Within a separate conversation on Prokaryotes, Eukaryotes and their cousins, the name of this interesting cellular organelle popped up: mitochondria. This called my attention and raised my curiosity. There’s a least one conversation topic devoted to mitochondria barcodes. But maybe this cellular organelle deserves to be reviewed completely in a separate topic? Any objections?
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Here’s an interesting paper on this topic:
Mitochondria in innate immune signaling
Balaji Banoth, Suzanne L. Casse
DOI: 10.1016/j.trsl.2018.07.014
Mitochondria are functionally versatile organelles. In addition to their conventional role of meeting the cell’s energy requirements, mitochondria also actively regulate innate immune responses against infectious and sterile insults. Components of mitochondria, when released or exposed in response to dysfunction or damage, can be directly recognized by receptors of the innate immune system and trigger an immune response. In addition, despite initiation that may be independent from mitochondria, numerous innate immune responses are still subject to mitochondrial regulation as discrete steps of their signaling cascades occur on mitochondria or require mitochondrial components. Finally, mitochondrial metabolites and the metabolic state of the mitochondria within an innate immune cell modulate the precise immune response and shape the direction and character of that cell’s response to stimuli. Together, these pathways result in a nuanced and very specific regulation of innate immune responses by mitochondria.
Very interesting, isn’t it?
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Here’s another interesting article on this topic:
Mitochondria, Oxidative Stress and Innate Immunity
DOI: 10.3389/fphys.2018.01487
Canonical functions of mitochondria include the regulation of cellular survival, orchestration of anabolic and metabolic pathways, as well as reactive oxygen species (ROS) signaling. Recent discoveries, nevertheless, have demonstrated that mitochondria are also critical elements to stimulate innate immune signaling cascade that is able to intensify the inflammation upon cytotoxic stimuli beyond microbial infection.
Mitochondria are not only house machineries that support cellular essential activities, but also important sources of endogenous DAMPs including ROS as well as necessary triggers for inflammasome signaling. A large number of evidence has emerged linking dysfunctional mitochondria to aberrant innate immune responses. Nevertheless, our understanding of precise roles the inflammasomes in response to mitochondrial malfunction and ROS are still lacking. Many significant questions regarding the molecular machineries which initiate inflammasome activation upon mitochondria disorder and ROS remain to be addressed. Further elucidation of the interplay of ROS, mitochondrial function and inflammasome pathways might open up a new horizon for the development of immunotherapeutic strategy for chronic inflammation diseases such as cardiovascular diseases.
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Microsoft OneNote is great tool for web clipping and taking notes. 
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From my understanding of this research, the mitochondria is like a canary in a coal mine. If the mitochondria are damaged by things like infections, lack of oxygen, or other factors it starts to leak out proteins. There are other proteins in the cytoplasm of the cell that bind to these mitochondrial proteins, and this triggers a whole host of cellular responses. One of those responses is autophagy (translation = self eating). Yoshinori Ohsumi is the scientist who discovered this process for which he was awarded the Nobel Prize in 2016.
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Deep mitochondrial origin outside the sampled alphaproteobacteria
Joran Martijn, Julian Vosseberg, Lionel Guy, Pierre Offre & Thijs J. G. Ettema
Nature volume 557, pages 101–105 (2018)
Mitochondria are ATP-generating organelles, the endosymbiotic origin of which was a key event in the evolution of eukaryotic cells. Despite strong phylogenetic evidence that mitochondria had an alphaproteobacterial ancestry, efforts to pinpoint their closest relatives among sampled alphaproteobacteria have generated conflicting results, complicating detailed inferences about the identity and nature of the mitochondrial ancestor.
previous hypotheses on the nature of the mitochondrial ancestor should be re-evaluated.ATP? Huh?
Is this ATP related to the Association of Tennis Professionals? 
Does this ATP deserve a separate conversation topic?
More on mitochondria:
Structural Patching Fosters Divergence of Mitochondrial Ribosomes
Anton S Petrov, Elizabeth C Wood, Chad R Bernier, Ashlyn M Norris, Alan Brown, A Amunts
Molecular Biology and Evolution, msy221
DOI: 10.1093/molbev/msy221
Mitochondrial ribosomes (mitoribosomes) are essential components of all mitochondria that synthesize proteins encoded by the mitochondrial genome. Unlike other ribosomes, mitoribosomes are highly variable across species. The basis for this diversity is not known.
since the toolkits of elements utilized for structural patching differ between mitochondria of different species, it fosters the growing divergence of mitoribosomes.
Mitochondria are organelles that perform multiple functions within eukaryotic cells including the production of chemical energy. They contain their own mitochondrial genome (mt-genome) and translational machinery.
The origin of non-proteobacterial components as well as the complete history of mitochondrial evolution remain a subject of ongoing studies
Despite the proposed common ancestry, mitoribosomes are morphologically diverse and vary in protein and mt-rRNA content in different species
It has recently become apparent that mitoribosomes have undergone substantial changes within a relatively short evolutionary period in response to a host environment and subsequent diversification of the eukaryotic species
mitoribosomes evolved, and gained new functions, through a “structural patching” of the archetypical ribosome driven by destabilizing changes in mt-rRNA.
it is likely that the more diverse taxa have lineage-specific proteins that are yet to be identified.
the mitoribosome is a molecular symbiont with a complex evolutionary history.
Further complexity likely comes from constructive neutral evolution, in which structural features become fixed into the mitoribosome through subsequent co-dependent mutations without the apparent evolution of novel functions
Additional structural and phylogenetic analyses will be required to track the specific details of early evolutionary changes within mitoribosomes of bikont species.
