In the 1970s, when scientists compared the sequences of DNA in genes with the sequences of RNA encoded by those genes, they made a puzzling discovery: the DNA of most genes in animals, plants, and other eukaryotes contains too much information. The extra segments of largely useless information were named introns, and they must be cut out of RNA before the protein is made. Exons are the portions of the gene that remain in the RNA after the introns have been removed.
- Relics of Eden
At every turn evolutionists are faced with inventing yet another story. But that’s ok because, to paraphrase dazz, they are used to it by now.
At some point in some lineage in the history of life it must have been advantageous to insert crap into the genome. But that’s simply not allowed, under the central dogma. Even so, some mechanism must have evolved to make it possible to insert crap into the genome, and then yet another mechanism evolved to remove the crap from the DNA so that protein could still be produced from genes in spite of the fact that genes had become filled with junk.
At some point, the evolutionary story stretches credulity.
Assume a gene without an intron. Now imagine a scenario in which some piece of crap of indeterminate length gets inserted into that DNA sequence. Imagine more than one. Imagine that protein manufacture continues unabated in spite of the insertion. Imagine now an imaginative mechanism arises to excise the crap out of the gene. Let your imagination run wild!
It’s simply difficult for me to believe that “it just happened, that’s all” is rational. It throws rationality, and science, out the window.
What is the most recent and the most plausible explanation for the rise and fall of introns?
The whole point is that genome size is not a good proxy for percentage of non-protein-coding DNA.
There is a table of the percentage of non-coding DNA in selected sequenced genomes here
From the table we can see that this percentage for the following organisms is:
Yeast 27.2%
Nematode worm 72%
Fruitfly 81.8%
Human 97.2%
I will insert the table below.
Do you understand the difference between relative size and absolute size? Guinea pigs have heads which in proportion to their overall size is larger than giraffe’s heads to their overall size. It does not then follow that guinea pigs have larger heads than giraffes.
The research can only go one way.
From Wikipedia:(WARNING – unreliable source) about the protein titan.
Mutations to this protein can cause all sorts of problems so I would say that the production and distribution of isoforms must be very tightly controlled.
Can you not see why only sequenced data were used in the chart? It does not matter if only two of three species from different phyla were used in the chart the conclusion would have been just the same. Percentage non-coding DNA varies greatly throughout the living world.
When we get down to organisms such as bacteria then the non-coding portion of their genome is a very small fraction of the total genome. Most of their genomes are translated. Over 80% of the bacteria genome is translated into proteins compared with less than 2% for humans.
Then, as in the protein titan I mentioned above, how does the cell decide which isoform to use in the various parts of the body? Surely having all that noise floating about the cell would be detrimental to its health.
Using scrabble letters, take all the characters that make up a short story and put them in a bag. There is an astronomical combination of ways that these can be arranged, the vast majority of which will be jibberish. And if they are removed randomly this is what you will get. But give the bag to an adult human who knows the language and s/he will be able to make up a vast amount of short stories from these available letters.
Modularity is something which is used in gas turbine engine design. But it wasn’t always so. Engines have only a handful of modules which can be easily exchanged, but the way engines were constructed had to be extensively modified in order to allow this capacity. It wasn’t just a matter of simple modifications to existing engines. It took designers much time and effort and learning from previous unthoughtful design to come up with successful modular designs. And gas turbine engines are extremely simple structures compared to living organisms.
Sounds like the designer of organisms didn’t take the time and effort
And to think it all evolved from a simple self-splicing intron. The selective pressure to evolve a better way of RNA splicing must have been ginormous!
CharlieM,
Argument by rubbish analogy Part 1. Protein segments are actual 3D ‘things’, not sentence fragments.
Argument by rubbish analogy Part 2. What are they, sentences or machines? Make your mind up. If you can cut up a turbine and rearrange it in multiple ways for functional product, maybe you would have the grain of a point.
Mung,
It certainly screws with your proteins if you don’t do it right.
The Designer seems to have omitted doing something about the potentially invasive intron fragments that result from this process. Once you have a halfway decent spliceosome, introns can hop around ad lib, cackling maniacally. And transposons can hop inside them, smirking. All that enhancement is just asking for trouble.
Thanks Charlie M.
