Year of Award

2018

Document Type

Dissertation - Campus Access Only

Degree Type

Doctor of Philosophy (PhD)

Degree Name

Organismal Biology, Ecology, and Evolution

Department or School/College

Division of Biological Sciences

Committee Chair

John P. McCutcheon

Commitee Members

Douglas J. Emlen, Lila Fishman, Jeffrey M. Good, Scott R. Miller

Abstract

Symbioses in which a bacterium resides solely within another organism have arguably been the most important interspecies interactions in the history of life on Earth – bacterial endosymbionts facilitated the evolution of both all eukaryotic and plant life, and have played important roles in many other organisms. There is a consistent pattern of reduction in genome size and content as free-living bacteria enter into long-term endosymbiosis, as has happened in organelles and many nutritional endosymbionts of insects. The evolutionary pressures driving these changes, though, are less well understood. Endosymbiont genome reduction may be beneficial to the endosymbionts, but since endosymbionts are susceptible to inefficient selection it has been hypothesized that mutation and genetic drift play an important role in the process of endosymbiont genome reduction. This hypothesis for endosymbiont genome evolution does not suggest that natural selection plays no role in endosymbiont evolution. Instead it implies that genome reduction in long-term endosymbionts is not primarily the result of symbiont-level positive selection, but rather reflects the host’s struggle to limit mutational meltdown of its endosymbionts. The aim of this dissertation is to understand the evolutionary forces that have allowed the genome of one endosymbiont of cicadas, Hodgkinia, to become incredibly complex. Hodgkinia produces the same nutrients for all cicadas in which it is present. Despite this functional stability, Hodgkinia’s genome has undergone severe instability. Rather than a single circular chromosome, as is typical of bacteria, Hodgkinia’s “genome” in some cicadas has split into many lineages that each contain some subset of the ancestral gene set.

To understand how and why Hodgkinia has become so complex, ideally one would test the fitness of Hodgkinia and cicadas with varying levels of Hodgkinia complexity. Unfortunately, these tests are not plausible given the long cicada lifecycles and the inability of Hodgkinia to be cultured in the lab. Therefore, I focus on ways that Hodgkinia’s evolution can be understood from an evolutionary perspective. After providing some background information on symbiosis and Hodgkinia’s genome, I compare Hodgkinia in several different closely related cicada species to show that Hodgkinia evolution occurs idiosyncratically as the cicada species themselves diverge. I then show one way in which the host responds to the increase in Hodgkinia complexity is to transmit more Hodgkinia cells to its offspring, negating one of its mechanisms of host- symbiont conflict mediation. Finally I show how changes in important host life history traits can increase the likelihood of Hodgkinia becoming more complex, without it being beneficial for host or symbiont. While I cannot definitively pinpoint the causes of Hodgkinia’s incredible complexity at this time, my research provides considerable circumstantial evidence that mutation and genetic drift have played an important role in driving increases in Hodgkinia genome complexity.

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© Copyright 2018 Matthew A. Campbell