How could there be no junk DNA? There are plenty of inserted regions of repeating codons, between regions that are read (outside of replication). DNA replicators are very simple machines, they copy until they’re told to stop, I agree that any junk DNA in the human genome has been there for a very long time, but it’s not difficult to find single cell organisms that have introduced previously non-self DNA in their genome. If that DNA isn’t used besides replication then it’s junk is it not?
Also telomeres are pretty synonymous with junk DNA, until they aren’t, or is every shortening of the telomere removing information vital to a cells function?
I’m not an expert on the subject. I can only repeat what Venter said: “the only junk DNA is in my colleagues brains”. He claims that all DNA has function and that it should not be referred to as junk just because we don’t know the function yet.
Junk DNA is repeating codons, or codons that occur in areas that are outside of the “start/stop” codon triplicate pairs. A DNA transcribing protein will read the genetic code from a start signal, until it gets to a stop signal. Then it clips itself off the chain and re-binds the chain together for the next transcriber to use. Sometimes there are extra codons between a stop signal and the next start signal, sometimes there are hundreds of thousands of extra codons. They aren’t there for structural reasons, all DNA is the same 4 codons linked together over and over, all the different chromosomes are different sizes. All of this DNA is reported when the cells divide, that’s the only time those regions between the stops and starts actually come into play. This is very easily proven, we know the structure of the reading proteins down to the molecule (indeed there are starts and stops and triplicate base pairs that design these transcribing proteins). The “important” junk DNA that has significance while not being in a “start->stop” zone are the codons that occur before the first start codon on either side of a DNA strand, when DNA is replicated the protein that starts replicating it has to start at 1 end of 1 side of the DNA in order to be able to read it, except it needs to find the end first, and to make sure it’s all the end it “clips” the first 6 (? Maybe more maybe less, it’s been decades since I’ve studied this) codons from the strand of DNA, this is lost for all future replications of the cell, your DNA actually gets shorter every time your cells reproduce (except your miosis division cells, they have a special replication process that keeps the full length of every chromosome).
Sorry for the wall of text, but there’s plenty of examples of blatantly junk DNA, and there are known methods of how it occurs. Anyone who says every codon pair has a purpose has a screw loose and is ignorant to the mechanics of evolution.
Junk DNA is repeating codons, or codons that occur in areas that are outside of the “start/stop” codon triplicate pairs.
Those sequences do things and have effects. In fact, the coding regions are often less functional than the non-coding ones.
They aren’t there for structural reasons, all DNA is the same 4 codons linked together over and over, all the different chromosomes are different sizes.
Sometimes they ARE there for structural reasons? Read: enhancers, or CTCF binding sites? Among many other myriad examples of functional noncoding regions? Also, nucleotides =/= codons. There are 64 codons.
All of this DNA is reported when the cells divide, that’s the only time those regions between the stops and starts actually come into play. This is very easily proven, we know the structure of the reading proteins down to the molecule (indeed there are starts and stops and triplicate base pairs that design these transcribing proteins).
That’s bull. You’re out of your depth. A contemporary college molecular biology course would show your examples to the contrary.
The “important” junk DNA that has significance while not being in a “start->stop” zone are the codons that occur before the first start codon on either side of a DNA strand, when DNA is replicated the protein that starts replicating it has to start at 1 end of 1 side of the DNA in order to be able to read it
I feel like a broken record but Enhancers! lncRNAs! siRNAs! Binding sites! Other gene regulatory regions! Epigenetic nucleosome modifications! Chromatin remodeler sites!
except it needs to find the end first, and to make sure it’s all the end it “clips” the first 6 (? Maybe more maybe less, it’s been decades since I’ve studied this)
Oh, there’s your problem. A lot has changed. You refuse to see the sea change happening around you because it means you’re out of date.
Sorry for the wall of text, but there’s plenty of examples of blatantly junk DNA, and there are known methods of how it occurs. Anyone who says every codon pair has a purpose has a screw loose and is ignorant to the mechanics of evolution.
I was happy to reply to you and engage pleasantly originally but you are only engaging with people that know less about biology than you do. You are not an expert if you last studied biology decades ago and can’t remember the details. You certainly aren’t enough of an authority on the subject to question a contemporary article published in Science or the work of other researchers currently in the field.
I really, really encourage you to read these papers thoroughly. You are the target audience-- people who learned the machine model of the cell and who are gripping it so tightly that they are blind to the nuance that we’ve uncovered. I also encourage you to not write insults about people who disagree with you, especially people with more domain knowledge than you have.