The complexity of a vocabulary isn’t defined by the alphabet that spells its words. The Chinese are astonished that the English language has only 26 letters in its alphabet.
The complexity of a novel is not rooted solely in the number of words that can be found in its dictionary.
In like manner, the complexity of the human isn’t solely in the protein sequences, but how the sequences are put together. It looks to me the ncDNA in humans is provides a lot of complexity to what makes humans human, especially the brain and the rest of the central nervous system.
I’ve already listed a three specific classes of ncDNA , two of which are implicated in human neural development:
1 Alus: about 11% of the genome
2 Introns: about 30% of the genome
3 LINE-1: about 16% of the genome
The Alus in combination with introns are unique in the way they are used in primates, especially the nervous system. LINE-1 use is also special to the central nervous system.
If each creature has some aspects of how it uses its DNA that are unique to that species, that will explain the C-value paradox. The Alus are a case in point to that effect since they are primate specific, and hence have primate specific behavior of ncDNA.
Do we have as much data as we’d like to know the details. Not yet, but it’s looking promising.
stcordova,
That is one heck of a long shot. Indeed, one is going down to within-baramin level for such distinctions.
Though maybe the primates inherited them from a common ancestor.
And Allan’s argument is via bald assertion.
Current theory says it came from 7SL RNA, which I believe is conserved beyond primates. The issue is why the primates have so many copies of this particular sequence, in humans about a million copies. The Alus are used in ways described above.
Agreed, but I’ll take that bet, the only question is when the question can be settled to everyone’s satisfaction. Given there are about 90,000 lncRNAs (including Larry’s LOLATs) and that we’ve really successfully identified the mechanism of 10-400 of them (HOTAIR, XIST, FIRRE, NEAT1…) just in humans alone, we could be waiting a long time to settle the issue.
stcordova,
Of course it is. The mutation(s) that led it to become a transposon in primates occurred in the primate common ancestor, not 7SL RNA itself.
Because it’s a transposon. You can even see which copies are related to which – there are several families. Any theory must try and explain why there is apparent sequence divergence.
Clearly not to the satisfaction of someone who thinks their eternal soul rides on the answer.
Sure. Like, forever.
I wish you would get your story straight. That was your third reversal. You had just told me that Mattick’s claim was your point, and he said that there wasn’t much difference in amount of coding DNA among species.
A few carefully selected sequenced genomes, which, as I explained, were selected for their small sizes, except for the human.
I understand. It seems that you don’t. Your table is directly related to genome size. Given that the absolute amount of protein-coding sequence doesn’t change much, the percentage of non-coding DNA is directly related to genome size. Salamanders have a much higher percentage of non-coding DNA than humans. They are therefore, I suppose, the pinnacle of creation. Or would be if the record-holder were not an amoeba. You don’t seem to understand any of this.
Ah, but how far can it go? That’s the question. I don’t see any point regarding Titin. Does it have no isoforms?
Of course it varies greatly. The point is that it doesn’t vary in any systematic way with organismal complexity, however you try to measure that.
Yes, and there’s a well-understood reason for that which has to do both with population size and selection on replication efficiency. Your table is merely a text version of the dog’s-ass plot, and has the same flaws.
Your list seems to contradict your claim. The bigger the genome, the larger the percentage of it is non-coding. Which is what John Harshman basically said.
You really should read this paper: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4571570/
What’s in a genome? The C-value enigma and the evolution of eukaryotic genome content
Tyler A. Elliott and T. Ryan Gregory
As we can see there is a very strong correlation. In general, the bigger the genome, the bigger the non-coding percentage.
That depends on expression levels. Splice-variants expressed due to noisy transcription are expressed at extremely low levels. When we are talking about “all that noise floating about the cell” we are some times talking about something as low as a single copy pr. cell (I’m talking about pervasive transcription as a phenomenon here, not alternative splicing of Titin in particular).
It might be the case that Titin is a protein that has functional splice-variants. I have no reason to outright reject that claim. But the mere fact that it IS alternatively spliced does not demonstrate that those splice-variants are functional. So how do splice-variants avoid causing disease? With very very low expression levels.
If the expression levels become high enough, that can either be due to mutation which can result in disease, or yes, the protein might in fact have functional splice-variants. But the mere detection of a splice-variant in itself is not an indication of functional alternative splicing. It is more likely to be noise. Why do we claim it is more likely? Because those splice-variants are usually expressed at unbelievably low levels. And in the majority of cases where splice-variants are known to be expressed in large amounts approaching the “primary” coding isoform, the result is some sort of disease.
