Dosage compensation in Drosophila is mediated by the MSL complex, which increases male X-linked gene expression approximately 2-fold. The MSL complex preferentially binds the bodies of active genes on the male X, depositing H4K16ac with a 3@ bias. Two models have been proposed for the influence of the MSL complex on transcription: one based on promoter recruitment of RNA polymerase II (Pol II), and a second featuring enhanced transcriptional elongation. Here, we utilize nascent RNA sequencing to document dosage compensation during transcriptional elongation. We also compare X and autosomes from published data on paused and elongating polymerase in order to assess the role of Pol II recruitment. Our results support a model for differentially regulated elongation, starting with release from 5@ pausing and increasing through X-linked gene bodies. Our results highlight facilitated transcriptional elongation as a key mechanism for the coordinated regulation of a diverse set of genes
CITATION STYLE
Ferrari, F., Plachetka, A., Alekseyenko, A. A., Jung, Y. L., Ozsolak, F., Kharchenko, P. V., … Kuroda, M. I. (2013). “Jump Start and Gain” model for dosage compensation in drosophila based on direct sequencing of nascent transcripts. Cell Reports, 5(3), 629–636. https://doi.org/10.1016/j.celrep.2013.09.037
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