Every sperm isn’t sacred and every piece of DNA isn’t with purpose, otherwise explain ferns and plants having hundreds of times more DNA than higher functioning life forms.
So I think I can make the claim that I am an expert in this, at least compared to 95%+ of biological researchers. My research foci include epigenetic and emergent interactions like the ones discussed in the article, and although I am not going to back this up by identifying myself, please believe me when I say I’ve written some papers on the topic.
The concept of junk DNA is perhaps the problem here. Obviously there are large swaths of our genome that do not encode anything or have instructions for proteins. However, dismissing all non-coding DNA as “junk” is a critical error.
Your telomeres are a great example. They don’t contain vital information so much as they serve a specific function-- providing a buffer region to be consumed during replication in place of DNA that does contain vital information. Your cells would work less well without telomeres, so calling them junk is inaccurate.
Other examples of important non-coding regions are enhancer and promoter regions. Papers describing the philosophical developments of stochasticity in cellular function note how enhancers are vital for increasing the likelihood of transcription by making it more likely that specific proteins floating in the cellular matrix interact with each other. Promoter regions are something most biologists understand already, so I won’t describe them here (apologies for anyone who needs to go read about them elsewhere!). Some regions also inform the 3D structure of the genome, creating topological associated domains (TADs) that bring regions of interest closer together.
Even the sequences with less obvious non-coding functions often have some emergent effect on cellular function. Transcription occurs in nonsense regions despite no mRNA being created; instead, tiny, transient non-coding RNAs (ncRNAs) are produced. Because RNA can have functional and catalytic properties like proteins, these small RNAs “do jobs” while they exist. The kinds of things they do before being degraded are less defined than the mechanistic models of proteins, but as we understand more stochastic models, we are beginning to understand how they work.
One last type of DNA that we used to consider junk: binding sites for transcription factors, nucleosome remodelers, and other DNA binding proteins. Proteins are getting stuck to DNA all the time, and then doing things while they’re stuck there. Sometimes even just being a place where a nucleosome with a epigenetic flag can camp out and direct other cellular processes is enough to invalidate calling that region “junk”.
Anyway I’m done giving my spiel but the take home message here is that all DNA causes stochastic effects and almost all of it (likely all and we haven’t figured it out yet) serves some function in-context. Calling all DNA that doesn’t encode for a protein “junk” is outdated-- if anything, the protein encoding regions are the boring parts.
Thank you for taking the time to respond, I respect your knowledge and agree with you for the most part. From an evolutionary perspective there’s very little pressure to cull genetic material that does not have a purpose, genome replication is already taking place and takes very little overall energy/time.
There may not be as much useless DNA in the system as previously thought, but not every codon pair has a use. There are undoubtedly identical transcription codes being suppressed in one section of DNA that are active in other regions, and it may have been useful to have that extra region available if pressures ever applied that caused that region to be reactivated, but if mutation occurred and caused that region to no longer have the original blueprint it was coding for, it could theoretically create actual evolutionary pressure to eliminate/suppress that section of the genome, it could be suppressed/inactive harmful DNA, not junk but also not beneficial.
My biggest hang-up on the whole “every codon has a purpose” argument is that it blatantly ignores the evidence occurring so much more frequently at “lower” life forms. Eukaryotic single cell organisms swap DNA rather readily, it’s a much higher risk/reward mechanism of evolution, a lot of that DNA, if it turns out to be beneficial, will be ancillary to the actual genes with benefit. Plants have genomes that vary in length from generation up generation, often times much larger than required, maybe it’s because they chill in the sun all day and are more susceptible to genetic mutation, but just because there’s extra targets for codon swapping, doesn’t mean that DNA is set there with purpose. It just exists. It may have been beneficial at one point, but it’s only there because it isn’t detrimental enough to have selection pressure repercussions. If pressures were high enough they every codon mattered, (or if it were designed intelligently so that every codon mattered) a lot of genomes (I’m not to nervous to claim I believe all genomes) would be shorter due to junk culling, it’s just such a small factor in the schema that it isn’t ever selected against.
You feel that if a codon isn’t meant for something, if it doesn’t have a purpose– then it is junk. This is a mindset that is reflective of the machine model of the cell. We used to expect that each protein was bespoke for a function, each transcript necessary.
