Wednesday, April 09, 2014
This link came to me from Bill Lagakos via Facebook. It covers a lot of ground and is, unavoidably, a little superficial in places when the subject matter is very deep. He mentions his work with mice made heteroplasmic for two different strains of mitochondria, the NZB and the 129. Both work perfectly well as the sole mitochondrial population giving normal mice. Engineering heteroplasmy produces mice with a stack of problems in high energy demand tissues.
I got to this point, about half way through the presentation, before the penny dropped that the speaker was Doug Wallace, group leader of the people who published this paper
There is a more detailed analysis of this aspect in Nick Lane’s comment in the same edition of Cell about why heteroplasmy might be a Bad Thing, especially in high ATP demanding cells.
I spent much of the presentation thinking that there was no mention of nutritional tools for managing mitochondrial heteroplasmy and very little about mitochondrial mutations and ageing but these came up in the Q and As at the end. The nicest question was about intermittent fasting but Wallace immediately threw in a ketogenic diet as a potential technique for clearing out deleterious heteroplasmic mitochondrial sub populations. He also mentioned the ubiquity of low level heteroplasmy and pre ovulatory selection for optimal mitochondrial population in oocytes...
A lot of ground. Much there which makes sense.