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First epigenetics, now epigenomics

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The people standing athwart epigenetics and yelling “Stop!” probably won’t like epigenomics either.

From Nature:

Obesity may be written not only in the genes, but also on top of them. One of the largest studies so far to probe the human epigenome — the collective name for the patterns of chemical groups that adorn DNA sequences and influence their activity — has found some tags that are linked to differences in body mass index (BMI).

Chemical alterations in a gene thought to be involved in metabolism were identified in the blood and fat cells of more than 2,500 people, scientists reported last month. The work, led by Nilesh Samani at the University of Leicester, UK, is part of an emerging line of research that is probing disease through epigenome-wide association studies (EWAS). Those in the field hope that because many epigenetic changes are influenced by the environment, such studies will reveal mechanisms of disease that have remained elusive. However, many scientists remain sceptical.

Obesity is a stubborn, growing problem in non-starving societies. Billions can be made off diets and treatments that don’t really work. Treatment that did work would be a far smaller industry. But seriously, we need to know more about why some people, surrounded by an abundance of food, don’t eat so as to become obese, but close relatives do. Maybe they have mostly the same genes but are getting different sets of signals. So we shouldn’t be looking for a special “fat gene” but a signalling pattern about when and how much it feels right to eat.

That said, it’s a long road and we don’t know the territory at all well:

Stephan Beck, a medical genomicist at University College London, thinks that epigenomic epidemiology is at the same stage genomic epidemiology was at eight years ago, when most studies were small and rarely identified the same genetic variants for any one disease. That changed in 2007, when the Wellcome Trust Case Control Consortium, an effort by research groups to identify genetic variants linked to common diseases, set standards for GWAS that emphasized the importance of large numbers of patients and reproducibility.

Beck sees signs that EWAS are headed in the same direction. For example, in the past few years several studies have reproduced the finding that a gene called AHRR is epigenetically modified in the blood cells of adult smokers and their newborn children. And some epigenome studies — including the BMI research1 — now verify discoveries made in one group of patients in separate cohorts of the same study. From More.

As with obesity, why do some people become addicted to nicotine, and relatives—surrounded by opportunities to buy and smoke it—never do. Or do it once or twice, get bored, and quit without damaging their lungs. Is there a “nicotine gene” that one relative happened to get and the other happened not to? Or will a science-based answer sound more like epigenomics and less like the selfish gene?

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See also: DNA doesn’t even tell teeth what they should look like

“If DNA really rules, why did THIS happen?”, where human neurons, transplanted into a mouse, had a mouse morphology.

Jonathan Wells: Far from being all-powerful, DNA does not wholly determine biological form (Mutate a fruit fly embryo in every possible way, and observe only three possible outcomes: a normal fruit fly, a defective fruit fly, or a dead fruit fly.)

Jonathan Wells: We are far from a good theoretical model of organisms’ development (We are far from having a complete list of the components, as a matter of fact.)

 

16 Replies to “First epigenetics, now epigenomics

  1. 1
    Dionisio says:

    How much of the DNA does correspond to actual genes that code for proteins (yes, after splicing, cut&paste and all that)?
    What happens with the rest of the DNA? what is it for?
    Do the DNA and the other machines within the cell have to be setup in such a way so that it reacts to environmental signals in the right way in order to function and build as it does? How does that operate?
    How does it happen that the zygote goes through several iterations of symmetric cellular divisions until a point, then cells start dividing asymmetrically? What determines the cell fate in those cases? what determines their migration paths?
    the first few days they were all apparently equivalent, weren’t they? so what makes them turn into one or another type, and position themselves in this or that location? how does that work? what part of the DNA is involved in all that? are many parts of the DNA, beyond the genes, involved in a way or another in all that orchestration and choreography?
    Got more questions, but let’s pause at this for now.
    Looking forward to hearing your comments on this. Thank y’all in advance.

  2. 2
    Dionisio says:

    Please, don’t be hard on me for my stupid questions. I’m a software developer who started to like this whole biology thing.

  3. 3
    Andre says:

    I’m starting to feel sorry for our Darwin friends they have gone into full damage control mode, how much longer before we chuck put the random, blind luck and lots of time just so story?

  4. 4
    News says:

    They’re not stupid, you’re right to ask. Hope an expert will answer.

  5. 5
    News says:

    Andre, what’s amusing is listening to them claim that everyone knew all along the very things making headlines and publications in the science media today, and we alone just discovered them. We don’t see many headlines out of: Water freezes at 0 degrees, do we? More to come, by the way. We are handicapped in how fast we can report, due to having day jobs, etc.

