Phys.org. Researchers find mitochondria to nucleus messenger protein

Thanks for posting. From my level of ignorance, this looks interesting!

I hope it is something which would be feasible to investigate in ME to see if it is of relevance, or not.

https://phys.org/news/2018-03-mitochondria-to-nucleus-messenger-protein.html

"Mitochondria are special organelles that contain their own DNA. However, the information they store is not sufficient to sustain their own activity or biogenesis. Instead most of the genetic information for mitochondrial proteins is stored in the nuclear DNA. Thus, when the mitochondria are under stress they need to communicate with the nucleus so that it can respond appropriately to help restore their activity or increase in number."

When I had testing done a good many years ago now via Biolab/Myhill on mitos and function I only had 60% of the normal number of mitos.
 
The researchers conducted their study in cell cultures and experimental models that had been genetically modified to lose the expression of GPS2. "Using a combination of imaging techniques, biochemical approaches and next-generation sequencing experiments, we were able to show that the total number of mitochondria in the cells and the fat tissue without GPS2 was considerably lower than in the normal ones. We also showed that in absence of GPS2, cells were not able to recover when exposed to mitochondrial stress"

Interesting @Daisymay. I was just about to ask if there's been any research that has found lower numbers of mitochondria in the cells of people with ME. I vaguely recall there was some research although I can't remember what was found.
 
Link to the actual paper, paywalled, is http://www.cell.com/molecular-cell/fulltext/S1097-2765(18)30096-0

Highlights
  • •GPS2 binds to the promoters of neMITO genes and regulates their transcription
  • •GPS2-mediated inhibition of Ubc13 regulates H3K9 demethylation and POL2 activity
  • •Mito-to-nucleus translocation of GPS2 mediates mitochondrial stress response
  • •GPS2 is required for sustaining mitochondrial biogenesis in brown adipose tissue
Summary


As most of the mitochondrial proteome is encoded in the nucleus, mitochondrial functions critically depend on nuclear gene expression and bidirectional mito-nuclear communication. However, mitochondria-to-nucleus communication pathways in mammals are incompletely understood. Here, we identify G-Protein Pathway Suppressor 2 (GPS2) as a mediator of mitochondrial retrograde signaling and a transcriptional activator of nuclear-encoded mitochondrial genes. GPS2-regulated translocation from mitochondria to nucleus is essential for the transcriptional activation of a nuclear stress response to mitochondrial depolarization and for supporting basal mitochondrial biogenesis in differentiating adipocytes and brown adipose tissue (BAT) from mice.

In the nucleus, GPS2 recruitment to target gene promoters regulates histone H3K9 demethylation and RNA POL2 activation through inhibition of Ubc13-mediated ubiquitination. These findings, together, reveal an additional layer of regulation of mitochondrial gene transcription, uncover a direct mitochondria-nuclear communication pathway, and indicate that GPS2 retrograde signaling is a key component of the mitochondrial stress response in mammals.
 
"The researchers conducted their study in cell cultures and experimental models that had been genetically modified to lose the expression of GPS2."

Just want to point out that the 'experimental models' are mice, which bear little resemblance to humans, especially if they have been genetically modified.

My own studies have shown that such experiments bear little promise for humans.
 
"The researchers conducted their study in cell cultures and experimental models that had been genetically modified to lose the expression of GPS2."

Just want to point out that the 'experimental models' are mice, which bear little resemblance to humans, especially if they have been genetically modified.

My own studies have shown that such experiments bear little promise for humans.
Ah ... :(
 
Thanks @MeSci just shows how easy it is for non scientist like me to get hooked in by a title:whistle:
I'm not necessarily saying that there is nothing to be said for cell cultures, just that using the wrong species gives the right answer so rarely that it's really not worth doing. It just means a huge amount of suffering. The animals are almost always killed, and large numbers are used in producing the 'right' genotypes.
 
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