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In partial fulfillment of the requirements for the degree of
Doctor of Philosophy in Biology
in the
School of Biological Sciences
Wen Xu
will defend her dissertation
Nematodes Adapt Using Yin-yang Isoforms of a NURF Subunit
Tuesday, March 19th, 2019
9:00 AM
Engineered Biosystems Building (EEB)
Children's Healthcare of Atlanta Seminar Room
Thesis Advisor:
Dr. Patrick T. McGrath
School of Biological Sciences
Georgia Institute of Technology
Committee members:
Dr. Jeffrey T. Streelman
School of Biological Sciences
Georgia Institute of Technology
Dr. Greg Gibson
School of Biological Sciences
Georgia Institute of Technology
Dr. Annalise B. Paaby
School of Biological Sciences
Georgia Institute of Technology
Dr. David Katz
Department of Cell Biology
Emory University
Summary
Convergent or parallel evolution is the repeated evolution of the same genotype in independent populations in response to similar environmental changes. A growing number of examples of parallel evolution are accumulating in the literature (e.g. cis-regulatory changes in the shavenbaby developmental regulator in Drosophila species result in dorsal cuticle hair loss (Sucena & Stern 2000), repeated selection on the Eda TNF ligand causes stickleback low-plated phenotype (Colosimo et al. 2005), and deletion of chemoreceptor genes contribute to the insensitivity to a specific pheromone in Caenorhabditis species (McGrath et al. 2011)). In this dissertation, I will discuss my studies of how Caenorhabditis elegans strains adapt to laboratory environments. I will describe how two C. elegans strains N2 and LSJ2, who share a common ancestor but have evolved independently in laboratory conditions have increased fitness in their respective environment. I will show that part of adaptation in the LSJ2 strain is caused by a 60 bp deletion in nurf-1 gene, a subunit of nucleosome remodeling factor NURF. Next, I will describe my finding about that adaptation of the N2 lineage is partially caused by a SNV in the 2nd intron of nurf-1. This work suggests that nurf-1 is a common target of evolution in response to laboratory growth. Finally, I will describe my work to understand why nurf-1 might be targeted, which I propose is due to the antagonistic function (here I refer as Yin-yang) of two major nurf-1 isoforms on the sexual fate during gametogenesis. My doctoral thesis study advance our understanding of how nucleosome remodeling factor may work and that isoform-level study of complex genes is feasible and necessary.