Notice these are statements about probabilities and relative proportions. Not absolute claims. Alternative splicing is mostly noise. Mostly does not mean functional alternative splicing doesn’t exist at all. It does, there are known cases of it. But they’re exceptions, not the rule.
CharlieM,
Sorry, I omitted to respond to this. This question exists regardless whether a particular set of isoforms has just one, or many functional members. They aren’t all functional in all cells, where all are functional, so cells must regulate isoform expression either way.
Regardless whether a given isoform is ‘noise’ in all cells, or just in all cell types but one, cells need a means to upregulate the mRNAs for the ‘correct’ form, and/or downregulate the rest. I don’t actually know how this is done, but something like it needs doing in either scenario.
I don’t see why, actually. If a transcript with all introns spliced out and all exons spliced together is the sole functional variant, then no regulation is necessary; just let the usual process act, and accept the occasional errors as cost of doing business.
But that’s good thing.
Another good thing. Didn’t you read my post?
No fear, the magical forces of evolution are on the job!
Mung,
It’s a thing. Whether good or bad depends on your PoV. If carrying surplus DNA at a site you don’t even need an exon break is a good thing then yeah, it’s a good thing. But the result is 25% of our genome in introns, only < 2% in exons. Seems OTT to me.
You’ll have to be more specific. You make many posts.
I don’t recall the one where extending the genome even more was good. If all you need is an exon junction, I can think of many less ridiculous ways to do it. But then, I’m not a mad bodger like your Designer appears to be.
John Harshman,
In that instance, I guess. But other scenarios are available. As soon as a second functional isoform becomes available, there needs to be regulation of one or both pathways. That gives us 2 possible answers to ‘how does it deal with all the noise’.
LoL! You couldn’t even begin to design living organisms. And BTW, what we are looking at now is after many generations of genetic entropy
Frankie,
Of course not. No-one could.
Some one did
No human. And God is unthinkable. Maybe it was space aliens.
God is thinkable, the question then is how did He choose to do it? Of course space aliens are ok with ID.
How did the designer begin?
Mung,
That would be ‘someone’ (in all cases). And still leave the question of ‘quis designiet ipsos designori’ (yes, my Latin too is flawless … ) as a rather unsatisfactory loose end.
newton,
At The Very Beginning. A very good place to start, as Nobel Laureate Julie Andrews was wont to say.
By outsourcing to space aliens.
Only to you, perhaps. Why does the designer require a designer? Please be specific and show your work.
Umm that’s “when” not “how”. We may never know how the designer began when it comes to living organisms just like we may never know how the builders of Nan Madol began when building what they did. But we study the design to answer the more important and pressing questions.
Hi Allan,
Genes In Conflict arrived today. I see Group I introns and Group II introns in the index. What should I look for to find the other classes of introns?
Genes In Conflict is a book about “selfish genetic elements, those stretches of DNA that spread in spite of being injurious to the individuals they occupy. (p. viii)”
Given that Group I and Group II introns are both self-splicing, in what way are they injurious to the individuals they occupy?
Seems like a reasonable question to me.
Actually that is the most realistic answer yet, thanks.
Mung,
First, intron transcription is costly (although the partial cost varies depending on the organism’s overall budget). 25% of the genome is intronic, but < 2% is protein coding. This slows down replication, and transcription, as well as adding to the energy and material costs of both. RNA polymerase ii only manages about a base a second, so intronic transcription adds hours.
Second, splicing is not done perfectly 100% of the time. There will be a proportion of splice errors due to the need to remove the intron, even if it does it itself.
Third, the need for recognition sequences adds a mutational load – the entire intron sequence is not free to change at the neutral rate, even if much of it is. Mutations in the intron can be just as damaging as coding mutations – often more so.
Frankie,
Have you ever got an answer after ‘study’ that you didn’t already figure you knew?
I don’t know if intron transcription is “costly” or not. What do you mean by costly?
The claim is that Type I and Type II introns are “injurious.” But it’s pretty clear to me from reading the preface that by “injurious” he means should have been selected against. And yet they persist. LoL.
One of the original points I made in this thread.
