In fact, everywhere you look in the night sky with a high-quality telescope, you can see objects whose light started the journey to the telescope hundreds of millions, even billions of years ago.
So…What is the message that God has written in the heavens? What do these billions of galaxies tell us about when God created the universe?
Grace and peace,
Chris Falter
That was fascinating.
Some comments with screenshots.
Doesn’t that assume all non-coding DNA is of equal value?
If a specific type of non-coding DNA had adaptive value, and it could proliferate the genome, it could be selected for, right?
Wouldn’t you just have to see what type of DNA causes the difference in the genome size for those species, and if there is a pattern, create a hypothesis around that? For instance, transposons inserted in introns in salamanders.
Well, I’ve understood it as as a hypothesis based on common ancestry (not an argument from ignorance) that is slowly being chipped away at as more function is found for junk DNA.
Please share this evidence. This is what I’m curious about.
Good point. I have to think in an evolutionary paradigm sometimes.
I would suggest using a scientific mindset. One of the most prominent parts of that mindset is the ever present question, “What should I observe if I’m wrong?”. Scientists can spend more time trying to prove themselves wrong than in proving themselves right.
It also helps to keep a broad view of biology and not focus in too much on one aspect of biology.
Did you? I don’t remember you arguing this, and I don’t see why you would even have to as it’s not something anyone here would dispute. Yes smaller populations allow more deleterious mutations because the strength of selection is reduced relative to the power of genetic drift.
You might have read Sanford state as much(he’s just got that idea from standard population genetics), but that doesn’t mean his case for genetic entropy is true, as the idea that the effect of drift and selection depend on population size is pretty standard result of population genetics and in no way entails the inevitable fitness decline to extinction of natural populations that GE demands.
Bigger populations → less influence of drift =/= genetic entropy is true.
No. Why would it?
Though common ancestry is a fact, nothing in that talk was really about establishing that (though some of the topics basically just take that as background knowledge that was already established). It was more about understanding how the different aspects of population genetics influences and explains cellular characteristics such as genome size, cell size, and metabolic rate.
Whether you think different species share common ancestry or not it would still be a fact that the strength of selection depends on population size, and therefore would influence things like genome size, complexity, growth rate and so on.
The question being explored there is really just one about what happens if a population is of a certain size, and what happens on the long term if you make it much smaller, or much bigger, and about trying to understand why that is.
I’m not sure I understand the question. Value in what sense?
I am saying that the idea of a unique explanation for non-coding DNA in every single species is very poor scientific reasoning, and basically scientifically useless, especially for research purposes. You’d want principles you can apply more broadly so that what you learn from studying one or a few species (or one area of the genome) can help you understand and guide your understanding of other species (or other areas of the genome). The idea that each species (or each genomic locus) has it’s own unique functions in non-coding DNA is totally useless. It stops being predictive science that can model the phenomenon of life generally, and instead just becomes a matter of ad-hoc storytelling.
Now you might say who cares about whether it is scientifically useless, what if it is true? There’s just no precedent for thinking something like this (and it doesn’t make biochemical sense), and on the contrary, the idea that there are broadly applicable principles has been extremely successful in all other areas of genetics and molecular biology.
The principles learned from Mendel’s work on pea plants helped understand rules of heredity all other organisms. The base-pairing rules for DNA bases apply in all species, and even in RNA too. All species carry essentially the same genetic code, essentially the same translation system, transcribe RNA from their DNA genomes etc.
Proteins with similar sequences (both in the same and in different species) usually have the same or similar structures and functions, the atomic and molecular forces that explain their function are the same of course (electrons and protons still attract each other in mice, fish,in flies, in yeast, onions, and in E coli). All organisms must eat and take in nutrients to survive and to synthesize and rebuild their own constituents. We’re all stuck to the surface of this planet because we are all subject to the pull of gravity, etc. etc.
One could go on and on. There’s just no good reason to think this isn’t also true for non-coding DNA, and in fact we really do actually understand the physics and biochemistry of non-coding DNA pretty well. DNA binding transcription-initiators(or repressors) bind to non-coding portions and cause their effects by similar principles in all species, and so on and so forth. And there are perfectly good biochemical and explanations for how it got there and what proportion of it is functionless junk in different species.
Yes, definitely.
Yes and in fact that is thought to be one of the primary causes of non-coding genome size expansions. High activity of transposons. But that merely explains how it got there, the next step is to also try to work out what fraction of it is functional and what fraction is not. The mere fact that it exists does not mean it is functional, and the mere fact that it grew in size mostly due to transposon activity does not mean it is all non-functional either, of course.
Partly true, at least. Sequence conservation inferred by comparing the genomes of different species is one argument for junk-DNA. But it’s not the full thing.
Yeah unfortunately that’s somewhat misleading, because the conclusion that most non-coding DNA in many species is nonfunctional junk was never sold as the conclusion that it’s all nonfunctional junk, and the case for the functionality or not of some locus was always probabilistic in nature.
