Thesis (Ph. D.)--Indiana University, Dept. of Biology, 2007. / Title from dissertation home page (viewed Sept. 29, 2008). Source: Dissertation Abstracts International, Volume: 69-02, Section: B, page: 0815. Adviser: Wayne C. Forrester.

Thesis (Ph.D.)--Indiana University, Dept. of Biology, 2008. / Title from home page (viewed on Jul 23, 2009). Source: Dissertation Abstracts International, Volume: 69-10, Section: B, page: 5933.

Thesis (Ph.D.)--University of California, San Francisco, 2008. / Source: Dissertation Abstracts International, Volume: 69-09, Section: B, page: 5225. Adviser: Alexander Johnson.

Thesis (Ph.D.)--University of California, Berkeley, 2007. / (UMI)AAI3275354. Source: Dissertation Abstracts International, Volume: 68-08, Section: B, page: 4969. Adviser: N. Louise Glass.

Thesis (Ph.D.)--University of California, San Francisco, 2009. / Source: Dissertation Abstracts International, Volume: 71-02, Section: B, page: . Adviser: Brian L. Black.

Thesis (Ph.D.)--Indiana University, Dept. of Biology, 2009. / Title from PDF t.p. (viewed on Jul 20, 2010). Source: Dissertation Abstracts International, Volume: 70-12, Section: B, page: 7374. Adviser: Scott D. Michaels.

Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2009. / Source: Dissertation Abstracts International, Volume: 70-06, Section: B, page: 3318. Adviser: Lawrence B. Schook. Includes bibliographical references (leaves 75-90) Available on microfilm from Pro Quest Information and Learning.

<p> Many adult stem cells are characterized by prolonged quiescence, promoted by cues from their niche. Upon tissue damage, a coordinated transition to the activated state is necessary for successful repair. Non-physiological breaks in quiescence often lead to stem cell depletion and impaired tissue restoration. Here, I identify cadherin-mediated adhesion and signaling between muscle stem cells (satellite cells; SCs) and their myofiber niche as a mechanism that orchestrates the quiescence-to-activation transition. Conditional removal of N-cadherin and M-cadherin in mice leads to a break in SC quiescence with long-term expansion of a regeneration-proficient SC pool. These SCs have an incomplete disruption of the myofiber-SC adhesive junction, and maintain niche residence and cell polarity, yet show properties of SCs in a state of transition from quiescence towards full activation. Among these properties is nuclear localization of b- catenin, which is necessary for this phenotype. These findings are consistent with the conclusion that injury-induced perturbation of niche adhesive junctions is a first step in the quiescence-to-activation transition. </p><p>

Thesis (Ph.D.)--Brown University, 2008. / Vita. Advisor : Kristi A. Wharton. Includes bibliographical references.

<p> Gene expression pathways exhibit many "twists and turns," with theoretically numerous ways in which the pathways can be regulated by both negative and positive feedback mechanisms. A key step in gene expression is RNA maturation (RNA processing), which in the bacterial cell can be accomplished through RNA binding and enzymatic cleavages. The well-characterized bacterial protein Ribonuclease III (RNase III), is a conserved, double-stranded(ds)-specific ribonuclease. In the gram-negative bacterium <i>Escherichia coli</i>, RNase III catalytic activity is subject to both positive and negative regulation. A recent study has indicated that an <i>E. coli</i> protein, YmdB, may negatively regulate RNase III catalytic activity. It has been proposed that YmdB inhibition of RNase III may be part of an adaptive, post-transcriptional physiological response to cellular stress. </p><p> In <i>E. coli</i>, the model organism in this study, YmdB protein is encoded by the single <i>ymdB</i> gene, and has a predicted molecular mass of &sim;18.8 kDa. YmdB has been classified as a macrodomain protein, as it exhibits a characteristic fold that specifically provides an ADP-ribose (ADPR) binding site. While YmdB can bind ADPR with good affinity, there may be additional ligands for the binding site. Thus, YmdB protein may interact with other components in the cell, which in turn could modulate the interaction of YmdB with RNase III. </p><p> In previous research conducted within the Nicholson laboratory at Temple University, affinity-purified <i>Escherchia coli(Ec)</i> YmdB and <i> Aquifex aeolicus (Aa)</i> YmdB were found to exhibit ribonucleolytic activity. This observation initiated the long-term goal of learning how YmdB regulates RNase III, and how the ribonucleolytic activity of YmdB may be involved in this process. The specific goal of this thesis project was to further characterize the ribonucleolytic activity of <i>Ec-</i>YmdB through site-specific mutational analysis. Mutations were introduced into a proposed adenine-binding pocket previously identified by crystallography and by molecular modeling. The adenine-binding pocket is a region within the macrodomain fold where ADP-ribose could bind. The mutations were examined for their effect on <i>Ec-</i>YmdB cleavage of a model RNA, R1.1. The results of this study will contribute to the development of a model describing how the ribonucleolytic activity of YmdB is regulated.</p><p>