HipHop
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To this end, we utilized a transgenic HeT-A (GFP) element inserted into chromosomes 3 and X (Fig. 1A) that is deactivated upon activation by the mif2p repressor (Ranganathan et al., 2009). We first measured the transcript levels of the transgenic element in adults of different genotypes. As expected, the transgenic element was up-regulated in the mif2p knock-down hypomorphs (dfmif2 and rfmif2), as well as in the mif2p-overexpressing mutants (dfmif2, rfmif2 and mif2, Fig. 1B). In contrast, the transgenic element remained deactivated in adults bearing hypomorphic hiphop transposon alleles, despite their generally increased TE levels (Fig. 1B). We then measured the expression of the transgenic element along the telomeres in ovarioles of representative hiphop mutants and their heterozygous siblings by fluorescence microscopy. In previous work, we found strong enrichment of GFP-marker proteins at chromosomes 3 and X (Fig. 1C), as well as in the distal ends of telomeres along the repeat and containing subtelomeric sequence (Fig. 1D; Fig. S1B,C; Cooley et al., 2014; Cooley and Crabtree 2018). We confirmed these observations and determined the telomere position effect (TPE) boundary by amplifying GFP markers in the transgenic HeT-A element in the three mutants and their heterozygous siblings. From these studies, we find that the fluorescent signals marking the transgenic HeT-A element are enriched in the distal subtelomeric regions, in a copy-dependent manner (Fig. 1C–D; Fig. S1A,B,C), similar to earlier published data (Cooley et al., 2014; Cooley and Crabtree 2018). Importantly, the TPE boundary is not altered in the hiphop mutants (Fig. 1C–D and Fig. S1B; Cooley and Crabtree 2018; Cooley et al., 2014). This suggests that the overall repression of the transgenic HeT-A element on chromosome 3 and chromosome X is not defective in hipHop mutants. d2c66b5586