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Modifiers of P-element-dependent silencing in Drosophila melanogaster.
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- Author / Creator
- McCracken, Allen TM
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If all cells in a multicellular organism contain exactly the same genetic information, the question arises of how tissue types with distinct gene expression profiles are formed and maintained over the life of the organism. These different temporal and spatial gene expression patterns are thought to be built by activating and repressing proteins and RNAs to create self-perpetuating chromatin states. Identifying these components is the first and fundamental step in understanding this type of control of gene expression, and is the focus of this thesis. My model system centers on P{lacW}ciDplac , a white (w+) transgene insert on chromosome 4 of
Drosophila melanogaster. P{lacW}ciDplac is a previously characterized enhancer trap of ciD that should be sensitive to many of the proteins that regulate ci during development. Normally, the white gene within P{lacW}ciDplac is expressed throughout the adult eye and presents a
uniform red eye phenotype. However, the presence of other P elements results in stochastic silencing of the w+ of this transgene and a variegated phenotype in a process called P element dependent silencing (PDS). A derivative allele of P{lacW}ciDplac was isolated, called E1, that contained a distal gypsy element insertion. This allele variegates in the absence of
other P elements, and the variegating phenotype can be suppressed by and enhanced by modifiers of wm4 in a manner similar to heterochromatic Position Effect Variegation (hPEV). I performed a genetic screen formodifiers of E1 variegation and isolated mutations that fell into complementation groups on both the second and third chromosomes. I identified 5 of these groups as: TAF4, a general transcription factor; cg, an already characterized regulator of ci; ash1 and trx, known regulators of homeotic genes not previously shown to act at ci; and CG8878, a putative protein kinase of unknown specificity. I also isolated a complementation group that was too weak in phenotype to accurately map via
recombination and several singles, which were not pursued farther. I chose to investigate the alleles of ash1, trx, and CG8878. This thesis describes their generation, isolation and further characterization. -
- Graduation date
- Spring 2013
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- Type of Item
- Thesis
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- Degree
- Doctor of Philosophy
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- License
- This thesis is made available by the University of Alberta Libraries with permission of the copyright owner solely for non-commercial purposes. This thesis, or any portion thereof, may not otherwise be copied or reproduced without the written consent of the copyright owner, except to the extent permitted by Canadian copyright law.