A particular locus being well conserved(highly similar or identical between many species) would make it much more likely to be functional (it’s conservation imply it was under selection against accumulating deleterious mutations), and a locus being less conserved implied it was under relaxed selection, therefore more free to accumulate mutations, and since most mutations are deleterious, if it is free to accumulate deleterious mutations it’s much less likely to have a function.
In this way sequence conservation would provide a general guide to finding things more or less likely to be functional. It’s important to understand here that most non-coding DNA appears to be not conserved at all, and is accumulating mutations pretty close to the rate at which they occur. And this can be shown even without assuming common ancestry, by looking at the amount of variation there is in non-coding DNA within the same population.
It’s also important to understand that many of the papers claiming to have found a function for some piece of junk DNA merely detect some sort of biochemical activity associated with some locus (RNA is transcribed from here and binds over there), and are inferring a function from this despite not showing what that function is supposed to be. And they never actually show that the particular locus they worked on really was something that was inferred to be junk DNA based on considerations of conservation and DNA type(pseudogene, transposon, intron, repetitive element, or whatever). Often times they just claim that “transposons used to be thought of as junk”, essentially strawmanning the case for junk-DNA into having claimed that in so far as something is a transposon it must be junk by definition.
Though it is true functions are occasionally found for bits and pieces here and there, it is much more rarely found in the least conserved parts (if ever?), and at the current rate it’ll be maybe a few million years before all of it is found to be functional in any species.
I think you should read Larry Moran’s sandwalk blog on his posts about junk DNA. Particularly this post:
I’ve pointed her there before. Maybe you will have better luck.
Just to clear this up a bit . . .
All junk DNA is going to be non-coding DNA. Not all non-coding DNA is thought to be junk. To use a different example, all bears are mammals, but not all mammals are bears. Junk DNA is a subset of non-coding DNA. Junk DNA is not a synonym for non-coding DNA.
There are tons of examples of functional non-coding DNA. Examples of functional non-coding DNA include genes for ribosomal RNA, microRNA, transfer RNA, gene promoters, and 3’ UTR’s.
For the human genome, it is estimated that between 90 and 95% of the genome is junk DNA. That’s about 2.8 billion bases of junk DNA. When some scientists find a few thousand bases of non-coding DNA that have function, that doesn’t move the needle.
Very true, and in this one sees some of the true art of the swindler. It’s fairly impressive how books like Darwin’s Doubt work: convincing the rube that the evidence, fairly viewed, can point only to divine oogity-boogity, and that the reason the scientific establishment doesn’t see it that way is that scientists are blinkered by an atheistic/materialistic worldview. One of the things this really clarifies, even to someone outside of science, if he has some notion of what the evidence actually is, is that there is and can be no project to seek any credible scientific agreement with this bizarre position.
But, you know, that works for their audience. They’ve already got a culture-war audience which believes that “experts” are at the core of most problems. Abolish experts, and solve the problems. From “strict construction” in the law to the gold standard in monetary systems, to Ivermectin for COVID patients – all across the board, how much better our lives would be if the people who actually know something about law, economics and medicine could all be removed from power! Why should a program like that not extend to biology?
Indeed. And it generally is really difficult for people to pull their prejudices out of judging any question where they feel they have a stake in the thing. But I will also say that one of the sad things about actually trying cases before juries is that juries are composed of ordinary people, and ordinary people are profoundly bad at weighing evidence in relation to questions, when their feelings can be stirred in another direction. As a civil rights lawyer I hated to work before juries – my cases tended to be “disagreeable individual versus noble public servant” cases, where if personalities were to decide the matter, jurors were liable to think my client was a bit touched in the head and that he should have understood that when local government tells you to do something, you do it. The nice thing about a bench trial in such a case is that you can have a judge of the facts who understands that disagreeable people have rights, too. Kitzmiller, for different but related reasons, would have looked VERY different as a jury trial, which is why the plaintiffs didn’t ask for any relief which would give the defendants the right to jury trial.
We who care about how this plays out have to remember that in some ways we are in that jury trial. If you want to convince scientists that IDC is garbage, you can rest now, because you’re already there. But if there is value to winning the hearts and minds of the public, that’s a wholly different problem, and the culture warriors of the DI understand that. We’d best understand it, too.
It would be a huge accomplishment if Valerie stopped invoking this particular equivocation, but admitting that it’s a farce would also implicitly admit that a huge amount of IDcreationist propaganda is, too.
To answer @thoughtful, no. We KNOW that all non-coding DNA does not have equal value. We have evidence.
That’s why in the ERV thread, I offered questions that would help a truly curious person to understand the absurdity of the equivocation:
Aren’t you curious, Valerie?
But you’re not going to a place where you are a witness to the evidence.
There you go again, denying the very existence of the scientific worldview. In science, we bake in the interpretations while predicting the data. You are falsely portraying science as mere retrospective interpretations, instead of its foundation of testing the empirical (IOW, independent of interpretation) predictions of hypotheses.
