Thesis (Ph.D.)--University of California, San Francisco, 2009. / Source: Dissertation Abstracts International, Volume: 70-06, Section: B, page: 3311. Adviser: Marc I. Diamond.

Thesis (Ph.D.)--University of California, San Francisco, 2009. / Source: Dissertation Abstracts International, Volume: 70-06, Section: B, page: 3337. Advisers: Graeme W. Davis; Robert H. Edwards.

Thesis (Ph.D.)--University of California, San Francisco, 2009. / Source: Dissertation Abstracts International, Volume: 70-04, Section: B, page: 2108. Adviser: Roger Nicoll.

<p> Life exists in complex environments, requiring organisms to have adaptive developmental strategies in order to survive. The nematode <i>Caenorhabditis elegans</i> has evolved a developmental polyphenism whereby it may arrest development in the dauer diapause state when environmental conditions are not suitable for reproductive growth. The relative simplicity of the <i>C. elegans</i> nervous system, together with its robust molecular and genetic tool set, make it an ideal system in which to study how environmental stimuli are sensed and integrated to drive developmental plasticity. Food availability, temperature and the presence of dauer pheromone each inform the dauer fate decision. I have taken molecular and genetic approaches to study the mechanism by which pheromone signals are transduced by <i> C. elegans</i> sensory neurons and also to understand how food and pheromone signals are integrated to drive an adaptive developmental choice. I have identified roles in dauer formation for the protein scaffold QUI-1, the rough endoplasmic reticulum protein MACO-1 and a putative Tau tubulin kinase, which we have named PHD-1. I have also identified a critical role for the calcium/calmodulin-dependent protein kinase 1 CMK-1 in encoding the food signal and integrating this information in the dauer fate decision. Furthermore, these studies have led to the previously unrecognized roles for the ASH and AWC neurons in the regulation of dauer formation.</p>

<p> In both mice and humans, males and females exhibit differences in behavior and response to neurological and psychological diseases that are linked to the cortex and hippocampus. The perinatal exposure of males to testosterone secreted by the testes creates alterations in neural structures and behaviors that can persist throughout their lives; however, the molecular mechanisms that underlie the actions of sex steroids to produce these lasting changes are still unclear. Given that regulation of gene expression is a primary mechanism whereby sex steroids exert changes to an organism, I sought to identify genes expressed at different levels between the sexes in the cortex and hippocampus and to determine the effect of testosterone on expression of these genes. Using gene expression microarrays and RT-qPCR, I identified genes that are differentially expressed between the sexes in the neonatal mouse cortex and hippocampus; however, whether perinatal testosterone is regulating these differences remains unclear.</p>

<p> Neural stem cells (NSCs) participate in a delicate balance between maintaining cellular identity through self-renewal and differentiating into myriad neural cell types. Understanding exactly how epigenetic mechanisms regulate this balance and the subsequent differentiation process in adult mammalian brain is an ongoing effort. We conducted a genome wide association study to elucidate the roles of genes in neural progenitors regulated by chromatin modifications. Neural progenitors of baboon SVZ were examined using ChIP-Seq (chromatin immuneprecipitation followed by deep sequencing) to determine genome wide gene targets of three histone modifications: H3K4me3, H3K9me3 and H3K27me3. Our data suggest these chromatin marks are associated with genes responsible for cellular organization and morphology, proliferation and survival, neuron development. Taken together these processes suggest histone modifications, predominantly H3K27me3, are responsible for maintenance of NSC identity. Our findings also highlight the importance of using in vivo models to study the SVZ neurogenic niche and compel examination of the H3K27me3 catalyzing enzyme EZH2. In the future, the role of EZH2 will be determined by EZH2 conditional knockout and overexpression models, using stereotaxic injections of novel Cre protein and lentiviral delivery of EZH2, respectively.</p>

Thesis (Ph.D.)--University of California, San Francisco, 2006. / Source: Dissertation Abstracts International, Volume: 68-01, Section: B, page: 0119. Adviser: Arturo Alvarez-Buylla.

Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2007. / Source: Dissertation Abstracts International, Volume: 68-06, Section: B, page: 3581. Advisers: Esmail Meisami; Philip Best. Includes bibliographical references (leaves 98-117) Available on microfilm from Pro Quest Information and Learning.

Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2007. / Source: Dissertation Abstracts International, Volume: 69-02, Section: B, page: 0859. Adviser: Michael Glaser. Includes bibliographical references (leaves 137-158) Available on microfilm from Pro Quest Information and Learning.

Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2007. / Source: Dissertation Abstracts International, Volume: 68-11, Section: B, page: 7124. Adviser: Martha Gillette. Includes bibliographical references. Available on microfilm from Pro Quest Information and Learning.