Pitfalls of Mapping High-Throughput Sequencing Data to Repetitive Sequences: Piwi’s Genomic Targets Still Not Identified

•Published ChIP-seq datasets do not reveal Piwi’s genomic binding sites•Loss of Piwi does not lead to a broad redistribution of Pol II to transposons

SummaryHuang et al. (2013) recently reported that chromatin immunoprecipitation sequencing (ChIP-seq) reveals the genome-wide sites of occupancy by Piwi, a piRNA-guided Argonaute protein central to transposon silencing in Drosophila. Their study also reported that loss of Piwi causes widespread rewiring of transcriptional patterns, as evidenced by changes in RNA polymerase II occupancy across the genome. Here we reanalyze their data and report that the underlying deep-sequencing dataset does not support the authors’ genome-wide conclusions.