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
I think I now understand why other blogsites can have so much profanity!
Damn!!!!!!
Did Sal just give John the PHD finger?
I seem to remember something along these lines going down in flames on Larry’s sandwalk.blogsite… Specifically random transposon jumping somehow being different in different tissues and that somehow that proved non-randomness and as a result also proved Intelligent Design.
Can anybody help me out on this, not that it matters much, but I thought perhaps it was one of mregnor’s abominations on sandwalk.blogspot, maybe I am wrong.
meanwhile – what is the “sal”-connection. I must be new here – what’s a “sal”?
I will take one last stab at this.
stcordova Before going any further with your metaphor, could you please explain what you think “epigenetics” really is?
Your answer must somehow explain, what is being remembered and how. Understand that your answer CANNOT make reference to DNA methylation nor Histone acetylation because as Mark Ptashne explained, nucleosome modifications are by themselves not self-perpetuating and must therefore be considered peripheral to the epigenetic story. DNA methylation & Histone acetylation clearly are a result of “epigenetic memory” and not a cause.
Your answer must be able to explain the difference between a mule and a hinny! Let me explain: A female hinny zygote is a diploid cell with two sets of chromosomes: one set from a donkey and another set from a horse; which BTW describes the exact same scenario for the female mule zygote. Those differential nucleosome modifications you keep on going on about, should be identical in both zygote scenarios, yet hinnies and mules are quite different due to “epigenetics”.
So far I am convinced you are incoherent. I challenge you to prove me wrong. My challenge should not be too difficult given it can be answered by high school students.
Please answer me directly without resorting to puerile evasionary tactics or rhetorical questions.
TomMueller,
How did you/ they determine the transposon jumping was random?
stcordova,
I think I see your point. I missed the word substrate where you are not talking about accessing DNA but simply looking at the read write behavior of histones where DNA is the substrate that holds them. In a prior discussion you talked about DNA as functioning as wire that separated binding proteins by enough space so they can operate to function. Very interesting ideas.
When you roll a pair of fair dice, how do you determine invisible pixies didn’t consciously manipulate the outcome?
Many gamblers are convinced they do. And the pixies work for the house.
stcordova,
You are fond of paraphrases of positions which no-one holds. It must be the case, even on universal common ancestry, that ‘different species implement their genomes in different ways’. We observe them doing so.
But what you seem to be hinting at is that the assumed common ancestry of different onions of the same genus is some kind of ‘science-stopping’ blocker to the possibility that they have different epigenetic requirements. But even if they were separately created I wouldn’t take that possibility seriously. Common ancestry isn’t the issue, epigenetic operation is. There are many, many genera containing more than one species. If it were the case that any such species pairs had significantly different epigenetic unrolling … don’t you think someone might have noticed?
stcordova,
The key word missing there is SOME. SOME pseudogenes; SOME transposons. One cannot export the function of a subset of a class to the entire class. The term is ‘domestication’. Elements which do not as a rule have a positive effect on organismal fitness can evolve to do so. Individual instances, that is, not the entirety.
Transposons are generally considered junk because of the nature of transposition (and the fact that there is wide variation within species).
Some carnivores make very good pets.
stcordova
Coming soon to 24 hours by my clock… and still no reply except a puerile rhetorical question by Frankie.
At what point is defeat conceded?
When the last king is strangled with the entrails of the last priest. Or, in this case, when all of the adherents are deceased and forgotten and all the scriptures turned to dust.
Intelligent design creationism is and always has been a religious and political movement, never driven or supported by science. They will never concede defeat. The best we can hope for is to use elections and the courts to limit the damage they can do until they’re no longer a political threat.
Do creationists ever concede defeat?
Have you tried asking them?
Sure. Just like you conceded defeat to keiths.
You never do even though it has been proven that your position makes untestable claims and because of that is not science.
Talk about total unawareness…
LoL! And I notice that you are too afraid to answer my question. However Spetner, 1997, 2014 makes the case that refutes your claim.
