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The l(2)03605 P element induced lethality is not caused by disruption of the Drosophila melanogaster high mobility group genes D (HMG-D) or Z (HMG-Z)

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Title: The l(2)03605 P element induced lethality is not caused by disruption of the Drosophila melanogaster high mobility group genes D (HMG-D) or Z (HMG-Z)
Author: James, Erick Robert
Degree Master of Science - MSc
Program Zoology
Copyright Date: 1999
Abstract: Chromatin is functionally defined as DNA, histones and non-histone chromosomal proteins (NHCP). The High Mobility Group (HMG) 1/2 proteins represent one well defined set of NHCP in eukaryotes . These proteins are thought to act as architectural components of chromatin and are well characterized biochemically but not biologically. HMG 1/2 proteins have been implicated in transcription, DNA replication, chromatin assembly and stability. The Drosophila HMG1 homologues are HMG-D and HMG-Z. The Drosphila HMGs are thought to play a role in establishing developmental specific regions of chromatin that are silent and easily replicatable, albeit at different developmental times and locations, but again their biological role is speculative. Unfortunately, no mutations exist in the HMG 1/2 class of proteins and mutants would be extremely useful in assigning a biological function to these proteins. However, the Drosophila HMG gene are cytologically mapped to a precise region, banded region 57F8-11 on chromosome 2. I attempted to identify P element insert mutations in HMG-D/Z using the Berkeley Drosophila Genome Project P element insertion lines. The Berkeley Drosophila Genome Project has undertaken the daunting task of P element tagging essential genes in Drosophila. Their P element inserts are mapped cytologically and the expression pattern of enhancer trap expression are known. One such recessive lethal line, l(2)03605/CyO has a P element inserted at 57F8-10, the same cytological location as HMG-D/Z. In addition, the insert shows fi-galactosidase expression in the nervous system, while HMG-D/Z mRNA is also found in embryonic neural tissues. This coincident expression pattern and the cytological location suggest that the 1(2)03605 P element insertion may have disrupted either or both genes. Therefore, I set out to determine whether the 1(2)03605 P element is either inserted into and/or disrupting the HMG-D/Z genes. This work shows the 1(2)03605 P element does not affect either HMG-D or HMG-Z and most likely disrupts another gene in the 57F8-10 region.
URI: http://hdl.handle.net/2429/9061
Series/Report no. UBC Retrospective Theses Digitization Project [http://www.library.ubc.ca/archives/retro_theses/]

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