Correction: Temporal Dissection of Rate Limiting Transcriptional Events Using Pol II ChIP and RNA Analysis of Adrenergic Stress Gene Activation

S1 Fig. Analysis of Pol II density across the transcriptional units following gene activation. ChIP density estimates of Pol II density during the indicated period of maximal, activated expression following α1aAR stimulation. Primer locations associated with 5’ end of upstream primer relative to the transcription start site (i.e. TSS bp is 1). (A) Pol II density on Fos, expressed as the number of precipitated DNA copies from a maximum of 200 copies, was constant across proximal and distal regions indicating a complete abrogation of proximal pausing. (B) Elevated promoter proximal Pol II density on Nr4a3 (500 copies max.) shows incomplete abrogation of pausing, while a distal decrease in density was reported by regression analysis as a negative slope (-0.28 copies/kbp) that was statistically significant (p = 0.022). Lower density in distal regions is a consequence of partial transcription termination at an internal polyadenylation site at 14,004 bp. (C) Pol II density across the dominant transcriptional unit of Nr4a1 (200 copies max) displays no systematic variation; however, the TSS appears to be associated with modest promoter proximal pausing. (D) For Dusp5 (500 copies max), elevated promoter proximal density even after activation suggests only partial abrogation of pausing. (E) Density across Gpcr5a shows no systematic variation in Pol II density following abrogation of an internal transcriptional pause. Because the values from each primer are not independent (due to use of a common quantitation curve), error bars show standard deviation. Linear regression analysis was done using the average value observed for each primer pair within the time period indicated. (TIF)