Mitochondria are old free-living organisms that came together with whatever chimera originated the Eukaryotic Cell we are all based upon; A remarkable discovery by one giant Lynn Margulis. Like ribosomes, they likely vary between cell lines in the same organism. I wonder if this brillant research and breakthrough (congrats) relate to heteroplasmy in any way... Hypocondriac mitochondria?!
Endosymbiosis is not the same process as formation of chimera (cell lines with distinct nuclear origins within the same organism, iirc). Again iirc, most of the original bacterial DNA has become nuclear, with only a portion remaining in our mitochondria.
@@Talus-Gort Check the early century work by W. Ford Doolitle. Eukarya cells seem to have sets of genes from eubacteria (mainly those related to metabolism), some related to Archea (those related to the Central Dogma processes) and some apparently from something else (maybe a deceased lineage). Some even extend the endosymbiosis premise to the cell nucleus (it has two sets of double-lipid layers). So, yes, ultimately the endosymbiosis scenario, of multiple lineages of organisms amalgamating into one coherent hole could be portrayed by a Chimera metaphor, a term that in Cellular and Molecular Biology alone has more than one potential figurative meaning (e.g. a chimeric recombinant DNA stretch). If one cell is spliced from two or three different organism (simultaneously or in steps) it seems chimeric to me. Reference 127 here supports both of our claims, in a way: www.nature.com/articles/s41586-024-07677-6
@@Talus-Gort ...and not only a portion of the proteobacteria-like ancestral DNA remaining in our mitochondria but, as the video explains, with several vital processes encoded from old nuke genes now found in the mtDNA. A sort of resident hostage scenario of Game of Thrones (or the War of the Roses if you prefer): Hey mitochondria, hold my beer, er, I mean, hold my genes.This way both parties are heavily dependent on one another...
@@Mob1bo wow didn't know that, definitely stem cells have stored energy. When kids are born, they have brown fat cells in higher number than white cells, also number of mitochondria per cells in kids are higher. May be stem cells have something in them.
It was not clear if these "two types of mitochondria" are actually two separate lines ("species") of mitochondria, with different genetics, or are the same genetic type of mitochondria expressing their genes in very different ways, that is, specializing in the same way as the cells of multicellular organisms specialize into different types of cells.
It's interesting that aerobic exercise training can induce mitochondrial biogenesis, meaning the creation of more mitochondria. Considering exercise training is also linked to improved cellular health and muscle growth or maintenance, the question arises, does exercise training also stimulate the production of these alternative mitochondria that aid in building a cell?
@@livephysiology probably. If these segregated Mt are related to stress or cell damage. Just like adults lose brown fat but athelets have more brown fat in them. Same with mitochondria.
Excercise induces an hypoxic environment in cells meaning they get starved of o2 because they dont get enough of it in time. This produces a chain reaction where your body gets the signal to produce more red blood cells, mitochondria in cells, growth hormone etc among other things to adapt to the metabolic stress. Blood flow restriction training actually takes advantage of this to help critically ill patients gain back their strength. Hour long high intensity training is equivalent to short low intensity training under BFR
This "begging the question" narrative is a stretch, but yeah obviously they've done these studies on mitochondria without the knowledge of their subpopulations so they were inclusive of all results which includes the "other" mitochondria
Right. Something is missing because when you have CFS/ME most people are hurt further with excersises. Not just resistant but one could just stop functioning mid functioning ya know?
@ have not watch any Dr Crusher podcasts. But if I understood the video correctly the data indicates that this function is something that can be activated while fasting. Is there a podcast you can recommend for me to introduce myself to Dr Crusher? Thank you
My question is how did this thing evade discovery for so long? It does look visibly different enough for someone to have said, "Wait -- what's that one, and why does it look like that?" I have a feeling that it tended to be pointed out by first-year students, and the professor replied, "Well, some mitochondria just look like that, we don't know why. Moving on ... " That happens more than we would like in the sciences, where a potential discovery is staring us in the face, but the n00bs are the ones who see it, and they are often instructed to stop noticing it until someone higher up decides right, we're going to look into this.
