Speakers

Nels Elde

University of Utah

Evolutionary innovations from biological collisions between microbes and their hosts

Biological collisions, for example virus infection of hosts, influence the fate of populations. These associations whether transient or seemingly permanent can provoke genetic conflicts of recurring, counteracting adaptations crucial for cell functions at the interfaces. I will discuss our work probing variation in primates and other mammals, which is revealing the far-reaching impact of selfish genetic elements on the origins and regulation of immune functions.

Jennifer Mandel, Assistant Professor

The University of Memphis

Department of Biological Sciences

Plant organellar genomes: heteroplasmy and its evolutionary consequences

The occurrence of within individual organellar genomic variation, i.e., heteroplasmy, has been described and studied since at least the 1970s. However, recent studies have revealed that heteroplasmy is more common and widespread than once thought. In particular, advances in sequencing technologies now allow for the study of entire organellar genomes within individuals as compared to one or a few genes. The occurrence of within individual genetic variation raises profound questions relating to evolutionary processes: can individuals (as collective populations of organellar genomes) evolve? How sexual are organellar genomes? Does heteroplasmy influence cytonuclear interactions? Is there genetic conflict among genomes within individuals? I will provide an overview of our recent work in this area using the natural plant system, wild carrot, for both plastid and mitochondrial genomes including population genetic and cytonuclear linkage disequilibrium consequences of heteroplasmy. Finally, I will demonstrate a prototype of a software that enables visualization of heteroplasmy candidates at the genome-wide level.

Amanda M. Larracuente, PhD

Assistant Professor

University of Rochester

Meiotic drive and satellite DNA in Drosophila melanogaster

Conflicts arise within genomes when genetic elements are selfish and fail to play by the rules. Meiotic drivers are selfish genetic elements found across a wide variety of taxa that cheat meiosis to bias their transmission to the next generation. We are interested in the evolution of drive systems, their mechanisms of cheating meiosis, and impacts on genome evolution. Our model system is an autosomal male meiotic driver found on the 2nd chromosome of Drosophila melanogaster called Segregation Distorter (SD). Males heterozygous for SD and sensitive wild type chromosomes transmit SD to >95% of their progeny, whereas female heterozygotes transmit SD fairly, to 50% of their progeny. SD is a sperm killer that targets large blocks of tandem satellite repeats (called Responder) for destruction through an unknown mechanism. We will discuss the impact of SD on the regulation and evolution of the Responder satellite, and how this may lend insight into mechanisms of meiotic drive.

Erin Kelleher

Assistant Professor

Department of Biology and Biochemistry

University of Houston

Host tolerance of invading transposable elements.

Transposable elements (TEs) are obligate genetic parasites that propagate in host genomes by replicating in germline nuclei, thereby ensuring representation in offspring genomes. This selfish replication not only produces deleterious insertions: in extreme cases, TE mobilization induces germline genome instability that prohibits the development of viable gametes. To avoid these fitness costs, animal and plant genomes are known to repress germline TE activity through small-RNA-mediated silencing. However, it remains unknown whether host genomes may also evolve tolerance of TEs, by desensitizing gametogenesis to TE activity. In part, this absence of research on tolerance reflects a lack of opportunity, as small-RNA- mediated repression masks variation in tolerance and evolves rapidly after a new TE invades.

We have exploited the recent the historical invasion of the Drosophila melanogaster genome by P- element DNA transposons in order to study tolerance of TE activity in the absence of repression. By performing genome-wide association on a panel of 1600 recombinant inbred lines that lack small-RNA- mediated silencing of P-elements, we have uncovered two major QTL that determine the tolerance of oogenesis to P-element mobilization. The first QTL harbors a well-studied regulator of oogenesis, suggesting that differences in the timing of gamete development could confer robustness to TE activity. By contrast, the second locus spans a centromere, and is explained by differential abundance of the pericentromeric satellite repeat Responder. Repetitive DNA could contribute to host tolerance of TE activity by determining sensitivity to DNA damage. Taken together, our results reveal that individuals differ in their response to germline TEs, and that these differences may reflect a range of developmental and genomic factors.

