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
No No and NO again!
Sal – all you have proven is that you have no shame! You have no right to show your cyber-face on this forum any more.
My original challenge was quite straight forward:
You still are INCOHERENT!!!
Here is the rub… you suggested that epigenetics could be described with a metaphor along the lines of “RAM memory”
You then went on to explain why
We then pointed out to you that your explanations in your own OP contradicted your very thesis and that in fact you were chasing your tail and even contradicting your contradiction to your contradictions in and endless cycle of contradictory confusion.
After a while the joke got stale and you were no longer amusing.
Do you think me wrong? Then follow up on your own suggestion and invite your professors to adjudicate. Failing that – just go away… please!
Sal – in case you did not get it the first time
I will repeat in terms you can understand:
To paraphrase Wolfgang Pauli:
You are not just WRONG – you are so WRONG, that you are not even WRONG anymore…
I challenge you to prove me wrong – simply invite your professors to adjudicate who in fact is correct – you or your detractors.
Sal –
If you are at a loss for words and want to pose your professors a specific question:
ask them whether the article you cite above does or does not confirm Mark Ptashne’s version of events that you dismissed as incorrect.
Ptashne nailed it, Classical Geneticists have known for decades that there exist gene regulatory models where Positive Feedback control in fact maintains homeostasis, if by homeostasis we understand “status quo”! The maintenance of one “status quo” over another could be deemed your “memory” …of sorts. It gets better: irreversible commitment points often occur in Biology. Self-perpetuating responses are then required long after the triggering stimulus is removed and these responses occur as a result of positive feedback as well as double-negative feedback mechanisms as first described by Jacob and Monod.
http://tinyurl.com/pqx4jom
A fellow Canadian James Ferrell does an excellent job of elucidating these difficult concepts.
http://www.medicine.mcgill.ca/physio/mackeylab/courses_mackey/pdf_files/ferrell_2002.pdf
What you fail to understand that despite all your incoherent flip-flopping you somehow tenaciously managed to maintain Ptashne as “WRONG” even though the latest article you cite in fact agrees with Ptashne’s version of events!
Please do not return in the absence of the professorial adjudication you promised earlier
Moved a comment to Guano. Do not accuse other participants of being dishonest.
I never promised to invite my professors to TSZ. That’s stupid to involve them in this sort of extra-curricular banter.
You’re making a false claim and repeating it. Support your false claim or retract it. Link to where I said it or otherwise issue an apology and a retraction for spreading false claims about what I said.