Note on Histone Butyrylation and Propionylation

What I meant in the last posting (http://hardcorephysiologyfun.blogspot.com/2009/06/histone-butyrylation-and-propionylation.html) is that the transcriptional responses to the butyrylation of histones might be similar to the responses produced by the acetylation of histones, and the butyrylated histones might be poorer substrates for histone deacetylases than acetylated histones are. In the context of histone propionylation, I was thinking that propionylated histones might produce either similar or different transcriptional responses (via the ensuing ATP-dependent, chromatin remodeling) and that those responses (defined in very vague and totally unspecified terms, here) might, by any number of mechanisms, partially account for some of the adverse effects associated with propionyl-CoA accumulation (or, incidentally, some of the "positive" or "desirable" effects that have been associated with treatments with anaplerotic, odd-chain fatty acid supplements). (I mean that histone propionylation could, up to a point, produce therapeutic effects and that those effects might be inappropriately attributed to "anaplerosis" per se.) The fact that histone propionylation can occur might also tend, in my opinion, to call into question the measurements used to assess "propionate overload" in people who are receiving odd-chain fatty acid supplements (such as triheptanoin). Researchers have tended to evaluate the potential for propionyl-CoA overload (and also propionate overload) by measuring plasma or urinary methylcitrate and other organic acids, but it's possible that excesses of propionyl-CoA might be used as substrates for histone acetyltransferases (rather than being cleaved to yield propionate and then its abnormal metabolites) and confound attempts to evaluate the extent of the propionyl-CoA accumulation.