DNA is not just a static read-only memory (ROM) for coding proteins, but hosts dynamic random access memory (RAM) in the form of methylations and histone modifications for regulation of gene expression, cellular differentiation, learning and cognition, and who knows what else. The picture below depicts how rapidly the RAM aspect of DNA is changed during embryogenesis.
Many of the DNA methylation patterns are in non-coding repetitive regions. This suggests at least some of the roles of non-coding DNA are involved in supporting the complex epignomic memory in each cell.
Depicted below are changes in epigenetic methylation marks on the DNA in the stages of embryo development. The light green colors indicate epigenetic methylations and the darker blue colors indicate absence of epigenetic methylations. In boxes “a” through “l”, the bottom part is the DNA from the mother and the top part is the DNA from the father. Eventually the DNA from mom and dad mix in the 4 cells of box “m”.
Note how the epigenetic marks are erased from the parternal DNA first!
The depiction below shows how rapidly epigenetic changes happen even in time frames as short as hours. Each cell has a slightly different methylation pattern and hence each cell’s RAM has some unique information. If we consider that the human has 100 trillion cells and that each cell has 30 million potential methylation sites, the sum total of RAM memory implemented by epigenetic cytosine methylation alone is on the order of sextillions of bits of Shannon information. Like histones, DNA methylations can be written, erased and read.
When scientists inhibit epigenetic changes, the results are usually lethal. So we know the epigenetic component of the DNA is vital to life.
a–e, Anti-5-methylcytosine (MeC) immunofluorescence of mouse one-cell embryos. a, Zygote 3 h after fertilization with intense MeC labelling of both pronuclei (>10). Numbers in parentheses indicate the number of embryos analysed. b Paternal and maternal pronuclei at 6 h (>10). c, Undermethylated paternal pronucleus at 8 h (>20). The smaller female pronucleus remains methylated. d, Aphidicolin-treated one-cell embryo displaying demethylation of the male pronucleus (>20). e, First metaphase (>5). f–j, Controls. Anti-DNA immunofluorescence of one-cell embryos demonstrates that both chromatin sets are accessible to antibody molecules. f, 3 h (>5). g, 6 h (>5). h, 8 h (>5). i, Aphidicolin treatment (>5). j, First metaphase (2). k,l, MeC staining of two-cell embryos at 22 h (>20) (k) and 32 h (>20) (l) shows that the paternal and maternal compartments have different methylation levels. m, Four-cell embryo at 45 h (>10). The MeC-staining intensity of the maternal half of the nucleus is weaker than in two-cell embryos. Scale bar, 10 mum.
http://www.nature.com/nature/journal/v403/n6769/fig_tab/403501b0_F1.html#figure-title
http://www.nature.com/nature/journal/v403/n6769/fig_tab/403501b0_ft.html
Isn’t this research murder?
If there is a point to this post, I’m not getting it.
It was listed under the category of life sciences.
I wanted to see if there were objections to my characterization of DNA as a substrate for random access memory (RAM) and not just merely read-only-memory (ROM).
This sort of has a bearing on the junk DNA debate since it is visually apparent by the referenced experiment all that “junk DNA” is getting lit up like a computer RAM!
The OP showed a picture of the global methylation patterns.
There has to be attendant machinery that writes, erases, and reads this DNA RAM we call the methylome as well as the “histone-ome”. This is a conceptual depiction of some of machinery which tells me the RAM of the epigeneome cannot be a minor part of the information processing in biology.
The black “wires” in the diagram that coil around the drums — that’s DNA.
http://alfin2100.blogspot.com/2010/11/fine-meth-ylome-youve-gotten-us-into.html
Objections — no.
Laughter – yes, lots of that.
Personally I don’t think of DNA as either ROM or RAM. It’s a specification.
Of course, a biological system is going to change over time, especially during development. And there’s no surprise if that changes existing structures. But the methylization does not seem important for inheritance. Whether it is actually being used to track development changes, I will leave to the biochemists to invesigate.
As a non-biologist, I am not seeing anything here that particularly surprises. Well, I see Sal jumping to conclusions. But that doesn’t seem surprising either, given how often it happens.
“Gee, this is so complex! It must have been designed!”
Episode #28,346 of Personal Incredulity Theater.
From the Why Evolution is True blog:
https://whyevolutionistrue.wordpress.com/2011/05/14/development-is-epigenetic/
stcordova,
So Sal finds his god-of-the-gaps in methylation. When that gap is closed, I wonder where he will next look.