It's not about noticing the mitochondria under the microscope but rather about finding the right conditions which will cause cells to produce the second kind of mitochondria
@@kektimus_prime9899 Still though, they must have been seen before now. Those conditions must have obtained in cells on slides before, meaning that they must have been visibly present before this researcher finally decided to find out what was up with them. I'm surprised it took this long for someone to ask the question.
we should digitalise research, especially the data collection part into bigger databases. Correlations of stuff happening occasionally 6 times out of 10 is not itneresting, but 5200 out of 10000 is. This way the rarer phenomena would not evade the only narrow minded people who are lucky enough to see it. Also with this particular example... effects after starvation means someoner forgot to feed the samples in the petri dishes, so they are hush hush about it.
Look up cell danger response. Dr. Robert Naviaux of UCSD. I'll be honest, it seems like there is some kind of resistance within academia to do certain kinds of research linked to chronic disease. It doesn't seem like it's that hard to observe this mitochondrial behavior, but it does seem like young postgrads are steered away from advancing research in metabolic disorders and disease stemming from innate immunefunction.
Considering that non-OXPHOS, P5CS-containing mitochondria also need ATP for the first step (Gamma-glutamyl kinase activity): Glutamate + ATP → Gamma-glutamyl phosphate + ADP, and NAD(P)H for the second step (Gamma-glutamyl phosphate reductase activity): Gamma-glutamyl phosphate + NADPH + H+ → Glutamate-5-semialdehyde + NADP+ + Pi, where does the ATP and NAD(P)H come from?
Cells may have many mitochondria, some might have hundreds if I recall correctly. Each mitochondria might have multiple copies of the mitochondrial DNA.
besides this, being round and relatively short is the reason it is such a primary seat for varied genetic markers, such as species barcodes. Easy to recover even from degraded DNA... The Ouroborus...
Synthases "do not require energy from adenosine triphosphate (ATP) or other nucleoside triphosphates to form bonds. They are classified as lyases, which are enzymes that cleave chemical bonds without using hydrolysis or oxidation." Does this lack of reliance on ATP explain the segregation of pyrroline-5-carboxylate synthase (P5CS) activity?
of course. all such investigations have the same perspective: we are investigating the evolutionary biology of an organism which develops from a progenitor cell which we use to identify that organism. For example, when I say, "your cat", I am referring to all cells of which the progenitor cell was your cat's mom's egg which "became" your cat.
@@Talus-Gort Why do you think we JUST went over the video together yesterday? Otherwise, there would have been no video. Are you expecting everyone to believe that how much you understand is a total mystery to everyone until we've already taught you what you didn't know (just so you can convince yourself that you didn't say anything embarrassing), while other people all around the world are constantly making fun of each other for not understanding things? I'm done explaining this to you like a robot. You're clearly trying to make it so that "only women can work as educators". Bam Margera never did THAT
I'd love to know how this relates to ME/CFS where mitochondrial damage is one of the theories and issues recycling ADP back to ATP seem to be compromised.
Are you trying to say that usually proline doesn't express in mitochondria, but in damaged cells they do make proteins. And presence of these same proteins in cancer cells too shows that when ever cells are in stress they make proline based proteins? Does that mean if we remove these segregated mitochondria from cancer cells, we can control cancer?
Look up cell danger response hey Dr Robert Naviaux. Yes, cells under stress do this. In cancer cells I think this is called the Warburg effect, but all cells with mitochondria can do this.
Yes, however most of the proteins localized inside the mitochondria are from both parents, such as P5CS. The electron transport chain proteins are however only inherited from the mother as they are encoded by the mitochondrial DNA that most of the time only passes down maternally unless rare circumstances.
In theory, yes. But, as this is a new discovery, a lot more research is going to have to be done into what even causes this secondary mitochondria to form and how it affects cell growth and function.