Oh, and he admits to excluding bacteria and viruses. What are we to make of that if we want to discuss Type I introns and Type II introns?
If that was the case you would study it to confirm what you already figured you knew. But anyway we still don’t know what Stonehenge was for. The same goes for Nan Madol. But we study them to try to determine what’s up
https://en.wikipedia.org/wiki/Group_I_catalytic_intron
https://en.wikipedia.org/wiki/Group_II_intron
In the continuing saga of meeting Larry’s challenge to learn about intron evolution from reading biochemistry textbooks, I cracked open Stryer’s Biochemistry.
Part I. Molecular Design of Life.
I shit you not.
Let’s hope they fixed that in later editions.
Mung,
I mean that organisms have to get their energy and materials, which are often limiting. To spend it on unnecessary activity reduces that available for other things. And what, in any case, of my other two points?
Perhaps you should read the book to find out the ‘and yet’.
I recommended the book as a useful guide to the world of genetic conflict – including both introns and transposons – not as a Guide To Intron Evolution. It is a dimension of which many are unaware, and one you are clearly having a hard time assimilating into your cartoon view of evolution.
If you are just going to read it and post your gotchas as you go, I’m not sure how much help I can be.
Mung,
We know, Mung. Alternative splicing. It’s a thing, and has been mentioned several times already.
Mung,
What’s the point of all this if, as per your OP, evolution is about to collapse anyway? All that wasted learning! Those 17 books read without point!
The problem is, evolution is taking foreeeeeever to collapse.
“Today, at the dawn of the new century, nothing is more certain than that Darwinism has lost its prestige among men of science. It has seen its day and will soon be reckoned a thing of the past.” -Eberhard Dennert, At the Deathbed of Darwinism, 1904
I’m always looking to add to my library of cartoon guides!
The Cartoon Guide to Physics (Cartoon Guide Series)
The Cartoon Guide to Statistics
The Cartoon Guide to Genetics
And one we already addressed. I got the impression you got it, but now you’re bringing it up again?
Once again, one part of the problem is how effective selection is. With very large population sizes, those found to be typical of prokaryotes and single-celled eukaryotes, population sizes in the tens to hundreds of billions, or even trillions, selection is strong enough to almost totally eliminate introns. Almost.
Prokaryotes still retain some group II elements, but they almost never insert in coding regions and are usually intergenic instead, meaning they’re often not transcribed, meaning their “cost”(in terms of how much energy the organism takes to produce them is only effectuated at binary fission, when the entire genome is replicated, and since they aren’t transcribed they don’t have a time-cost during gene-expression). If they insert in coding regions, their cost becomes “visible” to selection and they’re quickly eliminated. But between the protein coding genes they can still hide away relatively successfully.
In the populations of large multicellular eukaryotes, the picture changes. Population sizesmay reach millions or billions, but they also go through periods of bottlenecks, such as when small groups become geographically isolated, during which populations are as low as some few thousands. In these situations, drift can overwhelm selection allowing selfish elements to run rampant. They can insert in coding regions, become large and so on with little hinderance.
And this is before we even consider the mechanisms these elements exploit to make copies of themselves. As Allan Miller also mentioned earlier, the size of introns are also relevant. The bigger they are, the higher the cost.
An important concept to assimilate here is that of levels of selection. But since people seem to have trouble even with the most basic idea, that of selection among individuals (genome selection, one might call that, a special case of a more general principle), I don’t hold out much hope.
In the space below, Frankie will paste his pet quote from Mayr. Again. And maybe phoodoo will return and honour us with ‘it’s an after the fact assessment’. It’s a tautology I tells ya. And so it continues.
Mung,
The cartoon guide to genetics has the DNA flip from right-handed (correct) below what I presume to be RNA polymerase, to left-handed above it. This cannot be correct. RNA polymerase would stall at such a junction, which also presumes the availability of biochemical pathways for both D and L ribose, and all downstream consequences of that – basically, a complete set of duplicate pathways for everything. There will be much flipping of coins in this cell. 🙂
Stryer’s Biochemistry on introns.
Again nothing on how introns evolved, only in how they possibly got weeded out after they were already present.
Further:
According to a program? No wonder biochemists [erm, I mean IDiots] talk the way they do.
😀
Heads I win tails you lose?