Cobalamin Depletion and mtDNA Transcription

This article [Leeds and Brass, 1994: (http://www.jbc.org/cgi/content/abstract/269/6/3947) (http://www.ncbi.nlm.nih.gov/pubmed/7508436?dopt=Abstract)] is interesting and shows that experimental cobalamin deficiency, induced in rats by hydroxycobalamin [c-lactam], causes the transcription of mitochondrial genes to be decreased. I haven't seen as much research on deficits in mtDNA transcription underlying mitochondrial dysfunction, but a decrease in the mtDNA copy number, a variable that is itself implied by a reduction in the overall cellular mtDNA content, implies that the transcription of mitochondrial genes will be reduced. There is research showing that, to the extent that uridine or other nucleosides can influence different aspects of mtDNA turnover, the total RNA contents can be influenced by the pools of exogenous or endogenous nucleotides. In the articles discussing propionyl-CoA accumulation in response to experimental cobalamin depletion, it's reasonable to assume that the accumulation is secondary to a decrease in methylmalonyl-CoA mutase activity. In this article, I think it's not clear that that's the case. Part of the effect may be due to a decrease in methionine synthase activity.