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RESEARCH COMMUNICATION

Transcription elongation controls cell fate specification in the Drosophila embryo

¹ Department of Biochemistry and Cell Biology and the Center for Developmental Genetics, Stony Brook University, Stony Brook, New York 11794, USA; ² Graduate Program in Biochemistry and Structural Biology, Stony Brook University, Stony Brook, New York 11794, USA; ³ Center for Gene Regulation, Department of Biochemistry and Molecular Biology, The Pennsylvania State University, University Park, Pennsylvania 16802, USA

The simple combinatorial rules for regulation of the sloppy-paired-1 (slp1) gene by the pair-rule transcription factors during early Drosophila embryogenesis offer a unique opportunity to investigate the molecular mechanisms of developmentally regulated transcription repression. We find that the initial repression of slp1 in response to Runt and Fushi-tarazu (Ftz) does not involve chromatin remodeling, or histone modification. Chromatin immunoprecipitation and in vivo footprinting experiments indicate RNA polymerase II (Pol II) initiates transcription in slp1-repressed cells and pauses downstream from the promoter in a complex that includes the negative elongation factor NELF. The finding that NELF also associates with the promoter regions of wingless (wg) and engrailed (en), two other pivotal targets of the pair-rule transcription factors, strongly suggests that developmentally regulated transcriptional elongation is central to the process of cell fate specification during this critical stage of embryonic development.

[Keywords: Segmentation; ChIP; DNase I hypersensitivity; in vivo footprinting]

Received December 5, 2006; revised version accepted March 13, 2007.

E-MAIL pgergen{at}life.bio.sunysb.edu; FAX (631) 632-8575.

Article is online at http://www.genesdev.org/cgi/doi/10.1101/gad.1521207

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