Ancient Genes for Symbiosis Hint at Mitochondria’s Origins
quantamagazine.org
quantamagazine.org
In this case, you should know that the phagocytic model of endosymbiosis has been radically upended since the successful culturing of a Lokiarchaeota in (ecto)symbiosis with a delta-proteobacterium in 2019 by Imachi et al.
"Isolation of an archaeon at the prokaryote–eukaryote interface" https://www.nature.com/articles/s41586-019-1916-6 doi.org/10.1038/s41586-019-1916-6
The striking images of the branching, filamentous prokaryotic Lokiarchaeotum grappling its metabolic partner resembled nothing I had ever seen in biology before, save maybe the mycorrhizal root nodules of a legume at a ~2000x smaller scale. The prevailing model of the process of eukaryotic endosymbiosis is now "entangle-engulf-endogenize", rather than phagocytosis, which might be a secondary post-mitochondrial lifestyle adaptation.
If the Nature paper is difficult for you to read or access, this summary is well written and provides better citations than the Quanta article.
"Challenging Eukaryogenesis: The Story of the Eukaryotic Ancestor" https://arxiv.org/abs/2008.06608 doi.org/10.48550/arXiv.2008.06608
If you are interested in this topic, I cannot praise Nick Lane's nonfiction trilogy of books on mitochondria and evolution highly enough:
• "Oxygen: The Molecule that Made the World" (2002)
https://www.amazon.com/Oxygen-Molecule-that-Made-World/dp/0198508034
• "Sex, Power, Suicide: Mitochondria and the Meaning of Life" (2005)
https://www.amazon.com/Power-Sex-Suicide-Mitochondria-Meaning/dp/0192804812
• "The Vital Question: Energy, Evolution, and the Origins of Complex Life" (2015)
https://www.amazon.com/Vital-Question-Evolution-Origins-Complex/dp/0393088812In fluid dynamics, their pages on why turbulence is hard [0] don't mention the actual reason turbulence is hard: It has a really high computational complexity. There is no mystery here. The math behind it is pretty simple. I guess this doesn't sell the article though, so a journalist won't say that. Though I'm not sure the people at Quanta Magazine are aware!
Quanta Magazine also spends an extremely disproportionate amount of articles on the (constant viscosity) Navier-Stokes existence and uniqueness problem [1]. This is essentially a pure math problem, in my view, of no practical consequence [2]. Contrary to what Quanta Magazine writes, this has nothing to do with turbulence beyond that both use the Navier-Stokes equations.
[0] https://www.quantamagazine.org/the-trouble-with-turbulence-2... https://www.quantamagazine.org/what-makes-the-hardest-equati...
[1] https://www.quantamagazine.org/deep-learning-poised-to-blow-... https://www.quantamagazine.org/famous-fluid-equations-spring... https://www.quantamagazine.org/for-fluid-equations-a-steady-... https://www.quantamagazine.org/what-makes-the-hardest-equati... https://www.quantamagazine.org/mathematicians-find-wrinkle-i... https://www.quantamagazine.org/a-fluid-new-path-in-grand-mat...
[1] - https://www.youtube.com/watch?v=06e-PwhmSq8 [video]
As for cell division, the simplest and maybe partial but best explanation would be that prior to cell cloning, the cell induce mitochondria cloning proactively. Therefore it would have excess mitochondria in order to havz them already ready for the cloning stage.
My limited understanding is that can is the key word. There are apparently factors that can lead to the cell switching from OxFox to the primitive method of ATP generation which may actually be the original default state of operation for the cell prior to mitochondria being introduced. This may be an early state that existed prior to there being much O2 in the atmosphere when lifeforms were much more primitive. Again, this is not my area of expertise and I am not sure that scientists fully understand this yet either.
> "The ‘reverse’ Krebs cycle was first proposed in 1966. It does exactly the opposite; it uses energy to react the gases hydrogen and carbon dioxide to make Krebs-cycle intermediates, turning simple gases into the molecules of life. The bacteria that live this way are a billion years older than the first photosynthetic cyanobacteria and thrive in environments where life might have started, such as hydrothermal vents."
https://www.ukri.org/blog/understanding-the-origins-of-life-...
