FIG. 7.

Model explaining the differential role of DSIF inhibition of elongation in nonstimulated and stimulated cells. In unstimulated cells (upper panel), the promoters of rapidly induced NF-κB target genes, like A20, are bound by the entire Pol II transcription apparatus, but the basal activity is low since this complex is capable of initiation but not reinitiation (1). Under these conditions, a factor that binds ELIE on the A20 promoter inhibits the basal transcription at the level of elongation via DSIF. This effect is required to keep the basal activity of the prebound transcription complex much lower until NF-κB is stimulated. After NF-κB is induced, it enhances the reinitiation rate but, on the other hand, is responsible for inhibition of elongation by DSIF. This inhibition might serve to load the elongating polymerase with pre-mRNA processing factors in order to ensure that each transcript that has been initiated will be completely processed into mature and translatable mRNA. Alternatively, this inhibition may be used to control the level of activation of the A20 gene by NF-κB, which might be important under certain physiological conditions. CTD, C-terminal domain; GTFs, general transcription factors; TBP, TATA binding protein.