Probably, scientists were able to evolve a single cell colony of fungus into a multicellular being, so i can't see why they can't just transform the living cousins of mitochondria into it
I was told ribosome are places to make protein. Didn't know that mitochondria can make proteins 😮 I have slight memory that mitochondria have their own apparatus and may be thus they can make their own RNA or proteins. Need to recall and read about it.
Yeah mitochondria have their own genome and their own ribosome. There's only a small number of mitochondrial genes left in the mitochondria though and alot of them have been ported to the nuclear genome, get made into protein by the host ribosome, then trafficked back into the mitochondria.
Ribosomes perform translation --- they *read mRNA codons* to assemble amino acids into peptides and proteins. "Pyrroline-5-carboxylate synthase (P5CS) catalyzes the synthesis of pyrroline-5-carboxylate (P5C), a key precursor for the synthesis of proline (a secondary amino acid) and ornithine (non-essential and nonprotein amino acid)." Perhaps the fact that these are not the amino acids typically assembled into proteins at ribosomes explains an essential part of the difference.
@@Talus-GortUnderstood first part. For second part, are you trying to say that amino acids formed inside mitochondria are non essential because they do not form any protein or peptide? Why you gave example of proline? Sorry if my question is not clear. But the video says that the second type of mitochondria are full of proteins. Or you are trying to say that usually proline doesn't make proteins, but in damaged cells they do make proteins. And presence of these same proteins in cancer cells too shows that when ever cells are in stress they make proline based proteins?
CDR, Dr. Robert Naviaux, professor at UCSD. I've got a kind of CFS myself and it's just painful how slow research is going, but the UCSD genetics lab has been extremely busy last 10 years
Fun fact: You inherit your mitochondrial dna exclusively from your mother so if you are a guy then a massive mitochondrial descendent line just ended with you 😅
Very interesting, mitochondria are to me amazing. Now they are specialising. Sure there is more to mitochondria at the quantum level but I need someone who can explain it. We know that they do not depend on the food we consume alone to produce energy, they mainly use light. Did not realise how deep the energy of light penetrates our bodies. Please if you're interested look at mitochondria and light, melonin, deturium depleted water. Mitochondria produce water and use water. I have also watched videos of how our bodies produce light internally, to me mitochondria are interesting.
BABE WAKE UP NEW MITOCHONDRIA JUST DROPPED
😂😂gold.
I bestow you the title "winner of the internet" for today.
👇
Well damn, that is interesting. My mitochondrial education continues.
Mitochondria are old free-living organisms that came together with whatever chimera originated the Eukaryotic Cell we are all based upon; A remarkable discovery by one giant Lynn Margulis. Like ribosomes, they likely vary between cell lines in the same organism. I wonder if this brillant research and breakthrough (congrats) relate to heteroplasmy in any way... Hypocondriac mitochondria?!
Endosymbiosis is not the same process as formation of chimera (cell lines with distinct nuclear origins within the same organism, iirc). Again iirc, most of the original bacterial DNA has become nuclear, with only a portion remaining in our mitochondria.
@@Talus-Gort Check the early century work by W. Ford Doolitle. Eukarya cells seem to have sets of genes from eubacteria (mainly those related to metabolism), some related to Archea (those related to the Central Dogma processes) and some apparently from something else (maybe a deceased lineage). Some even extend the endosymbiosis premise to the cell nucleus (it has two sets of double-lipid layers). So, yes, ultimately the endosymbiosis scenario, of multiple lineages of organisms amalgamating into one coherent hole could be portrayed by a Chimera metaphor, a term that in Cellular and Molecular Biology alone has more than one potential figurative meaning (e.g. a chimeric recombinant DNA stretch). If one cell is spliced from two or three different organism (simultaneously or in steps) it seems chimeric to me. Reference 127 here supports both of our claims, in a way:
www.nature.com/articles/s41586-024-07677-6
@@Talus-Gort ...and not only a portion of the proteobacteria-like ancestral DNA remaining in our mitochondria but, as the video explains, with several vital processes encoded from old nuke genes now found in the mtDNA. A sort of resident hostage scenario of Game of Thrones (or the War of the Roses if you prefer): Hey mitochondria, hold my beer, er, I mean, hold my genes.This way both parties are heavily dependent on one another...