LoL! If your position had something that could actually be tested Sal couldn’t do that. So time to step up and get to work. Complaining isn’t going to do it
Of course development is epigenetic. That’s what “epigenetic” means. How does this advance your claims of creationism?
Frankie:
LoL! If your position had something that could actually be tested Sal couldn’t do that. So time to step up and get to work. Complaining isn’t going to do it
If natural processes cannot be tested then ID is unfalsifiable since it would be impossible to show non intelligent agent design.
That doesn’t follow. ID is falsifiable and it isn’t ID’s problem that you cannot falsify it.
Epigenetic means development? Reference please
To pick one, Merriam-Webster:
Epigenesis. 1: development involving gradual diversification and differentiation of an initially undifferentiated entity (as a zygote or spore)
“Epigenetic” is just the adjective form, as in definition 1 below; it has lately accumulated additional meanings, as in 2 below; again from Merriam-Webster:
Epigenetic. 1: of, relating to, or produced by epigenesis. 2: relating to, being, or involving a modification in gene expression that is independent of the DNA sequence of a gene
But that second meaning is a contraction of the original meaning, which encompassed all the physical processes of development.
Frankie:
That doesn’t follow. ID is falsifiable and it isn’t ID’s problem that you cannot falsify it.
Per your criteria, it is unfalsiable if natural processes are untestable. One has to eliminate natural processes before one makes the design judgement, correct? There is no way to eliminate the untestable. Which is exactly the reason that an unknown designer with unknown abilities with unknown motivativations could ever be falsified.
I suggest you do some background reading. One good place to start may be right here:
http://sandwalk.blogspot.ca/2014/03/what-is-epigenetics.html?showComment=1395752770897#c3801031510809553494
Oh dear oh dear…
I do believe that Allan Miller already provided you the best response possible.
You didn’t ask me, but I would. I do have a foot in both camps, the informatic and the molecular biological, and I say ‘nah’. Same with ‘code’ 😉 Analogies are like bananas with an umbrella stuck in them, except when they are more like invisible battleships …
The crucial part you do not seem to be getting here is that Nucleosome Modification is clearly a result BUT NOT a cause of “Epigenetics”.
I direct your attention to mark Ptashne’s seminal work:
http://www.pnas.org/content/110/18/7101.full
Which is in direct contradiction to your thesis.
I guess the important point that Ptashne is emphasizing would be that nucleosome modifications are by themselves not self-perpetuating and must therefore be considered peripheral to the epigenetic story.
I once considered a metaphor my students may understand: If my every week my wife hides the cookies I purchase behind the bookshelf, then I will lose weight. Am I losing weight because the cookies are behind the bookshelf? Yes – of course that is true. But ultimately the real reason I am losing weight is a result of my wife’s actions, not the bookshelf’s location.
OK OK… I admit the metaphor is lame! … as lame as comparing epigenetics to bananas with an umbrella stuck in them, except when they are more like invisible battleships!
😉
I quickly dropped the whole idea of the metaphor. ITMT, and with all due respect, I suggest you may want to catch up on the subject, maybe by starting here: http://sandwalk.blogspot.ca/2014/03/what-is-epigenetics.html
best regards
Regarding stcordova’s quote:
Many of the DNA methylation patterns are in non-coding repetitive regions. This suggests at least some of the roles of non-coding DNA are involved in supporting the complex epignomic memory in each cell.
More than half of our genome consists of pseudogenes, including broken transposons and bits and pieces of transposons in scattered in various orientations over all our chromosomes.
That means it would be very important for eukaryotic cells to suppress the disastrous consequences of unequal or nonreciprocal crossover in so-called regions of junk DNA. That would be a more likely explanation for persistent nucleosome modification in non-coding repetitive regions. Any high school student could be expected to understand that! I should know – I am a high school teacher.
Of course the suppression of potential damage caused by active retroelements would be the second half of the contradiction to your line of conjecture.
You may find these two links helpful:
http://sandwalk.blogspot.ca/2013/07/five-things-you-should-know-if-you-want.html
http://atlasgeneticsoncology.org/Educ/HeterochromEng.html
If it is untestable it is eliminated. Science requires testability. And I said it is untestable because no one knows how to test it. That could change.
If it ever shown that stochastic processes are capable then ID falls.
He says that it is important in development. Epigenetics means do to something other than genetics- as in heritable changes in gene expression not due to changes in then genotype.
Perhaps we are just talking past each other
Uhmm… that would be incorrect!
Scientific statements must pass the test of “falsifiability”! Scientific statements do not need to pass some supposed test of “verifiability”.