The whole paradigm shift at hand is this model falls flat, even for coding regions. I think you’re actually very spot in here with the prokaryotic DNA or the plant genomes (love me some violets for their weird genomes). Some parts of a genome will rapidly change and appear to serve no real purpose, but the next bite is the important one: even if it seems like there isn’t a purpose, like a top-down prescription for functionality, those regions are still doing something while they are present.
For example, some long non-coding regions affect the likelihood that a person will develop Parkinson’s disease, or in the case of plants with various polyploidies, the relative expression of their genes won’t necessarily change, but the absolute expression may.
Basically, you aren’t wrong that these regions dont have a purpose, because no genes have a purpose. The cell isn’t a machine.
What do you mean by this? I feel like you think the meaning is obvious after everything you’ve said, but it’s not.
Even if we accept that everything you said is true, all it means is that the cell is a very, very complex machine. More complex than current models account for. It’s just chemistry, after all. The chemicals behave in predictable fashion or else life wouldn’t be possible at all. Molecules moving around, transforming, causing other molecules to transform, etc, etc, to turn food into shit and babies. You can always use the word “machine” to describe that, no matter how complex it is. Just like the word “algorithm” can be used to describe the function of code no matter how complex it is, whether it’s a simple path finding algorithm, or the newest machine learning one.
But I probably shouldn’t use the word “function” because that implies purpose, and, as you say, no part of the chemistry of life has purpose. I hope you can detect my snark. That’s a pretty lame argument that’s philosophical at best. The purpose of the machinations of the cell is to maintain life and reproduce. No mater how many times you say it, your words won’t change the fact that that is the purpose of the chemistry of life.
You’ve twisted around the word “purpose” in your head until it has no useful meaning. Nonsense. A molecule can many overlapping, hard to discern purposes. That does not mean it doesn’t have a purpose.
When I say “the cell isn’t a machine”, it is in specific reference to the machine model of the cell, which is a previously established conceptual framework in the field of molecular biology. If you want to understand why that model is falling out of favor today, you’re invited to read the article linked by OP and/or the articles I have linked in other comments.
The gist is that the cell is more complicated, flexible, and emergent than any machine has ever been and will be for the foreseeable future, and the idea that we can simply map the functions of each molecule in the cell to get a perfect “circuit diagram” of how everything plays together is defunct.
I don’t have time to mess with this thread any more. You can either accept what myself (an expert in this field), the author of this publication (which happens to be one of the most prestigious journals in the world), and others who do this research daily are saying about this, or you can not. Frankly, if you are an expert also, the field, the research, and the truth barely cares about our opinion-- it certainly doesn’t care about non-expert opinions on the internet.
How could there be no junk DNA? There are plenty of inserted regions of repeating codons, between regions that are read (outside of replication). DNA replicators are very simple machines, they copy until they’re told to stop, I agree that any junk DNA in the human genome has been there for a very long time, but it’s not difficult to find single cell organisms that have introduced previously non-self DNA in their genome. If that DNA isn’t used besides replication then it’s junk is it not?
Also telomeres are pretty synonymous with junk DNA, until they aren’t, or is every shortening of the telomere removing information vital to a cells function?
I’m not an expert on the subject. I can only repeat what Venter said: “the only junk DNA is in my colleagues brains”. He claims that all DNA has function and that it should not be referred to as junk just because we don’t know the function yet.
He talks about at intervals in this interview.
If there is a random mutation that is neither advantageous nor disadvantageous, wouldn’t that be junk DNA?
Are we going to say we need to see how every descendant of the creature fares before we can decide whether it was junk DNA or not?
Junk DNA is repeating codons, or codons that occur in areas that are outside of the “start/stop” codon triplicate pairs. A DNA transcribing protein will read the genetic code from a start signal, until it gets to a stop signal. Then it clips itself off the chain and re-binds the chain together for the next transcriber to use. Sometimes there are extra codons between a stop signal and the next start signal, sometimes there are hundreds of thousands of extra codons. They aren’t there for structural reasons, all DNA is the same 4 codons linked together over and over, all the different chromosomes are different sizes. All of this DNA is reported when the cells divide, that’s the only time those regions between the stops and starts actually come into play. This is very easily proven, we know the structure of the reading proteins down to the molecule (indeed there are starts and stops and triplicate base pairs that design these transcribing proteins). The “important” junk DNA that has significance while not being in a “start->stop” zone are the codons that occur before the first start codon on either side of a DNA strand, when DNA is replicated the protein that starts replicating it has to start at 1 end of 1 side of the DNA in order to be able to read it, except it needs to find the end first, and to make sure it’s all the end it “clips” the first 6 (? Maybe more maybe less, it’s been decades since I’ve studied this) codons from the strand of DNA, this is lost for all future replications of the cell, your DNA actually gets shorter every time your cells reproduce (except your miosis division cells, they have a special replication process that keeps the full length of every chromosome).
