Electronic Thesis and Dissertation Repository

Degree

Master of Science

Program

Biology

Supervisor

Dr. Anthony Percival-Smith

Abstract

Fushi tarazu (FTZ) is a pair-rule protein important for the development of the anterior-posterior axis during embryogenesis. Low level ectopic expression of FTZΔ148-206 from a Tubulin α1 promoter, but not FTZ1-410 (full length FTZ), results in the anti-ftz phenotype in developing Drosophila melanogaster larvae, indicating that FTZΔ148-206 is a hyperactive FTZ protein. Through deletion analysis, using a high level ectopic expression system and assaying survivorship, I narrowed the location of the negative regulatory domain (NRD) to the 178-206 amino acid region of FTZ. Mutations that mimic both constitutive phosphorylation and dephosphorylation in the NRD revealed that phosphorylation doesn’t control the activity of the NRD. When the NRD was deleted along with three important functional domains, the homeodomain, terminal tyrosines and the FTZ-F1 binding site, I found that both the FTZ-F1 binding site and terminal tyrosines were required for hyperactive activity and that the NRD may regulate homeodomain activity.


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