@@bigfootpegrande I know all this, but thanks for taking the time.
MITOCHONDRIA IS THE POWERHOUSE OF THE CELL
that's the only sentence I remember from biology class!!
Oh I didn't know this. Thanks
Stem cells can survive without mitochondria for more than 30 days. Where is the power coming from…?! 🤔
@@Mob1bo wow didn't know that, definitely stem cells have stored energy. When kids are born, they have brown fat cells in higher number than white cells, also number of mitochondria per cells in kids are higher. May be stem cells have something in them.
@@Mob1bocitric acid cycle happens in mitochondria, in stem cells they depends on glycolysis to produce ATP, which happens in cytosol.
It was not clear if these "two types of mitochondria" are actually two separate lines ("species") of mitochondria, with different genetics, or are the same genetic type of mitochondria expressing their genes in very different ways, that is, specializing in the same way as the cells of multicellular organisms specialize into different types of cells.
It's interesting that aerobic exercise training can induce mitochondrial biogenesis, meaning the creation of more mitochondria. Considering exercise training is also linked to improved cellular health and muscle growth or maintenance, the question arises, does exercise training also stimulate the production of these alternative mitochondria that aid in building a cell?
@@livephysiology probably. If these segregated Mt are related to stress or cell damage. Just like adults lose brown fat but athelets have more brown fat in them. Same with mitochondria.
Excercise induces an hypoxic environment in cells meaning they get starved of o2 because they dont get enough of it in time. This produces a chain reaction where your body gets the signal to produce more red blood cells, mitochondria in cells, growth hormone etc among other things to adapt to the metabolic stress.
Blood flow restriction training actually takes advantage of this to help critically ill patients gain back their strength. Hour long high intensity training is equivalent to short low intensity training under BFR
This "begging the question" narrative is a stretch, but yeah obviously they've done these studies on mitochondria without the knowledge of their subpopulations so they were inclusive of all results which includes the "other" mitochondria
Right. Something is missing because when you have CFS/ME most people are hurt further with excersises. Not just resistant but one could just stop functioning mid functioning ya know?
3:11 P5CS pyrroline-5-carboxylate synthase
Sounds like something Data and Dr. Crusher would be discussing.
@ have not watch any Dr Crusher podcasts. But if I understood the video correctly the data indicates that this function is something that can be activated while fasting. Is there a podcast you can recommend for me to introduce myself to Dr Crusher? Thank you
@@erikthompson404 It's a Star Trek reference.
My question is how did this thing evade discovery for so long? It does look visibly different enough for someone to have said, "Wait -- what's that one, and why does it look like that?"
I have a feeling that it tended to be pointed out by first-year students, and the professor replied, "Well, some mitochondria just look like that, we don't know why. Moving on ... " That happens more than we would like in the sciences, where a potential discovery is staring us in the face, but the n00bs are the ones who see it, and they are often instructed to stop noticing it until someone higher up decides right, we're going to look into this.
It's not about noticing the mitochondria under the microscope but rather about finding the right conditions which will cause cells to produce the second kind of mitochondria
@@kektimus_prime9899 Still though, they must have been seen before now. Those conditions must have obtained in cells on slides before, meaning that they must have been visibly present before this researcher finally decided to find out what was up with them. I'm surprised it took this long for someone to ask the question.
we should digitalise research, especially the data collection part into bigger databases. Correlations of stuff happening occasionally 6 times out of 10 is not itneresting, but 5200 out of 10000 is. This way the rarer phenomena would not evade the only narrow minded people who are lucky enough to see it. Also with this particular example... effects after starvation means someoner forgot to feed the samples in the petri dishes, so they are hush hush about it.
Look up cell danger response. Dr. Robert Naviaux of UCSD. I'll be honest, it seems like there is some kind of resistance within academia to do certain kinds of research linked to chronic disease. It doesn't seem like it's that hard to observe this mitochondrial behavior, but it does seem like young postgrads are steered away from advancing research in metabolic disorders and disease stemming from innate immunefunction.
