Repetitive DNA and ENCODE

[Here is something I just sent Casey Luskin and friends regarding the ENCODE 2015 conference. Some editorial changes to protect the guilty…]

One thing the ENCODE consortium drove home is that DNA acts like a Dynamic Random Access memory for methylation marks. That is to say, even though the DNA sequence isn’t changed, like computer RAM which isn’t physically removed, it’s electronic state can be modified. The repetitive DNA acts like physical hardware so even if the repetitive sequences aren’t changed, they can still act as memory storage devices for regulatory information. ENCODE collects huge amounts of data on methylation marks during various stages of the cell. This is like trying to take a few snapshots of a computer memory to figure out how Windows 8 works. The complexity of the task is beyond description.

To get a hint of the importance of the methylation marks see:
http://www.nature.com/nature/2015/180215/full/nature14310.html

So it’s just my conjecture, the repetitive DNA is there to act as dynamic store of data. We are fooled into thinking since the sequences don’t change much during an organism’s lifetime that it can’t act as an information processing system since we presume the relevant information is the DNA sequence, when in fact the critical information are the methylation marks.

The repetition is probably important for the organism to recognized the regions and say, “hey, here’s where a lot of RAM is for me to use.” The mistake is thinking the significant information content is in the “ACTG” sequences, it is not, it is in the methylation markings, and that could well be where some serious parts of ontogenic regulatory information is flowing through.

Gruar’s approach is akin to opening up a computer and examining the physical RAM in it and saying, “those VLSI transistors are all identical, look at all that repetition, therefore it’s junk!” What matters is when the computer is up and running and we’re seeing these transistors switching back and forth from 0 to 1. Those zero’s and ones are the DNA methylation marks for regulation (not the repetitive ACTG transistors), and that’s why I suspect Graur is way off mark. It really is too early to tell, I wouldn’t yet go out on limb, but Graur is going out on a limb, and if proven wrong, we can publicly call him on it.

Repetitive sequences are plug and play like computer RAM, and can be subject to some variation. But they need to be there.

102 thoughts on “Repetitive DNA and ENCODE

  1. stcordova,

    The functionality of DNA being recruited for optical lensing should be caution to being hasty in declaring DNA being junk.

    Are we nocturnal all of a sudden?

  2. More confirmation of my OP:

    http://www.sciencedirect.com/science/article/pii/S0888754311002400

    Abstract

    DNA methylation changes in repetitive elements (REs) are associated with the regulation of gene transcription, embryonic development, differentiation and carcinogenesis. However, genome-wide analysis of DNA methylation of human REs is lacking. Here, we performed genome-wide methylation analysis of REs in nine repeat types in human embryonic stem cells (H1) and fetal fibroblasts (IMR90), and found that the potential for changes in the DNA methylation of REs was different among the nine repeat types and within different genomic regions. DNA methylation changes in the nine repeat types were related to the GC content and CpG density of the sequence contexts. The differentially methylated REs and targeted genes of different repeat types were associated with gene silencing in the transition from H1 to IMR90 cells. Our results suggest that a quarter of REs are involved in the reprogramming of DNA methylation which may play important epigenetic roles during cellular differentiation.

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