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The end of the nineteenth century was an exhilarating and revolutionary era for the flute. This period is the Second Golden Age of the flute, when players and teachers associated with the Paris Conservatory developed what would be considered the birth of the modern flute school. In addition, the founding

The end of the nineteenth century was an exhilarating and revolutionary era for the flute. This period is the Second Golden Age of the flute, when players and teachers associated with the Paris Conservatory developed what would be considered the birth of the modern flute school. In addition, the founding in 1871 of the Société Nationale de Musique by Camille Saint-Saëns (1835-1921) and Romain Bussine (1830-1899) made possible the promotion of contemporary French composers. The founding of the Société des Instruments à Vent by Paul Taffanel (1844-1908) in 1879 also invigorated a new era of chamber music for wind instruments. Within this groundbreaking environment, Mélanie Hélène Bonis (pen name Mel Bonis) entered the Paris Conservatory in 1876, under the tutelage of César Franck (1822-1890). Many flutists are dismayed by the scarcity of repertoire for the instrument in the Romantic and post-Romantic traditions; they make up for this absence by borrowing the violin sonatas of Gabriel Fauré (1845-1924) and Franck. The flute and piano works of Mel Bonis help to fill this void with music composed originally for flute. Bonis was a prolific composer with over 300 works to her credit, but her works for flute and piano have not been researched or professionally recorded in the United States before the present study. Although virtually unknown today in the American flute community, Bonis's music received much acclaim from her contemporaries and deserves a prominent place in the flutist's repertoire. After a brief biographical introduction, this document examines Mel Bonis's musical style and describes in detail her six works for flute and piano while also offering performance suggestions.
ContributorsDaum, Jenna Elyse (Author) / Buck, Elizabeth (Thesis advisor) / Holbrook, Amy (Committee member) / Micklich, Albie (Committee member) / Schuring, Martin (Committee member) / Norton, Kay (Committee member) / Arizona State University (Publisher)
Created2013
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The RAS/MAPK (RAS/Mitogen Activated Protein Kinase) pathway is a highly conserved, canonical signaling cascade that is highly involved in cellular growth and proliferation as well as cell migration. As such, it plays an important role in development, specifically in development of the nervous system. Activation of ERK is indispensable for

The RAS/MAPK (RAS/Mitogen Activated Protein Kinase) pathway is a highly conserved, canonical signaling cascade that is highly involved in cellular growth and proliferation as well as cell migration. As such, it plays an important role in development, specifically in development of the nervous system. Activation of ERK is indispensable for the differentiation of Embryonic Stem Cells (ESC) into neuronal precursors (Li z et al, 2006). ERK signaling has also shown to mediate Schwann cell myelination of the peripheral nervous system (PNS) as well as oligodendrocyte proliferation (Newbern et al, 2011). The class of developmental disorders that result in the dysregulation of RAS signaling are known as RASopathies. The molecular and cell-specific consequences of these various pathway mutations remain to be elucidated. While there is evidence for altered DNA transcription in RASopathies, there is little work examining the effects of the RASopathy-linked mutations on protein translation and post-translational modifications in vivo. RASopathies have phenotypic and molecular similarities to other disorders such as Fragile X Syndrome (FXS) and Tuberous Sclerosis (TSC) that show evidence of aberrant protein synthesis and affect related pathways. There are also well-defined downstream RAS pathway elements involved in translation. Additionally, aberrant corticospinal axon outgrowth has been observed in disease models of RASopathies (Xing et al, 2016). For these reasons, this present study examines a subset of proteins involved in translation and translational regulation in the context of RASopathy disease states. Results indicate that in both of the tested RASopathy model systems, there is altered mTOR expression. Additionally the loss of function model showed a decrease in rps6 activation. This data supports a role for the selective dysregulation of translational control elements in RASopathy models. This data also indicates that the primary candidate mechanism for control of altered translation in these modes is through the altered expression of mTOR.
ContributorsHilbert, Alexander Robert (Author) / Newbern, Jason (Thesis director) / Olive, M. Foster (Committee member) / Bjorklund, Reed (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2017-05