Transposons carry within their sequence the coding for two of the enzymes required for it to move around. Please tell us how to test the claim that arose via stochastic processes- something scientific.
Or else admit that your claims are puerile
LoL! ID doesn’t have anything to do with any religion. However given the untestable claims of your position we can easily see that it relies solely on faith.
We will never concede defeat because you will never be able to test the claims of your position. And we understand that upsets you
Wedge document. And you knew that. You yourself used to write for a YEC website.
This is proving to be an interesting experiment.
Stcordova has evaporated without trace and Frankie persists in ignoring the original question by irrelevant posturing.
Frankie, to quote you: “I asked first!”
I wonder out loud; what is a reasonable time limit?
At what point has stcordova implicitly conceded defeat to my question as posed, not Frankie’s preoccupation with my inquiry regarding the identity of preposterous posters on a different blog.site
TomMueller,
Again- Spetner 1997, 2014, along with what I posted. The sequence contains the coding for two of the enzymes required for it to move around (actually that is also covered in the referenced material).
Just because we don’t understand what is happening isn’t any reason to classify them as random. You are assuming your conclusion.
Here is the question one last time:
I will take one last stab at this.
stcordova Before going any further with your metaphor, could you please explain what you think “epigenetics” really is?
Your answer must somehow explain, what is being remembered and how. Understand that your answer CANNOT make reference to DNA methylation nor Histone acetylation because as Mark Ptashne explained, nucleosome modifications are by themselves not self-perpetuating and must therefore be considered peripheral to the epigenetic story. DNA methylation & Histone acetylation clearly are a result of “epigenetic memory” and not a cause.
Your answer must be able to explain the difference between a mule and a hinny! Let me explain: A female hinny zygote is a diploid cell with two sets of chromosomes: one set from a donkey and another set from a horse; which BTW describes the exact same scenario for the female mule zygote. Those differential nucleosome modifications you keep on going on about, should be identical in both zygote scenarios, yet hinnies and mules are quite different due to “epigenetics”.
So far I am convinced you are incoherent. I challenge you to prove me wrong. My challenge should not be too difficult given it can be answered by high school students.
Please answer me directly without resorting to puerile evasionary tactics as seems to be Frankie’s wont or rhetorical questions.
I suggest a time limit before invoking an implied concession of defeat?
Suggestions? … Another 24 hours perhaps?
Frankie,
Why is this relevant? Transposase could have been designed; this would not tell us anything about whether transposons act on their own account or as part of the greater organismal whole. Transposition is a close relative of viral infectivity. No-one claims viruses are doing their hosts a favour.
Allan,
Thank you for taking Frankie off my back!
ITMT What would you suggest is a reasonable time limit for stcordova?
Best regards
TomMueller,
That is a task beyond my ability, I am afraid! There is, however, a handy little ‘Ignore Commenter’ button.
Sal has accepted points in the past; it’s not beyond the bounds of the possible that he will respond. Equally, I sometimes feel that some valid points have not even been read, let alone addressed. Either way, he does rather come and go.
Allan Miller,
what’s a “Sal”?
TomMueller,
Well, I hope I’m not outing, but the s in stcordova stands for ‘Sal’.
My favorite description is from ERV.
OK so you don’t have any justification for calling the actions of transposons random. And not all viruses are harmful. And some could very well be helpful.
TomMueller,
I have already answered the question about epigenetics. “Evolution in Four Dimensions” discusses the topic in detail
Another puerile evasionary tactic!
Please provide a brief and focused response to the question posed. One or two paragraphs should do. Otherwise I will have no more option but place you on IGNORE!
Remember that your answer must also be able to explain the difference between a mule and a hinny!
Frankie,
Changing the goalposts again. You brought up the enzymes involved in transposition, and said nothing about whether they were ‘random’ in operation. Just because they encode their own enzymes does not make their insertion positions surgical. They insert where they can.