I feel a little more smart today
*a little smarter
@@ricp7116I’m dead
Very, very cool study and finding! I'm sure Nick Lane will be all over this.
This video worth thousands of like thx for your incredible input ❤🌺
Considering that non-OXPHOS, P5CS-containing mitochondria also need ATP for the first step (Gamma-glutamyl kinase activity): Glutamate + ATP → Gamma-glutamyl phosphate + ADP, and NAD(P)H for the second step (Gamma-glutamyl phosphate reductase activity): Gamma-glutamyl phosphate + NADPH + H+ → Glutamate-5-semialdehyde + NADP+ + Pi, where does the ATP and NAD(P)H come from?
maybe this is new symbiotic relationship evolution? just like how chloroplasts and old mitochondria came into existence?
Cells may have many mitochondria, some might have hundreds if I recall correctly. Each mitochondria might have multiple copies of the mitochondrial DNA.
besides this, being round and relatively short is the reason it is such a primary seat for varied genetic markers, such as species barcodes. Easy to recover even from degraded DNA... The Ouroborus...
WOW!!! Cannot wait to learn MORE🥰❣️
Synthases "do not require energy from adenosine triphosphate (ATP) or other nucleoside triphosphates to form bonds. They are classified as lyases, which are enzymes that cleave chemical bonds without using hydrolysis or oxidation." Does this lack of reliance on ATP explain the segregation of pyrroline-5-carboxylate synthase (P5CS) activity?
of course. all such investigations have the same perspective: we are investigating the evolutionary biology of an organism which develops from a progenitor cell which we use to identify that organism. For example, when I say, "your cat", I am referring to all cells of which the progenitor cell was your cat's mom's egg which "became" your cat.
@@seanrowshandel1680 I know. The question was deeper than that.
@@Talus-Gort Why do you think we JUST went over the video together yesterday? Otherwise, there would have been no video. Are you expecting everyone to believe that how much you understand is a total mystery to everyone until we've already taught you what you didn't know (just so you can convince yourself that you didn't say anything embarrassing), while other people all around the world are constantly making fun of each other for not understanding things? I'm done explaining this to you like a robot. You're clearly trying to make it so that "only women can work as educators". Bam Margera never did THAT
scienctific discoveries from experimental data and hard analysis, yay!!! what a wonderful contrast to m a g a.
"We're doomed" - C3PO
Agreed. Also a wonderful contrast from 200+ different 'genders'...
Good. Now please try to figure out what is happening with the mitochondria of those of us living with ME/CFS. 😿
See Jack Kruse. He would undoubtedly say that you're getting insufficient full-spectrum sunlight, and/or too much blue light after sunset.
I'd love to know how this relates to ME/CFS where mitochondrial damage is one of the theories and issues recycling ADP back to ATP seem to be compromised.
Mitochondria is the powerhouse of the cell final boss
new mitochondria just dropped
Are you trying to say that usually proline doesn't express in mitochondria, but in damaged cells they do make proteins. And presence of these same proteins in cancer cells too shows that when ever cells are in stress they make proline based proteins? Does that mean if we remove these segregated mitochondria from cancer cells, we can control cancer?
I don’t think you even need to remove them, just inhibit them
Look up cell danger response hey Dr Robert Naviaux. Yes, cells under stress do this. In cancer cells I think this is called the Warburg effect, but all cells with mitochondria can do this.
Do both come from the mother?
Yes
Yes, however most of the proteins localized inside the mitochondria are from both parents, such as P5CS. The electron transport chain proteins are however only inherited from the mother as they are encoded by the mitochondrial DNA that most of the time only passes down maternally unless rare circumstances.
Fascinating stuff - thank you! ❤
Cool. Thanks for sharing.
Thank u for sharing sir
P5CS. Okay-I’m left hanging: What’s the function of this protein?
It synthesizes pyrroline-5-carboxylate which is required for the synthesis of proline
@@kektimus_prime9899 How does this relate to the anabolism of these mitochondria?
