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. Author manuscript; available in PMC: 2013 Apr 1.
Published in final edited form as: Trends Cell Biol. 2011 Dec 21;22(4):177–184. doi: 10.1016/j.tcb.2011.11.005

Figure 3. Potential mechanisms of tissue-specific gene activation by de-ubiquitination of ubH2B.

Figure 3

(A) SAGA-mediated de-ubiquitination of ubH2B at weak promoters might destabilize promoter nucleosomes, facilitating recruitment of Pol II. The acetylation of promoter-proximal nucleosomes by SAGA at these same weak promoters could also stimulate chromatin remodeling, thus enhancing the recruitment of Pol II. (B) At genes at which pausing of Pol II constitutes an important rate-determining step in transcription, de-ubiquitination of ubH2B by SAGA might enhance recruitment and/or retention of serine 2 CTD kinases that facilitate release of Pol II into productive transcription elongation. Adapted from [69].