Harmit Singh Malik

Howard Hughes Medical Investigator

Member, Division of Basic Sciences

Fred Hutchinson Cancer Research Center

"Genetic conflicts shape meiosis and species"

Selfishness pervades biology. Nowhere is the impact of selfish genes felt more strongly than during or in the aftermath of meiosis in many organisms. Using case studies in fission yeast and Drosophila, I will present some of our latest and ongoing work on how selfish elements shape fundamental aspects of meiosis, and may even provide the initial schism to reproductively isolate species.

Sarah Anderson

Department of Plant and Microbial Biology, University of Minnesota

Department of Plant Sciences, University of California Davis

Department of Plant Pathology, University of Minnesota

Analysis of transposon expression provides insights into TE-genome conflicts in maize

Transposable elements (TEs) comprise a large portion of many eukaryotic genomes and are unique in their ability to replicate and move within genomes. The size of the maize genome is largely inflated by TE insertions, with the majority of these sequences derived from LTR retrotransposons, which require transcription for movement. RNA-directed DNA Methylation (RdDM), one mechanism plants have evolved to silence transposons to prevent movement, also relies on transcription to produce small RNAs which target DNA methylation machinery to TE sequences. Despite the abundance of RNA-seq datasets published in maize, TE expression has been under-assessed due to challenges associated with annotating, mapping, and assigning reads to the repetitive sequences common in TEs. We have utilized the new structural annotation of maize TEs in combination with a novel read assignment approach that accounts for these repetitive sequences to assess TE expression on a per-family basis across development and in mutants with subtle defects in DNA methylation. We find substantial variation in the proportion of the transcriptome derived from TEs across development, and in the specific families with varied expression across development and in mutants. Furthermore, similarities between TE families expressed in RdDM mutants and in nutritive endosperm support a role for interactions between RdDM and certain TE families during seed development.

William Driscoll

The Biotechnology Institute, University of Minnesota

Department of Ecology, Evolution and Behavior, University of Minnesota

Social conflict during the experimental evolution of multicellularity

Multicellular life requires extensive inter-cellular cooperation, yet competition within multicellular groups favors ‘selfish’ lineages that forego cooperation. This tradeoff gives rise to a conflict between the interests of individual cells and multicellular collectives, which is widely viewed as a barrier to the evolution of multicellular life. Current models implicate selection to minimize such conflicts to explain pervasive features of modern multicellular organisms, including development from a single-celled propagule. However, direct tests of such hypotheses are impossible due to the ancient origins of modern multicellular lineages such as plants and animals. We employ experimental evolution to study the transition to multicellularity from a single-celled ancestor in the yeast Kluyveromyces lactis. We find evidence that contrasting selection at the levels of individual cells and multicellular clusters maintains both selfish unicellular and cooperative multicellular genotypes for > 300 generations in all ten replicate populations. Interestingly, complex life cycles involving phenotypic switching between unicellular and multicellular life stages evolved independently in 2/10 experimental populations, providing an opportunity to directly test hypotheses for the origin and evolution of this pervasive feature of multicellular organisms.

William Harcombe

Department of Ecology, Evolution and Behavior, University of Minnesota

The Biotechnology Institute, University of Minnesota

Systems biology and eco-evolutionary feedbacks in microbial communities

Conflict and cooperation between bacterial species drive the composition and function of microbial communities. Stability of these emergent properties will be influenced by the degree to which species’ interactions are robust to genetic perturbations. We use genome-scale metabolic modeling to computationally analyze the impact of genetic changes when Escherichia coli and Salmonella enterica compete, or cooperate. We systematically knocked out in silico each reaction in the metabolic network of E. coli to construct all 2,583 mutant stoichiometric models. Then, using a recently developed multi-scale computational framework, we simulated the growth of each mutant E. coli in monoculture and in the presence of S. enterica. The type of interaction between the species was set by modulating the initial metabolites present in the environment. We found that both the species ratios and community productivity are most robust to genetic perturbation when the two species cooperate. Additionally, the number of mutations that have a substantial effect is lower when the species cooperate than when they are competing. These results highlight the utility of connecting metabolic mechanisms and studies of ecological stability. Cooperation and conflict alter the connection between genetic changes and properties that emerge at higher levels of biological organization.