YEAHHHHH MITOCHONDRIA IS THE POWERHOUSE OF THE CELLL🔥🔥🔥🔥🔥
Thanks ❤❤❤
Should this not lead to pinpointing cures for autoimmune diseases
In theory, yes. But, as this is a new discovery, a lot more research is going to have to be done into what even causes this secondary mitochondria to form and how it affects cell growth and function.
When your mitochondria is damaged or faulty ... this is seriously news.
So not just powerhouse of the cell?
Efraim Racker gives this 👍
Bad news for bio students 😢
CAN I JOIN YOUR TEAM?? I’M REALLY INTO CANCER RELATED RESEARCH 😭😭😭😭😭😭😭😭😭
What's Mitochondria? Come on tell me what it is.
3:26 is this FISH imaging?
'Tis the bridge between worlds.
Awesome!
Do you think it possible too make Synthetic or "After market Mitochondria " ?
Probably, scientists were able to evolve a single cell colony of fungus into a multicellular being, so i can't see why they can't just transform the living cousins of mitochondria into it
Mitochondria is life.
We need a religion bowing down to Mitochondria 🙏
I was told ribosome are places to make protein. Didn't know that mitochondria can make proteins 😮 I have slight memory that mitochondria have their own apparatus and may be thus they can make their own RNA or proteins. Need to recall and read about it.
Yeah mitochondria have their own genome and their own ribosome. There's only a small number of mitochondrial genes left in the mitochondria though and alot of them have been ported to the nuclear genome, get made into protein by the host ribosome, then trafficked back into the mitochondria.
@justindie7543 yes, extra nuclear genome.
Ribosomes perform translation --- they *read mRNA codons* to assemble amino acids into peptides and proteins. "Pyrroline-5-carboxylate synthase (P5CS) catalyzes the synthesis of pyrroline-5-carboxylate (P5C), a key precursor for the synthesis of proline (a secondary amino acid) and ornithine (non-essential and nonprotein amino acid)." Perhaps the fact that these are not the amino acids typically assembled into proteins at ribosomes explains an essential part of the difference.
@@Talus-GortUnderstood first part. For second part, are you trying to say that amino acids formed inside mitochondria are non essential because they do not form any protein or peptide? Why you gave example of proline? Sorry if my question is not clear. But the video says that the second type of mitochondria are full of proteins.
Or you are trying to say that usually proline doesn't make proteins, but in damaged cells they do make proteins. And presence of these same proteins in cancer cells too shows that when ever cells are in stress they make proline based proteins?
@@Talus-Gortthat means if we kill these segregated mitochondria, cancers cells will not have supply for the protein needs and die too?
powerhouse of the cell yo
Dr Jack Kruse peaking head around corner
I wonder how this is a factor in my long COVID and post exercise exhaustion
CDR, Dr. Robert Naviaux, professor at UCSD. I've got a kind of CFS myself and it's just painful how slow research is going, but the UCSD genetics lab has been extremely busy last 10 years
We found new type of mitochondria before GTA 6 there are you happy?
Mitochondria 2
Fun fact: You inherit your mitochondrial dna exclusively from your mother so if you are a guy then a massive mitochondrial descendent line just ended with you 😅
For real? 🫠
Or did you just wanna say Massive mitochondrial descendent line?
Thats not true anymore. We used to believe that but now check the latest research on this you can also get it from your dad.
Learning something so fundamental, yet we keep hearing how to and how not to live at very high levels as they're absolute facts.
TALK! TALK! Quit your damn elocution.
"God moves in mysterious ways, Her wonders to perform".
Very interesting, mitochondria are to me amazing. Now they are specialising. Sure there is more to mitochondria at the quantum level but I need someone who can explain it. We know that they do not depend on the food we consume alone to produce energy, they mainly use light. Did not realise how deep the energy of light penetrates our bodies. Please if you're interested look at mitochondria and light, melonin, deturium depleted water. Mitochondria produce water and use water. I have also watched videos of how our bodies produce light internally, to me mitochondria are interesting.
it came from males
no not really??? from mother actually