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In species with highly heteromorphic sex chromosomes, the degradation of one of the sex chromosomes can result in unequal gene expression between the sexes (e.g., between XX females and XY males) and between the sex chromosomes and the autosomes. Dosage compensation is a process whereby genes on the sex chromosomes

In species with highly heteromorphic sex chromosomes, the degradation of one of the sex chromosomes can result in unequal gene expression between the sexes (e.g., between XX females and XY males) and between the sex chromosomes and the autosomes. Dosage compensation is a process whereby genes on the sex chromosomes achieve equal gene expression which prevents deleterious side effects from having too much or too little expression of genes on sex chromsomes. The green anole is part of a group of species that recently underwent an adaptive radiation. The green anole has XX/XY sex determination, but the content of the X chromosome and its evolution have not been described. Given its status as a model species, better understanding the green anole genome could reveal insights into other species. Genomic analyses are crucial for a comprehensive picture of sex chromosome differentiation and dosage compensation, in addition to understanding speciation.

In order to address this, multiple comparative genomics and bioinformatics analyses were conducted to elucidate patterns of evolution in the green anole and across multiple anole species. Comparative genomics analyses were used to infer additional X-linked loci in the green anole, RNAseq data from male and female samples were anayzed to quantify patterns of sex-biased gene expression across the genome, and the extent of dosage compensation on the anole X chromosome was characterized, providing evidence that the sex chromosomes in the green anole are dosage compensated.

In addition, X-linked genes have a lower ratio of nonsynonymous to synonymous substitution rates than the autosomes when compared to other Anolis species, and pairwise rates of evolution in genes across the anole genome were analyzed. To conduct this analysis a new pipeline was created for filtering alignments and performing batch calculations for whole genome coding sequences. This pipeline has been made publicly available.
ContributorsRupp, Shawn Michael (Author) / Wilson Sayres, Melissa A (Thesis advisor) / Kusumi, Kenro (Committee member) / DeNardo, Dale (Committee member) / Arizona State University (Publisher)
Created2016
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Description
In wild birds, the stress response can inhibit the activity of the innate immune system, which serves as the first line of defense against pathogens. By elucidating the mechanisms which regulate the interaction between stress and innate immunity, researchers may be able to predict when birds experience increased susceptibility to

In wild birds, the stress response can inhibit the activity of the innate immune system, which serves as the first line of defense against pathogens. By elucidating the mechanisms which regulate the interaction between stress and innate immunity, researchers may be able to predict when birds experience increased susceptibility to infections and can target specific mediators to mitigate stress-induced suppression of innate immune activity. Such elucidation is especially important for urban birds, such as the House Sparrow (Passer domesticus), because these birds experience higher pathogen prevalence and transmission when compared to birds in rural regions. I investigated the role of corticosterone (CORT) in stress-induced suppression of two measures of innate immune activity (complement- and natural antibody-mediated activity) in male House Sparrows. Corticosterone, the primary avian glucocorticoid, is elevated during the stress response and high levels of this hormone induce effects through the activation of cytosolic and membrane-bound glucocorticoid receptors (GR). My results demonstrate that CORT is necessary and sufficient for stress-induced suppression of complement-mediated activity, and that this relationship is consistent between years. Corticosterone, however, does not inhibit complement-mediated activity through cytosolic GR, and additional research is needed to confirm the involvement of membrane-bound GR. The role of CORT in stress-induced inhibition of natural antibody-mediated activity, however, remains puzzling. Stress-induced elevation of CORT can suppress natural antibody-mediated activity through the activation of cytosolic GR, but the necessity of this mechanism varies inter-annually. In other words, both CORT-dependent and CORT-independent mechanisms may inhibit natural antibody-mediated activity during stress in certain years, but the causes of this inter-annual variation are not known. Previous studies have indicated that changes in the pathogen environment or food availability can alter regulation of innate immunity, but further research is needed to test these hypotheses. Overall, my dissertation demonstrates that stress inhibits innate immunity through several mechanisms, but environmental pressures may influence this inhibitory relationship.
ContributorsGao, Sisi (Author) / Deviche, Pierre (Thesis advisor) / DeNardo, Dale (Committee member) / McGraw, Kevin (Committee member) / Orchinik, Miles (Committee member) / Moore, Michael C. (Committee member) / Arizona State University (Publisher)
Created2017
Description
The regulation of gene expression, timing, location, and amount of a given project, ultimately affects the cellular structure and function. More broadly, gene regulation is the basis for cellular differentiation and development. However, gene expression is not uniform among individuals and varies greatly between genetic males and females. Males are

The regulation of gene expression, timing, location, and amount of a given project, ultimately affects the cellular structure and function. More broadly, gene regulation is the basis for cellular differentiation and development. However, gene expression is not uniform among individuals and varies greatly between genetic males and females. Males are hemizygous for the X chromosome, whereas females have two X chromosome copies. Contributing to the sex differences in gene expression between males and females are the sex chromosomes, X and Y. Gene expression differences on the autosomes and the X chromosome between males (46, XY) and females (46, XX) may help inform on the mechanisms of sex differences in human health and disease. For example, XX females are more likely to suffer from autoimmune diseases, and genetic XY males are more likely to develop cancer. Characterizing sex-specific gene expression among human tissues will help inform the molecular mechanisms driving sex differences in human health and disease. This dissertation covers a range of critical aspects in gene expression. In chapter 1, I will introduce a method to align RNA-Seq reads to a sex chromosome complement informed reference genome that considers the X and Y chromosomes' shared evolutionary history. Using this approach, I show that more genes are called as sex differentially expressed in several human adult tissues compared to a default reference alignment. In chapter 2, I characterize gene expression in an early formed tissue, the human placenta. The placenta is the DNA of the developing fetus and is typically XY male or XX female. There are well-documented sex differences in pregnancy complications, yet, surprisingly, there is no observable sex difference in expression of innate immune genes, suggesting expression of these genes is conserved. In chapter 3, I investigate gene expression in breast cancer cell lines. Cancer arises in part due to the disruption of gene expression. Here I show 19 tumor suppressor genes become upregulated in response to a synthetic protein treatment. In chapter 4, I discuss gene and allele-specific expression in Nasonia jewel wasp. Chapter 4 is a replication and extension study and discusses the importance of reproducibility.
ContributorsOlney, Kimberly (Author) / Wilson, Melissa A (Thesis advisor) / Hinde, Katherine (Committee member) / Buetow, Kenneth (Committee member) / Banovich, Nicholas (Committee member) / Arizona State University (Publisher)
Created2021