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Dev Cell. 2015 Mar 23;32(6):765-71. doi: 10.1016/j.devcel.2015.01.013.

Pitfalls of mapping high-throughput sequencing data to repetitive sequences: Piwi's genomic targets still not identified.

Author information

1
Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA.
2
Department of Biochemistry, University at Buffalo, Buffalo, NY 14214, USA.
3
Institute of Molecular Biotechnology of the Austrian Academy of Sciences IMBA, Vienna Biocenter (VBC), 1030 Vienna, Austria.
4
Program in Bioinformatics and Integrative Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
5
Watson School of Biological Sciences, Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
6
Howard Hughes Medical Institute, RNA Therapeutics Institute and Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
7
Institute of Molecular Biotechnology of the Austrian Academy of Sciences IMBA, Vienna Biocenter (VBC), 1030 Vienna, Austria. Electronic address: julius.brennecke@imba.oeaw.ac.at.
8
Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA. Electronic address: kft@caltech.edu.

Abstract

Huang 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.

PMID:
25805138
PMCID:
PMC4494788
DOI:
10.1016/j.devcel.2015.01.013
[Indexed for MEDLINE]
Free PMC Article

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