Therefore what? All viruses are helpful? All transposons are helpful? We can just ignore the harmful ones because some aren’t?
Down for the count. Time’s up!
Another shibboleth slain! Judges 12:6
Apologies for sporadic visits, and thank you to all for pariticpating.
definition used by NIH researchers in the present day (though the term has evolved):
From the NIH Roadmap epigenetics project:
The roadmap project focuses on cytosine methylation and histone modication as epigenetic factors. Additionally DNase hypersensitive sites and chromatin remodelling is studied. Some people include ncRNAs as part of epigenetics because they are transmitted down somatic cell line. I usually don’t include ncRNAs right now in the defintion of epigenetics, but the NIH may change their mind because ncRNAs floating around in the cell are often integrated with histone modifications.
The ncRNAs are often phantom RNAs — about 10% of the RNA transcriptome has no direct analog in the DNA because of post transcriptional modification and who knows what else. The Fantom Transcriptome is starting to become a real issue because now we may have to have separate annotations for them.
Ptashne is old school obsolete.
From the NIH Roadmap project:
http://www.roadmapepigenomics.org/
The NIH Roadmap project is an almost 200 million dollar effort. They can define epigenetics for the rest of us with that sort of capital investment. I’m merely using their defintions not Ptachne’s — Ptachne obviously has a low opinion of NIH ENCODE and Roadmap.
Nah, most people know who I am in TSZ circles, ever since I was the featured in the cover story of the prestigious scientific journal Nature in 2005 and on National TV in 2006. 🙂
Speaking of that 2005 article in Nature that featured yours truly in the cover story:
http://www.nature.com/nature/journal/v434/n7037/
I’m also listed at #81 on encyclopedia of American Loons, ahead of Sean Hannity:
http://americanloons.blogspot.com/2010/10/81-salvador-sal-cordova.html
Gollygeewillakers, look at the title of this 2013 book (emphasis mine):
And here is a hint how c-values can vary between individuals of a species and thus fine-tune regulation. Even though it doesn’t talk about C-value per say, a little out-of-the-box thinking can enlighten as to how this can be important for C-value issues:
From a 2015 article:
Could you explain your thinking here? It’s too far outside the box for me to see it.
When I see the word “numerous” I want to know the percentages.
Too often, numerous means thousands, which is a trivial percentage of nearly any genome.
The problem is not that some non-coding DNA is functional. the problem is getting past 10 percent, for humans.
Sal, I edited your link as long URLs affect the display in smartphones. You can use Tinyurl or HTML tags (a href= etc).
Thanks Alan.
I’ll try to shrink the URL’s or provide hyperlinks.
If you read the paper, it isn’t even implied that the transposons are functional, and in fact the methylation is supposed to be a defense against the deleterious effects of insertions.
To the extent that there is an epigenetic ‘memory’ encoded with a parallel frequency to DNA sequence, how is this memory supposed to stretch beyond one generation? Bearing in mind that there are two copies, one from each parent, of any methylated or unmethylated sequence, but an exponential number of ancestors whose ‘memories’ are vying for representation in the strictly binary resource of a diploid locus.
If they are completely inert, what’s the point?
Allan Miller,
How am I changing the goalposts when that was my question from the beginning?
One possibility: to keep them from being transcribed and inserting somewhere else where they might cause a problem.
Frankie,
No it wasn’t. You made two completely different points:
This is about the origin of transposons. I queried the relevance of that to the discussion in hand, to which you responded:
This is about the action of transposons.
but wait, wait, waaaaaaaaaaaiiiiiiiiiiiiit , dammit.
Where’s Tom Mueller!!!
Its been over 24 hours now and no rebuttal to the rebuttal of the rebutted but.
Tom Mueller, down for the count !
Allan Miller,
The first question I raised was how did Tom know the movements were random. I then added the part of what a transposon is. And you don’t have any justification for calling their movements random