In contrast, depletion of Mael had no impact on nuclear Piwi levels ( Figure 1E). Defective piRNA biogenesis (e.g., armi KD) triggers loss of Piwi, presumably as unloaded Piwi is unstable ( Figure 1D). To identify the level at which Mael acts in the piRNA pathway, we monitored Piwi in clones of mael KD cells in the follicular epithelium. Our work illustrates the widespread influence of transposons and the piRNA pathway on chromatin patterns and gene expression. In contrast, loss of Maelstrom affects transposon H3K9me3 patterns only mildly yet leads to increased heterochromatin spreading, suggesting that Maelstrom acts downstream of or in parallel to H3K9me3. We show that Piwi is required to establish heterochromatic H3K9me3 marks on transposons and their genomic surroundings. ![]() Our data demonstrate piRNA-mediated trans-silencing of hundreds of transposon copies at the transcriptional level. Genome-wide assays revealed highly correlated changes in RNA polymerase II recruitment, nascent RNA output, and steady-state RNA levels of transposons upon loss of Piwi or Maelstrom. Here, we show that the HMG protein Maelstrom is essential for Piwi-mediated silencing in Drosophila. The piRNA pathway silences transposons in animal gonads, yet how this is achieved molecularly remains controversial. ![]() Eukaryotic genomes are colonized by transposons whose uncontrolled activity causes genomic instability.
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