Sorry for the wall of text, but there’s plenty of examples of blatantly junk DNA, and there are known methods of how it occurs. Anyone who says every codon pair has a purpose has a screw loose and is ignorant to the mechanics of evolution.
Those sequences do things and have effects. In fact, the coding regions are often less functional than the non-coding ones.
Sometimes they ARE there for structural reasons? Read: enhancers, or CTCF binding sites? Among many other myriad examples of functional noncoding regions? Also, nucleotides =/= codons. There are 64 codons.
That’s bull. You’re out of your depth. A contemporary college molecular biology course would show your examples to the contrary.
I feel like a broken record but Enhancers! lncRNAs! siRNAs! Binding sites! Other gene regulatory regions! Epigenetic nucleosome modifications! Chromatin remodeler sites!
Oh, there’s your problem. A lot has changed. You refuse to see the sea change happening around you because it means you’re out of date.
I was happy to reply to you and engage pleasantly originally but you are only engaging with people that know less about biology than you do. You are not an expert if you last studied biology decades ago and can’t remember the details. You certainly aren’t enough of an authority on the subject to question a contemporary article published in Science or the work of other researchers currently in the field.
I really, really encourage you to read these papers thoroughly. You are the target audience-- people who learned the machine model of the cell and who are gripping it so tightly that they are blind to the nuance that we’ve uncovered. I also encourage you to not write insults about people who disagree with you, especially people with more domain knowledge than you have.
Every sperm isn’t sacred and every piece of DNA isn’t with purpose, otherwise explain ferns and plants having hundreds of times more DNA than higher functioning life forms.
So I think I can make the claim that I am an expert in this, at least compared to 95%+ of biological researchers. My research foci include epigenetic and emergent interactions like the ones discussed in the article, and although I am not going to back this up by identifying myself, please believe me when I say I’ve written some papers on the topic.
The concept of junk DNA is perhaps the problem here. Obviously there are large swaths of our genome that do not encode anything or have instructions for proteins. However, dismissing all non-coding DNA as “junk” is a critical error.
Your telomeres are a great example. They don’t contain vital information so much as they serve a specific function-- providing a buffer region to be consumed during replication in place of DNA that does contain vital information. Your cells would work less well without telomeres, so calling them junk is inaccurate.
Other examples of important non-coding regions are enhancer and promoter regions. Papers describing the philosophical developments of stochasticity in cellular function note how enhancers are vital for increasing the likelihood of transcription by making it more likely that specific proteins floating in the cellular matrix interact with each other. Promoter regions are something most biologists understand already, so I won’t describe them here (apologies for anyone who needs to go read about them elsewhere!). Some regions also inform the 3D structure of the genome, creating topological associated domains (TADs) that bring regions of interest closer together.
Even the sequences with less obvious non-coding functions often have some emergent effect on cellular function. Transcription occurs in nonsense regions despite no mRNA being created; instead, tiny, transient non-coding RNAs (ncRNAs) are produced. Because RNA can have functional and catalytic properties like proteins, these small RNAs “do jobs” while they exist. The kinds of things they do before being degraded are less defined than the mechanistic models of proteins, but as we understand more stochastic models, we are beginning to understand how they work.
One last type of DNA that we used to consider junk: binding sites for transcription factors, nucleosome remodelers, and other DNA binding proteins. Proteins are getting stuck to DNA all the time, and then doing things while they’re stuck there. Sometimes even just being a place where a nucleosome with a epigenetic flag can camp out and direct other cellular processes is enough to invalidate calling that region “junk”.
Anyway I’m done giving my spiel but the take home message here is that all DNA causes stochastic effects and almost all of it (likely all and we haven’t figured it out yet) serves some function in-context. Calling all DNA that doesn’t encode for a protein “junk” is outdated-- if anything, the protein encoding regions are the boring parts.
Thank you for taking the time to respond, I respect your knowledge and agree with you for the most part. From an evolutionary perspective there’s very little pressure to cull genetic material that does not have a purpose, genome replication is already taking place and takes very little overall energy/time.
