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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.

Transcription elongation controls cell fate specification in the Drosophila embryo