Revision as of 12:22, 20 September 2006
Post discussion, questions, or comments about the Week 3 course material here.
Comments from the first paper (Brownell et al)
The authors show that p55 and Gcn5p both contain bromodomain; and that Hat1p doesn't possess a bromodomain. They speculate that the bromodomain tethers HAT A to other factors at specific chromosomal sites. This is remarkably accurate - later research has shown that bromodomains bind to acetylated lysine residues; helping regulate transciptional remodelling and transciptional activation (Zeng, L., Zhou, M.M. (2002)Bromodomain: an acetyl lysine binding domain. FEBS Letters. Vol 213, 124-128)
Question for Brownell et al:
At the end of the section Tetrahymena is Homologous to Yeast Gcn5p, the authors say that Gcn5p "migrates anomolously in SDS gels". Why would that happen?
Question for Taunton et al:
I noticed that they related RbAp48, the protein that binds to the retinoblastoma gene product, to histone deacetylase. They also found that inhibition of the deacetylase arrests the cell cycle. Could any of the research be useful for cancer treatment?