Skip to main content
. 2005 Sep 7;33(16):5045–5052. doi: 10.1093/nar/gki825

Figure 5.

Figure 5

Model depicting interactions among TFIIB, TFIIF and Rpb1 at the active center of RNAP II. The sua7-1 (TFIIB E62K) and sua8-1 (Rpb1 N445S) alleles confer similar growth defects and altered patterns of transcription start site selection at ADH1. The ssu71-1 and ssu71-1 alleles of TFG1 encode charged residue replacements of Tfg1 G363, which is predicted to lie at the Tfg1–Tfg2 dimer interface of TFIIF (Figure 1). Based on suppression by Tfg1 G363 replacements of the cell growth and start site defects associated with the TFIIB E62K and Rpb1 N445S replacements (Figures 3 and 4), we place the TFIIF dimer interface at the active center (purple dot) of RNAP II. The dotted black triangle denotes genetic, and presumably physical (Discussion), interactions among Tfg1, TFIIB and Rpb1. This model is consistent with earlier protein–DNA crosslinking data showing Tfg1 and Tfg2 contact points at the transcription start site (36).