The aim of this thesis is to find out the process carried out by many people to achieve a solo role for the tuba. It also explains which individuals people helped the development of the instrument so as how different composers have contributed to the music field and especially to the evolution and growth of the tuba in the last century. In the musical part, the thesis talks about different standard tuba pieces and their importance.

Concertino for Tuba, Winds, and Percussion is a work for solo tuba and an ensemble consisting of two flutes, two oboes, two clarinets, bass clarinet, bassoon, four horns, two trumpets, two trombones, bass trombone, and three percussionists. The percussionists play small, medium, and large suspended cymbals, triangle, tam tam, metal wind chimes, five tom toms, snare drum, tenor drum, bass drum, two sets of two timbales, five temple blocks, maracas, glockenspiel, vibraphone, chimes, xylophone, marimba, and five timpani. The three movements of the work follow the arrangement of the standard concerto format (fast-slow-fast). The lengths of the movements are approximately four minutes and fifteen seconds, two minutes and twenty-five seconds, and four minutes and ten seconds respectively. The total duration of Concertino is about eleven minutes.

The focus of this project is to examine current tuba and euphonium applied lessons syllabi and to create a New Orleans brass band curriculum supplement to enhance those existing courses. Through the addition of new method books, exercises, historical texts and articles, listening assignments, and performing experiences, collegiate tuba and euphonium students will be able to apply the knowledge gained in core academic music courses, such as music theory and music history, to mastering a new style of music. Emphasis has been placed on learning chord progressions, stylizations, and how to improvise and walk a bass line.

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Several pathogenic bacteria, including Listeria monocytogenes, use an F-actin-dependent motility process to spread between mammalian cells. Actin ‘comet tails’ propel Lm through the cytoplasm, resulting in bacteria-containing membrane protrusions that are internalized by neighboring cells. The mechanism by which L. monocytogenes overcomes cortical membrane tension to generate protrusions is unknown. In this work, I identify bacterial and host proteins that directly regulate the formation of protrusions. First, I show that efficient cell-cell spread in polarized epithelial cells requires the secreted Lm virulence protein, InlC. I next identify the mammalian adaptor protein Tuba as a ligand of InlC. InlC binds to a C-terminal SH3 domain in Tuba, which normally engages the human actin regulatory protein N-WASP. InlC promotes protrusion formation by inhibiting Tuba and N-WASP function, most likely by impairing binding of N-WASP to the Tuba SH3 domain. Tuba and N-WASP are known to control the structure of apical junctions in epithelial cells [1]. I demonstrate that, by inhibiting Tuba and N-WASP, InlC transforms taut apical cell-cell junctions into structures with a “slack” morphology. Experiments with Myosin II inhibitors indicate that InlC-mediated perturbation of cell junctions accounts for the role of this bacterial protein in protrusion formation. Collectively, my results suggest that InlC enhances bacterial dissemination by relieving cortical tension in apical junctions, thereby enhancing the ability of motile bacteria to deform the plasma membrane into protrusions to allow their spread into neighbouring cells.

Several pathogenic bacteria, including Listeria monocytogenes, use an F-actin-dependent motility process to spread between mammalian cells. Actin ‘comet tails’ propel Lm through the cytoplasm, resulting in bacteria-containing membrane protrusions that are internalized by neighboring cells. The mechanism by which L. monocytogenes overcomes cortical membrane tension to generate protrusions is unknown. In this work, I identify bacterial and host proteins that directly regulate the formation of protrusions. First, I show that efficient cell-cell spread in polarized epithelial cells requires the secreted Lm virulence protein, InlC. I next identify the mammalian adaptor protein Tuba as a ligand of InlC. InlC binds to a C-terminal SH3 domain in Tuba, which normally engages the human actin regulatory protein N-WASP. InlC promotes protrusion formation by inhibiting Tuba and N-WASP function, most likely by impairing binding of N-WASP to the Tuba SH3 domain. Tuba and N-WASP are known to control the structure of apical junctions in epithelial cells [1]. I demonstrate that, by inhibiting Tuba and N-WASP, InlC transforms taut apical cell-cell junctions into structures with a “slack” morphology. Experiments with Myosin II inhibitors indicate that InlC-mediated perturbation of cell junctions accounts for the role of this bacterial protein in protrusion formation. Collectively, my results suggest that InlC enhances bacterial dissemination by relieving cortical tension in apical junctions, thereby enhancing the ability of motile bacteria to deform the plasma membrane into protrusions to allow their spread into neighbouring cells.

Thesis (D.M.A.)--University of Texas at Austin, 2003. / Supervisor: Russell Pinkston. Vita. Includes bibliographical references. Available also from UMI Company.

Thesis (D.M.A.)--University of North Texas, 2006. / System requirements: Adobe Acrobat Reader. Accompanied by 4 recitals, recorded June 25, 2001, Nov. 18, 2002, Mar. 21, 2005, and Feb. 20, 2006. Includes bibliographical references (p. 44-48).

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