So a cell always has functional mitochondria. The mitochondria multiply within a cell (and their DNA is replicated), while the cell grows between divisions.
Nevertheless, not all ATP is produced by the mitochondria. For example ATP is produced by various chemical reactions that do not need dioxygen (i.e. which also work during anaerobic effort or whenever the power requirements exceed the maximum output of the mitochondria), e.g. by the hydrolysis of phosphocreatine (vertebrates) or of phosphoarginine (arthropods), or by the splitting of glucose into lactic acid.
So a cell can survive for some time without mitochondria, but it will exhaust quickly all its energy reserves.
Also if you really want an intellectual challenge and to help me on a problem I fail to understand, is the debate on mildronate vs ALCAR effect on health. Mildronate: The main cardioprotective effects of meldonium are mediated by the inhibition of GBB. By subsequently inhibiting carnitine biosynthesis, fatty acid transport is reduced and the accumulation of cytotoxic intermediate products of fatty acid beta-oxidation in ischemic tissues to produce energy is prevented, therefore blocking this highly oxygen-consuming process.[4] Treatment with meldonium therefore shifts the myocardial energy metabolism from fatty acid oxidation to the more favorable oxidation of glucose, or glycolysis, under conditions where oxygen is limited. It also reduces the formation of trimethylamine N-oxide (TMAO), a product of carnitine breakdown that has been implicated in the pathogenesis of atherosclerosis and congestive heart failure. https://en.wikipedia.org/wiki/Meldonium#Physio-pharmacology
https://en.wikipedia.org/wiki/Acetylcarnitine#Biochemical_pr... ALCAR has many many studies showing a potent improvement of health/metabolism and especially a reduction of oxidative stress. Despite this, ALCAR supposedly do the opposite of mildronate, it shift the mitochondria bioenergetics to an increase in beta oxidation and reduce glucose consumption. Beta oxidation is oxidative stress but I believed glucose oxidation leads to more oxidative stress?
How to make sense of those contradicting both positive narratives ?? Also weird detail: Excess acetyl-CoA causes more carbohydrates to be used for energy at the expense of fatty acids. This occurs by different mechanisms inside and outside the mitochondria. ALCAR transport decreases acetyl-CoA inside the mitochondria, but increases it outside.[4][5] plz halp
ATP is a highly unstable molecule, precisely due to its high energy content. It cannot be effectively supplemented exogenously.
... whatever that means
DNA in cells encode proteins that are used to construct things. this happens in centralized locations involving ribosomes, endoplasmic reticulum, blah blah lots of steps and you have a specific protein that may need to be used somewhere else.
The cell is built with strings like cables or chains (actin filament), each with the same repeating pattern of molecules. These get used like roads or tracks to move stuff (specific proteins) from one end of a track to the other.
But the both track the thing that needs to be moved just float in the cytoplasm and so we make these bizarre stick animal looking molecules (ATP) that literally walk along these roads and can carry a protein with them (way faster and more targeted than just floating).
nothing like deliberately climbing a rope with a load is free even if you are a just handful of atoms, there is an physical exchange (atom rearrangement) that changes each step the energy to effect the rearrangement that causes the "step" is taken from breaking up a sugar molecule. You do this allot. where that means you go through your own mass of these little beasts of burden ever day; where these little critters are produced is a "mitochondria" organelle.
So mitochondria produce little beasts of burden that can atomically walk along actin filaments while carrying more than just themselves. This can be used move stuff out by transporting it to the cell membrane, or bring things in, house-keeping tasks. But! you can also rig the actin (& myosin) up to pull one side of a cell against the other side of the cell and change the cells shape alot. (or quickly release a pulled cell)
This is how muscle work which is likely approaching the "powerhouse" concept without the mitochondria organelle (former parasite/symbiot now integrated) we would not have the genes to produce these wonderful little atomic constructs that can walk wherever we put path with a particular pattern on it all while carrying a comparatively heavy load.
I recall, but can not now find, an in-vivo video of this and being shocked at how fast they walk relative to their size. maybe someone with fresher brain cells can help.
They are like little stick men pulling stuff along the highways of the cell.