Thesis (Ph. D.)--University of Washington, 2005. / Vita. Includes bibliographical references (leaves 89-102).

Thesis (M.S.) -- University of Texas Southwestern Medical Center at Dallas, 2005. / Not embargoed. Vita. Bibliography: 32-34.

Dissertation (Ph.D.) -- University of Texas Southwestern Medical Center at Dallas, 2006. / Embargoed. Vita. Bibliography: 99-115.

No description available.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2005. / Härtill 4 uppsatser.

Thesis (Ph.D.). / Written for the Dept. of Biology. Title from title page of PDF (viewed 2008/07/24). Includes bibliographical references.

Diss. (sammanfattning) Stockholm : Karol. inst., 2004. / Härtill 4 uppsatser.

Thesis (Ph. D.)--University of Washington, 2003. / Vita. Includes bibliographical references (leaves 147-158).

Early Drosophila development is a coordinated series of temporal and spatial events leading to specific localized gene expression. The maternally expressed gene Bicaudal-C (Bic-C) encodes a KH-domain RNA binding protein required in the developing oocyte for anterior-posterior patterning and follicle cell migration. The dominant heterozygous phenotype results in the development of embryos with bicaudal and head defects. A two-hybrid screen using BIC-C as "bait" identified the novel protein ANTIMEROS (ATMS) and the SH3-domain containing protein MILE END (MILE). / ATMS is highly conserved between humans and mice, its expression is almost entirely female-specific, and is limited to certain developmental stages. Mutant alleles for atms are able to dominantly enhance the phenotype of Bic-C heterozygotes confirming the Bic-C-atms interaction. Here I show that NOS mislocalization causes the trans-heterozygous phenotype, as introduction of a nos mutation strongly suppresses the bicaudal phenotype. nos transcripts show a hyper-polyandenylation in atms mutant ovaries, an indicator of translational activation, suggesting that ATMS and BIC-C function as translational repressors of nos through changes in its poly(A) tail length. / MILE, contains two highly conserved SH3 domains at the C-terminus. Experiments involving the analysis of mutant alleles and overexpression mile transgenic lines show that MILE is a negative regulator of both Torso and Egfr RTK signaling. Its not clear what functional role BIC-C may have with RTK signaling, but recent evidence suggests that posterior group gene expression influence terminal pole RTK signaling.

Thesis (Ph.D.). / Written for the Dept. of Biology. Title from title page of PDF (viewed 2008/02/12). Includes bibliographical references.