There may not be as much useless DNA in the system as previously thought, but not every codon pair has a use. There are undoubtedly identical transcription codes being suppressed in one section of DNA that are active in other regions, and it may have been useful to have that extra region available if pressures ever applied that caused that region to be reactivated, but if mutation occurred and caused that region to no longer have the original blueprint it was coding for, it could theoretically create actual evolutionary pressure to eliminate/suppress that section of the genome, it could be suppressed/inactive harmful DNA, not junk but also not beneficial.
My biggest hang-up on the whole “every codon has a purpose” argument is that it blatantly ignores the evidence occurring so much more frequently at “lower” life forms. Eukaryotic single cell organisms swap DNA rather readily, it’s a much higher risk/reward mechanism of evolution, a lot of that DNA, if it turns out to be beneficial, will be ancillary to the actual genes with benefit. Plants have genomes that vary in length from generation up generation, often times much larger than required, maybe it’s because they chill in the sun all day and are more susceptible to genetic mutation, but just because there’s extra targets for codon swapping, doesn’t mean that DNA is set there with purpose. It just exists. It may have been beneficial at one point, but it’s only there because it isn’t detrimental enough to have selection pressure repercussions. If pressures were high enough they every codon mattered, (or if it were designed intelligently so that every codon mattered) a lot of genomes (I’m not to nervous to claim I believe all genomes) would be shorter due to junk culling, it’s just such a small factor in the schema that it isn’t ever selected against.
I would encourage you to read the linked Science paper and Dan Nichol’s paper, Is the Cell Really a Machine?
You feel that if a codon isn’t meant for something, if it doesn’t have a purpose– then it is junk. This is a mindset that is reflective of the machine model of the cell. We used to expect that each protein was bespoke for a function, each transcript necessary.
The whole paradigm shift at hand is this model falls flat, even for coding regions. I think you’re actually very spot in here with the prokaryotic DNA or the plant genomes (love me some violets for their weird genomes). Some parts of a genome will rapidly change and appear to serve no real purpose, but the next bite is the important one: even if it seems like there isn’t a purpose, like a top-down prescription for functionality, those regions are still doing something while they are present.
For example, some long non-coding regions affect the likelihood that a person will develop Parkinson’s disease, or in the case of plants with various polyploidies, the relative expression of their genes won’t necessarily change, but the absolute expression may.
Basically, you aren’t wrong that these regions dont have a purpose, because no genes have a purpose. The cell isn’t a machine.
What do you mean by this? I feel like you think the meaning is obvious after everything you’ve said, but it’s not.
Even if we accept that everything you said is true, all it means is that the cell is a very, very complex machine. More complex than current models account for. It’s just chemistry, after all. The chemicals behave in predictable fashion or else life wouldn’t be possible at all. Molecules moving around, transforming, causing other molecules to transform, etc, etc, to turn food into shit and babies. You can always use the word “machine” to describe that, no matter how complex it is. Just like the word “algorithm” can be used to describe the function of code no matter how complex it is, whether it’s a simple path finding algorithm, or the newest machine learning one.
But I probably shouldn’t use the word “function” because that implies purpose, and, as you say, no part of the chemistry of life has purpose. I hope you can detect my snark. That’s a pretty lame argument that’s philosophical at best. The purpose of the machinations of the cell is to maintain life and reproduce. No mater how many times you say it, your words won’t change the fact that that is the purpose of the chemistry of life.
You’ve twisted around the word “purpose” in your head until it has no useful meaning. Nonsense. A molecule can many overlapping, hard to discern purposes. That does not mean it doesn’t have a purpose.
When I say “the cell isn’t a machine”, it is in specific reference to the machine model of the cell, which is a previously established conceptual framework in the field of molecular biology. If you want to understand why that model is falling out of favor today, you’re invited to read the article linked by OP and/or the articles I have linked in other comments.
The gist is that the cell is more complicated, flexible, and emergent than any machine has ever been and will be for the foreseeable future, and the idea that we can simply map the functions of each molecule in the cell to get a perfect “circuit diagram” of how everything plays together is defunct.
I don’t have time to mess with this thread any more. You can either accept what myself (an expert in this field), the author of this publication (which happens to be one of the most prestigious journals in the world), and others who do this research daily are saying about this, or you can not. Frankly, if you are an expert also, the field, the research, and the truth barely cares about our opinion-- it certainly doesn’t care about non-expert opinions on the internet.