F. Ferrari1,*, Y. L. Jung1,2,*, P. V. Kharchenko1,3, A. Plachetka2,4, A. A. Alekseyenko2,4, M. I. Kuroda2,4,†, P. J. Park1,2,†
1Center for Biomedical Informatics, Harvard Medical School, Boston, MA 02115, USA.
2Division of Genetics, Brigham and Women’s Hospital, Boston, MA 02115, USA.
3Division of Hematology/Oncology, Boston Children’s Hospital, Boston, MA 02115, USA.
4Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.
†Corresponding author : F. Ferrari, Y. L. Jung
* These authors contributed equally to this work.
Conrad et al. (Reports, 10 August 2012, p. 742) reported a doubling of RNA polymerase II (Pol II) occupancy at X-linked promoters to support 5′ recruitment as the key mechanism for dosage compensation in Drosophila. However, they employed an erroneous data-processing step, overestimating Pol II differences. Reanalysis of the data fails to support the authors’ model for dosage compensation.