Popper described this as the demarcation problem. Of course, there exist many scientists (even now) on other nearby blogsites who embrace various different versions of empirical reductionism who also have similar difficulties to yours, when attempting to wrap their heads around the implications of what Karl Popper actually said.
I refer you to
http://plato.stanford.edu/entries/pseudo-science/#KarPop
I don’t think you get it… You asked for a reference confirming whether or not epigenetics was all about developmental biology. I provided a post within a thread that discussed that question in great detail. Don’t just read that solitary post.
You misunderstood me. I asked the definition of epigenetics that said epigenetics = development
Testability includes a falsification process
If you have the time, maybe you could provide me with the definition of frequency that says frequency = wavelength.
Yet another example of how evolutionary prejudice and “science” pollutes understanding of biological function and is a science stopper.
Pseudogenes serve as nice miRNA decoys in a ceRNA regulatory schema. Transposons jump in somatic cells during neuron development to create diversity even though we don’t see them jump in the same way in the germ line.
Actual physical and biochemical investigation should take priority over evolutionary speculations about function or lack there of.
The picture in the OP above demonstrates utility of the non-coding regions as scaffolds for the epigenomes of each cell. We’d be dead without such “junk” DNA to host the epigenetic memories or places for molecular machines to park.
About the only value in evolutionary theory is the idea of homology, but that was pioneered by the creaitonist Richard Owen before evolutionary theory distorted its meaning and value to understanding the structure and function of biological machines.
What is your understanding of the meaning of “homology”? And evolutionary theory didn’t distort any meanings, just explained how homology arises, which leads to a simpler and clearer definition.
I’m also quite curious about how a creationist would go about distinguishing homology from homoplasy.
John Harshman,
How do you do it? If it doesn’t fit your assumption of Common Descent then homoplasy and if it does the homology? To Creationists homology comes from a common design and Is based on the levels of archetype laid down in Linnaean classification.
So?
Frankie,
I’m also curious as to whether you have ever answered a direct question.
All you have is that single sentence “it’s getting lit up”. And by that you mean merely that histone mediated DNA methylations takes place throughout the genome. We’ve already been over this. You had nothing of value or consequence to say in response to the reality of pervasive transcription of even random synthetic DNA, and the c value paradox. Bring us your 30 million ad-hoc hypotheses for how this new memory device functions in it’s own unique way in every species ever, even closely related ones. Like Onions.
And yet millions and millions of species get by without it. And some very similar ones get by with tens to hundreds of times more than us, yet they’re tiny and simple by comparison.
So obviously clarification was needed. And Sal then tried to clarify, and a discussion proceeded from that. All of which was obvious to begin with. So why did you ask “So?”?
I have, however evolutionists don’t
Example of the “pseudogene” fallacy being an evolutionary left over. Even if it is, it is irrelevant since they are indicated to have function because of the ceRNA hypothesis.
The ceRNA hypothesis is advocated by some of my professors at the NIH. Fuz Rana at ReasonsToBelieve explains:
Just like the some of “vesitigial” organ hypotheses, it’s time to dump evolutionary theory as a means of judging non-funcitonality.
If Universal Common Ancestry advocates (UCAists) want to promote their conflicted unresolvable phylgenies as Darwin’s truth, that’s fine, but I do have a problem when UCAists start to impinge on advancement of medical understanding and human health.
Creationists have no problem with “evolutionary conservation” if it is treated simply as a euphemism for “God-designed similarity” according to the homology notions of Richard Owen (a pioneer of comparative anatomy). We could just as easily say, “God-designed similarity suggests function” and it will work just as well as saying “evolutionary conservation suggests function”, in fact it might work even better since there is no constraint on needing a conflicted phylogenetic story. For example, consider the “God-designed similarity” in this diagram, does it matter whether the similarities are due to common ancestry or God-made-similarity?
http://www.sci-news.com/genetics/article01036.html
How do you know there aren’t unique ways for each species. Yet another example again of UCAist non-sequiturs that go something like “they have a universal common ancestors, therefore species can’t implement epigenomes and genomes in different ways.”
UCA speculative non-sequiturs are not the way to solve empirical questions. As far as separate implementations and usage of genome and epigenome, Robert Tjian gave videos that highlighted the astonishment in the different kinds of regulatory schema in differing cell types, let alone different species.
I provided the video earlier. Did you look? Probably not, otherwise you wouldn’t be saying the following:
The c-values are different because Onions and humans don’t have the same friggin cell types! Sheesh! Differing cell types have differing regulatory mechanisms. Look at the Robert Tjian video. He is a scientist of no small reputation.
