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Sameny, A., La, A., Hanna, S., Locke, J. (2011). Point mutations in a Drosophila P element abolish both P element-dependent silencing (PDS) of a transgene and repressor functions.  Chromosoma 120(6): 573--585.
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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 P[SalI]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 P[hsp26-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 ( + ) 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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    Aberrations (1)
    Alleles (49)
    Genes (4)
    Natural transposons (1)
    Insertions (26)
    Transgenic Constructs (23)