The interdependency between genomic variation and plant-pathogen evolution /

The interdependency between genomic variation and plant-pathogen evolution /

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Bibliographic Details
Author / Creator:	Karasov, Talia, author.
Imprint:	2015. Ann Arbor : ProQuest Dissertations & Theses, 2015
Description:	1 electronic resource (121 pages)
Language:	English
Format:	E-Resource Dissertations
Local Note:	School code: 0330
URL for this record:	http://pi.lib.uchicago.edu/1001/cat/bib/10773245

Hidden Bibliographic Details
Other authors / contributors:	University of Chicago. degree granting institution.
ISBN:	9781339079974
Notes:	Advisors: Joy Bergelson Committee members: Jean Greenberg; Richard Hudson; Howard Shuman. Dissertation Abstracts International, Volume: 77-02(E), Section: B. English
Summary:	Every eukaryotic organism is challenged by pathogens and has evolved to suppress pathogenic disease. Conversely, every pathogen studied to date has evolved to evade the defenses of its hosts. The signature of this perpetual evolution is clearly evident in the respective genomes--the genetic loci underlying this interaction are among the most, if not the most, variable loci. Genomic variability can give insight into the mechanisms of host-pathogen evolution, indicating that certain functions are essential and invariant, others rapidly undergoing turnover, and others lost easily without significant cost. Such genomic variation does more than provide a historical perspective on the evolutionary process, though. It also shapes the evolutionary process. This point is illustrated in the comparison of resistance durability in agriculture versus in natural plant populations. Resistance in agriculture, in which the host is of one or a few genotypes, is frequently defeated within a few years, while in naturally more genetically diverse plant populations, resistance persists for millions of years. In Chapter I, I review what is known of the relationship between genomic variability and plant-pathogen evolution. Diversity at plant resistance loci is generated by high rates of mutation, then maintained by selection for diversity. Because the maintenance of these resistance polymorphisms is crucial for durable resistance, significant work has gone into determining the conditions that maintain them. Current models explain the maintenance of resistance polymorphisms as the consequence of a tight coevolution of a single host with a single pathogen and frequency dependent selection. The majority of pathogens infect multiple host species, however making this model inapplicable to the majority of interactions. Another layer of complexity stems from the fact that pathogens do not infect hosts in isolation. Instead, they reside in environments occupied by dozens to millions of other microbes. These co-residing microbes influence the interaction between a host and its pathogen, and alter the disease outcome. The discrepancy between the models of host-pathogen coevolution and the reality of multiple hosts interacting with multiple pathogens begs the question of how resistance polymorphisms are maintained in plant populations. Chapter II is aimed at resolving this question by studying the maintenance of a resistance polymorphism in a system in which the pathogen does not specialize on the host. Pseudomonas syringae has hundreds of known host plants but is nonetheless a dominant pathogen in Arabidopsis thaliana populations in the Midwestern USA. Furthermore, resistance to P. syringae is heterogeneous, and several resistance loci in A. thaliana encode resistance alleles that have been maintained for millions of years. This heterogeneity allowed us to clone an interacting plant R-gene and pathogen effector pair, and then study the evolution of the identified resistance and virulence loci. Chapter III studies the evolution of P. syringae in its non-specific interaction with A. thaliana. Although P. syringae is a dominant pathogen in A. thaliana populations, resident strains are of low virulence on A. thaliana . How these strains dominate in A. thaliana populations is unclear. Our first tactic to answer this question was to use comparative genomics to identify genetic variants characteristic of P. syringae collected from A. thaliana. By sequencing the genomes of 18 strains of P. syringae isolated from A. thaliana populations, and comparing these genomes to 22 genomes of P. syringae isolated from different crop species, we identified a genomic island enriched in the A. thaliana strains. This island encodes a toxin active against a broad range of hosts, but also known to be suppressive of a eukaryotic microbes and Gram positive bacteria. We find that a P. syringae strain from A. thaliana is capable of suppressing the growth of a more virulent strain of P. syringae. These results suggest that P. syringae in A. thaliana populations could gain dominance in part through suppressing other members of the microbiota. While these strains are not the most virulent, they may be able to infect widely and outcompete the surrounding microbiome. Together, my studies point to the influence of the surrounding microbiome, surrounding hosts, and microbe-microbe interactions on the evolution of plant and pathogen. At this point in time, though, the understanding of the plant microbiome is largely descriptive. Ultimately, finding the determinants that dictate the outcome of host-pathogen evolution will require a more detailed understanding of the interactions of microbes within the plant microbiome. (Abstract shortened by UMI.).