypes are straightforward to characterize in extant species but the selective pressures that drove their emergence at the transition(s) to multicellularity have yet to be fully characterized. Here we seek to understand how a dynamic environment shaped the emergence of two mechanisms of regulated cell survival: apoptosis and senescence. We developed an agent-based model to test the time to extinction or stability in each of these phenotypes across three levels of stochastic environments.
ContributorsDanesh, Dafna (Author) / Maley, Carlo (Thesis director) / Aktipis, Athena (Committee member) / Compton, Zachary (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2021-12
Description
Evolutionary theory provides a rich framework for understanding cancer dynamics across scales of biological organization. The field of cancer evolution has largely been divided into two domains, comparative oncology - the study of cancer across the tree of life, and tumor evolution. This work provides a theoretical framework to unify these subfields with the intent that an understanding of the evolutionary dynamics driving cancer risk at one scale can inform the understanding of the dynamics on another scale. The evolution of multicellular life and the unique vulnerabilities in the cellular mechanisms that underpin it explain the ubiquity of cancer prevalence across the tree of life. The breakdown in cellular cooperation and communication that were required for multicellular life define the hallmarks of cancer. As divergent life histories drove speciation events, it similarly drove divergences in fundamental cancer risk across species. An understanding of the impact that species’ life history theory has on the underlying network of multicellular cooperation and somatic evolution allows for robust predictions on cross-species cancer risk. A large-scale veterinary cancer database is utilized to validate many of the predictions on cancer risk made from life history evolution. Changing scales to the cellular level, it lays predictions on the fate of somatic mutations and the fitness benefits they confer to neoplastic cells compared to their healthy counterparts. The cancer hallmarks, far more than just a way to unify the many seemingly unique pathologies defined as cancer, is a powerful toolset to understand how specific mutations may change the fitness of somatic cells throughout carcinogenesis and tumor progression. Alongside highlighting the significant advances in evolutionary approaches to cancer across scales, this work provides a lucid confirmation that an understanding of both scales provides the most complete portrait of evolutionary cancer dynamics.
ContributorsCompton, Zachary Taylor (Author) / Maley, Carlo C. (Thesis advisor) / Aktipis, Athena (Committee member) / Buetow, Kenneth (Committee member) / Nedelcu, Aurora (Committee member) / Compton, Carolyn (Committee member) / Arizona State University (Publisher)
Created2023