The variable extent and rate of changes to the mt-genome and the different toolkits available in different species are responsible for promoting mitoribosomal diversity.Lots of highly persuasive arguments
Probably not. It stands for adenosine triphosphate. It’s the primary energy currency of your cells.
I see you have finally made a claim. Might we suppose it was facetious, and you are implying that the science is not, in your opinion, very good?
Why not?
What do you want to know? Why do you think it needs discussion?
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Excellent question. Thanks.
Everything that is knowable on this and other biology topics associated with developmental and systems biology. There’s a growing literature describing what is known today. But tomorrow we’ll know much more. Almost everything in modern biology research is highly fascinating. Definitely more than other areas of science. Biology research discoveries are happening at an accelerated speed. It’s hard to catch up with it.
Also I want to share whatever I learn about biology, so that other people can read it if they want to.
I think biology has become the new queen of science and engineering. Math, Physics, Chemistry, Computer Science, Engineering are serving Biology. I’ve read about physicists, mathematicians, chemists, computer scientists, engineers, who have ended up pursuing biology-related research or academic careers. However, don’t recall hearing of any biologist switching to math, physics, chemistry, computer science, engineering. Maybe those cases exist, but I’m not aware of them, maybe are rarer?
However, I’ll stop posting here as soon as the host of this website asks me to do so. This could happen anytime, but it hasn’t happened yet.
I encourage you to enjoy looking at what’s happening in biology research these days. You’ll appreciate it. One major obstacle is that spare time is very limited. We all experience its conspicuous scarcity.
Please, share here any interesting biology paper you read on the current topic. I and other folks will appreciate it very much.
No one could learn all of that material in a life time. You will have to narrow it down.
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But the question was about what I want to know, not how much I can learn. I think that’s very different. Isn’t it?
I may want to be healthy, but I can’t. I may want to be with my wife and my kids and my grandkids everywhere they are every day, but I can’t. I may want to be good, but I can’t.
Please, you may note that I’m trying to narrow down the overwhelming number of papers to a reader’s digest selection, but that’s not easy for me. I’m probably missing some good papers or referencing some papers that aren’t that representative. Somebody else could have done it better and much faster. But I’m learning in the process of doing this.
Some papers take me longer to read than others. The terminology and the concepts are quite difficult sometimes. Many things are new to me.
But leaning is fun.
Structural Patching Fosters Divergence of Mitochondrial Ribosomes
Molecular Biology and Evolution, msy221, DOI: 10.1093/molbev/msy221
Mitochondrial ribosomes (mitoribosomes) are essential components of all mitochondria that synthesize proteins encoded by the mitochondrial genome. Unlike other ribosomes, mitoribosomes are highly variable across species. The basis for this diversity is not known.
since the toolkits of elements utilized for structural patching differ between mitochondria of different species, it fosters the growing divergence of mitoribosomes.
Mitochondria are organelles that perform multiple functions within eukaryotic cells including the production of chemical energy. They contain their own mitochondrial genome (mt-genome) and translational machinery.
Mitoribosomes synthesize proteins encoded by the mt-genome.
ablation and expansion of mt-rRNA generates metastable regions of mitoribosomes that require patching by pre-existing elements that may confer new functions. The extent and type of modifications that can be made in different species are determined by the structural toolkits available. Fungal mitoribosomes have a structural toolkit that includes mt-rRNA expansion and protein acquisition, whereas metazoans appear to be restricted to only adding existing RNA elements and proteins. The variable extent and rate of changes to the mt-genome and the different toolkits available in different species are responsible for promoting mitoribosomal diversity.
Check this out:
Does Mitochondrial DNA Evolution in Metazoa Drive the Origin of New Mitochondrial Proteins?
S. L. van Esveld, M. A. Huynen
DOI : 10.1002/iub.1940
Most eukaryotic cells contain mitochondria with a genome that evolved from their α-proteobacterial ancestor. In the course of eukaryotic evolution, the mitochondrial genome underwent a dramatic reduction in size, caused by the loss and translocation of genes. This required adjustments in mitochondrial gene expression mechanisms and resulted in a complex collaborative system of mitochondrially encoded transfer RNAs and ribosomal RNAs with nuclear encoded proteins to express the mitochondrial encoded oxidative phosphorylation (OXPHOS) proteins.
It is tentative to argue that this co-evolution is driven by the mtDNA, given the relatively high rate at which it accumulates mutations in Metazoa (88), but evolutionary arguments are often rooted in wishful thinking. To make a more convincing argument we would have to observe such co-evolution in other parallel evolutionary lineages with a high accumulation of slightly deleterious mutations. Furthermore, even though we mapped the coevolution of the mitochondrial genome and the origin of new mitochondrial proteins by narrowing down events in both using phylogenetic analyses, we still face a chicken and egg problem: we do not know whether the origin of a new, nuclear encoded mitochondrial protein allowed the change in the mitochondrial genome, or whether a change in the mitochondrial genome provided the selective advantage for the maintenance of a new mitochondrial protein.
the reason why only Metazoa need these new proteins remains unclear. At the very least, the coincidence of the arrival of new mitochondrial proteins with changes in the mtDNA can provide hypotheses about the functions of those proteins and therewith drive experimental tests.
evolutionary arguments are often rooted in wishful thinking
Huh? What do they mean?
Also this:
we still face a chicken and egg problem
English is not my first language and my knowledge of biology is very weak to understand all this jargon.
Any comments?