Point mutations in a <Emphasis Type="Italic">Drosophila P</Emphasis> element abolish both <Emphasis Type="Italic">P</Emphasis> element-dependent silencing (PDS) of a transgene and repressor functions |
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Authors: | Alireza Sameny Anderson La Scott Hanna John Locke |
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Institution: | (1) Department of Biological Sciences, University of Alberta, Edmonton, Alberta, Canada, T6G 2E9; |
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Abstract: | The P elements of Drosophila melanogaster are well-studied transposons with both mobilizing and repressor functions. P elements can also variably silence the expression of certain other transgenes through a phenomenon known as P element-dependent silencing (PDS). To examine the role of the P repressor in PDS, we have induced, isolated, and characterized 22 point mutations in an archetype P element called PSalI]89D. All mutations showed a loss in the ability to silence one or more assays for the PDS phenotype. These mutants also lost
the ability to induce the suppression of variegation in Phsp26-pt-T]39C-12, another P element-dependent phenotype. A subgroup of 11 mutations was further assayed for their ability to act as a P repressor and silence the P element promoter transcribing a lacZ
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gene, and this function was lost as well. Taken together, this study supports a model of PDS acting through protein interactions,
not RNA, with heterochromatic proteins to modify the extent of variegation seen in PDS. Furthermore, the common loss of functions
for PDS and P repressor silencing (from another P promoter) argues for a common role of the repressor. This makes the PDS model a good system for examining P repressor functions and how they relate to transposon-mediated gene silencing in general. |
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