I don’t like the OP.
Yes, it certainly does. First I have to ask what you think that diagram shows; I’m not sure you understand it. But second, you need to provide a “god-designed” explanation for the nested hierarchy we generally encounter, one which despite your denigration is highly consistent among different sorts of data. (In case you were considering just answering “common design”, I will warn you right now that’s not an explanation.)
Now your diagram shows the results of a complex history of gene gain and loss in which all the individual events are obscured in two ways: by just being a count of the current situation and by just sampling four widely divergent species. You may be content to marvel at the wonders of creation, but an evolutionary biologist would try to get a larger species sample to investigate those individual events. Bet they’d form a nested hierarchy.
You consistently misunderstand the onion test. It isn’t about onions and humans but about onions and onions. Do different onion species in the same genus have different cell types? Or to turn it around, do humans, fugu, and salamanders have enough differences in cell types to account for their different genome sizes?
Onions can use DNA in different ways than humans. Extra DNA can have other purposes between species, not the least of which is extra storage of transgenerational heritable epigenetic memory as well as added redundancy.
Also, onions species with more DNA give it more epigenetic memory, and more epigenetic memory is useful if the plant needs a larger repertoire of memories to deal with the environment it is in. So it’s not just epigenetic memory in a heritable context but in a non-heritable context.
The problem with UCA-gene-centric thinking is that it has blinds thoughtful inquiry to other possibilities of how DNA can be used other than coding and for junk.
http://www.sciencedirect.com/science/article/pii/S1874939911000575
I guess Ryan Gregory, Dan Gruar, and Larry Moran are a bit blind to the possibilities that can be inferred known and accepted literature, some of it recent. Their junk DNA ideas are fossilizing more each day.
Man-made RAM:
https://upload.wikimedia.org/wikipedia/commons/6/61/Primitive_Magnetic_Memory.jpg
God-made RAM (note, the connecting wires are DNA):
Onions with more DNA = Onions with more RAM
Sal, so your argument is that histones are RAM because a photo of some core memory looks a little bit like someone’s cartoon of nucleosomes? Well, I’ll admit it’s just as convincing as most of what you say.
stcordova,
I think your analogy is interesting but I don’t think DNA acts like RAM as a computer functions. With computer RAM memory the data inside the cells (different depending on whether it is SRAM or DRAM) is as frequently accessed as written to. The epigenetic markers are generally reading or not writing to the DNA. Their job is to control the timing of gene expression. Two example exceptions would be HGT in the case of bacteria and a retro virus in the case of multicellular organisms. But in these cases, unlike RAM memory the, accessing of the memory is much more frequent then writing to the memory.
Why?
Why do some onions need more RAM than others Sal?
That argument can be made because life is run by the immaterial and DNA is part of the hardware that allows it to function in the physical world, ie the apparatus that serves life.
colewd,
Thanks for your comment.
The epigentic markers are constantly being exposed to “reading” mechanisms such as transcription machinery that would otherwise spontaneously attempt to initiate transcription.
Also histones are turned over (replaced) at a frequent rate on the order of minutes. That means the histone information must be transferred form the histone being removed onto the histone replacing it. We don’t know why this happens, but it happens. It reminds me of DRAM that has to be constantly refreshed.
That means when the histones are replaced, the information content has to be copied from the histone being removed to the histone that is coming in to replace it. An outstanding question is, why should there be any turnover or “refresh” at all. But we know it happens.
from wiki:
compare and contrast with histone turnover:
http://adsabs.harvard.edu/abs/2007Sci…315.1405D
It is noteworthy just how many co-authors are involved in the publication of each of these biochemically-based experiments. That speaks to the staggering laboratory effort needed to make measurements on a cell.
I was pointing out that an array of repetitive elements like the man-made magnetic memory is not evidence the repetitive elements are junk. In contrast that doesn’t stop “repetitive DNA-is-junk” proponents from saying “repetitive elements are junk because they are repetitive useless copies.”
The problem is “repetitive DNA-is-junk” proponents don’t really appreciate the role of DNA as part of a dynamically changeable memory device (aka RAM).
Since you continue to fail to acknowledge powerful evidence of histone memory, I now present this picture to you for the 3rd time — I seem to recall you didn’t like the fact that peer-reviewed scientific literature didn’t use scare quotes around the words “writer”, “eraser”, “reader” since it suggests analogies between God-made memory devices to man-made memory devices.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3342293/
Oh well, science seems to be progressing despite the junk-DNA-is-junk nay-saying going around.