It’s a very powerful method for overcoming biases.
Technically incorrect. There are definitely transient junk ORFs that are both transcribed and translated at low levels.
And there is a terminological question: whether intact and selfish DNA sequences like transposons or endogenous retroviruses should be considered junk, since they are non-functional from the perspective of the organism.
Thanks for the long reply. I read it initially when you responded and again just now. Lots I could respond to and would if my kids hadn’t thoroughly worn me out the last few days. And I need a brain break, so I’m choosing not to reply to specific statements to let the thread die, tbh. Just appreciated the length of your response and the links. I looked at the titles and skimmed a few, so far. They seem highly theoretical so if you have a favorite that is more practical, let me know. I could start with that.
I think that response reveals some confusion on your part. First of all the papers are no more theoretical than the entirely theoretical hypothesis that all(or almost all) DNA in all species is functional. Nobody has directly experimentally tested all DNA in any species. Even so, scientists are not opposed to the idea that there are species where the vast majority of DNA really is functional, such as prokaryotes, and viruses of course. But they have good reasons for thinking that in those cases, reasons which are lacking for other species where they think it’s mostly junk.
But in a way that’s the whole point here as we are trying to come up with a hypothesis that explains as much as possible about the DNA sequences of different species, all the different species, with as few ad-hoc assumptions as possible. Including everything from the differences in total genome size, the fraction of coding vs non-coding, and the more specific nature of different DNA elements(be they protein coding genes and their associated regulatory elements, intergenic regions, transposons, pseudogenes, repetitive elements etc. etc.)
The hypothesis of junk-DNA does that by bringing together a host of observations from the fields of population genetics(the relationship between mutation rate, genome size, and population size and so on affect the efficacy of purifying selection), comparative genetics(how are different species different form each other at the DNA sequence level), molecular biology(what types of sequences are genomes made up of) and biochemistry(what are the physical and chemical principles that govern the interactions of nucleic acids and other molecules in the cell).
I appreciate quality pedantry. 
The Larry Moran pie chart has functional transposons at 0.1% of the human genome. I think we can throw those in the functional bucket to be fair, but it doesn’t move the needle much.
Hmmm…I don’t think I’ve ever seen this before. Very helpful. Where can I learn more about “unknown” and how we know the transposons that make up 45% of the genome are defective.
With only between 3.3% definitely functional, 0.1% moves the needle by 3%.
That mostly comes from looking at their sequences and knowing what it takes for a transposon to be functional, and partly from conservation.
If they’re heavily fragmented with pieces crucial for the transposition function missing then they’re very unlikely to still be capable of transposition. And if they’re not able to transpose then why should there even be pieces of a transposon to begin with, if it is not simply a degraded remnant of one? You don’t need a broken transposon to regulate some downstream gene or whatever. This is the “if it looks like a duck…” argument.
Yeah, it looks like this car broke down.
I’m going to be bold and say I think it doesn’t work. Could it serve some other use? Hypothetically yes, but it honestly just looks like a broken car. Could that chain hanging over it still be used for something else? Maybe if it’s not too rusty, but you don’t need the rest of that broken car for that.
“Unknown” is just a number of random-looking sequences that don’t obviously fit into any of the other categories. They could easily have their origin in defective transposons, just too diverged from the original to tell. Transposons are defective if they no longer have the ability to transpose, and that can be determined from their sequences.
Your reply made me think of something I wanted to look up. I came across this:. https://genomebiology.biomedcentral.com/articles/10.1186/s13059-018-1577-z#ref-CR27
TEs occupy a substantial portion of the genome of a species, including a large fraction of the DNA unique to that species. In maize, where Barbara McClintock did her seminal work [28], an astonishing 60 to 70% of the genome is comprised of LTR retrotransposons, many of which are unique to this species or its close wild relatives, but the less prevalent DNA transposons are currently the most active and mutagenic [29,30,31,32] (Fig. 2). Similarly, the vast majority of TE insertions in Drosophila melanogaster are absent at the orthologous site in its closest relative D. simulans (and vice versa), and most are not fixed in the population [33, 34]. Many TE families are still actively transposing and the process is highly mutagenic; more than half of all known phenotypic mutants of D. melanogaster isolated in the laboratory are caused by spontaneous insertions of a wide variety of TEs [35]. Transposition events are also common and mutagenic in laboratory mice, where ongoing activity of several families of LTR elements are responsible for 10–15% of all inherited mutant phenotypes [36]. This contribution of TEs to genetic diversity may be underestimated, as TEs can be more active when organisms are under stress, such as in their natural environment [37, 38].
When I said this
I didn’t realize that it was known that there are huge TE differences between species or close relatives in all kinds of eukaryotes.
I see your point here now especially, but TE differences is definitely something I’m interested now in paying attention to, to see if any patterns like with the salamanders come up in the literature.
I guess I didn’t let this thread die. 
I’ll see if I have more questions after I finish reading that paper/article.