  6. 6
    gpuccio says:

    Dionisio:

    You ask very good questions.

    a) Protein coding genes are only a small minority of DNA in humans. Probably less than 2%. And they are about 20000.

    b) Non coding DNA is all the rest, but it is made of different things. More than 30% is introns, sequences inside protein coding genes. A smaller part is pseudogenes or gene fragments. The greatest part (about 60%) is intergenic non coding dNA. Much of that is made of transposons and repetitive sequences.

    c) The role of non coding DNA is probably mainly regulatory. But we still understand very little of how it works. This is a field which is growing every day. Really fascinating. Ah, I forgot: some important darwinists still seem to believe that most non coding DNA is junk 🙂

    d) Your question are mainly related to one of the most important problems in biology, which I usually sum up very simply in this way: where are the procedures?

    Indeed, the little we understand of how the genome works is about protein coding genes and proteins. Now, proteins are the final effectors. They are important, but much more important would be to understand the procedures which decide which proteins will be produced, in which sequence, and in which quantity, in each cell at any specific time.

    Of those procedures, we know almost nothing. They are not coded (if they are coded at all) according to what is known as “the genetic code”. That code is only to make proteins. The procedures are, at present, true “ghosts”.

    So, if you ask how it is that the zygote generates all the different kinds of cells in metazoa, the simple answer is that we don’t know.

    As I have already mentioned in my previous answer to you (in another thread) transcription regulation is the key.

    The main actors in that are, probably:

    1) Transcription factors (complex proteins)

    2) Various forms of nuclear RNA (miRNAs, lincRNA, and so on)

    3) Short regulatory peptides

    4) Epigenetic mechanisms (gene methilation, and so on)

    Many more things could be said, but that is just to begin 🙂

  7. 7
    Dionisio says:

    gpuccio @ 6
    Good to hear back from you! thank you so much for the supportive and encouraging words.
    I’m definitely struggling to understand so many terms and concepts in this fascinating field of science, but I’m excited about this switch I made from engineering apps software development to learning complex specified purpose-oriented functional information in systems biology.

  8. 8
    Dionisio says:

    News @ 4
    thank you so much for the supportive and encouraging words.
    As you well indicated, it didn’t take long for gpuccio -a very attentive expert- to respond my questions so clearly.
    I’m enjoying many OPs and comments in this UD blog.
    Please, keep up your good work.

  9. 9
    Dionisio says:

    gpuccio @ 6
    Thank you for the clear explanation you wrote. I’m copying it to my notes.
    I was on your time zone until last March 27, but now I’m on GMT-5.
    My niece and her fiancée are flying to Catania and going to Syracuse this summer.
    Have a good weekend.

  10. 10
    gpuccio says:

    Dionisio:

    Always a pleasure to hear from you 🙂

  11. 11
    DATCG says:

    News @ 5,

    You and ID guys are doing well. Good to see Sal back as well.

    The lamp’s flickering light pierces the darkness for those who have eyes to see the failure of Darwinism and Modern Synthesis.

  12. 12
    DATCG says:

    Gpuccio,

    Always appreciate your comments and responses. I suspect many more silent readers do as well.

  13. 13
    DATCG says:

    Question, When will Darwinian Geneticist and Epi-Geneticist drop the terminology of Non Coding from the vocabulary?

    It seems to be antiquated terminology, wrapped around ignorance, based upon blind processing opinions of Central Dogma. An opinion that dared not admit anything but the appearance of Design. And were loathe to admit appearance.

    Maybe, it will be dropped when Spell Checker recognizes the words Epi-Geneticist and Epigenome 🙂 As they become well recognized fields of research and operational activity.

    Non-Coding now covers every functional routine in a Programmers Guide of machine Architecture. From Interfaces, Subroutines and Database systems and tables for all kinds of variable input data, random or relational address access markers.

    “Non-Coding” genes provide smart selection for parsing Tables of Specified Information that bypass, interrupt, enhance, limit or promote different types of protein expressions.

    Like Frame Shifting can cause expression of a different Protein. Frame Shifting cannot be chanced to random selection due to point mutation without usual deleterious effect. So, wrong information gives a faulty jump, leads to nonsensical code. May entirely shut down protein expression.

    There’s NC regions to regulate the Regulators. cis-regulators, then guide RNA’s or gRNA and on and on.

    “Non-Protein-Coding” is used in attempt to recognize obvious Function. But that fails as well.

    It’s like saying an App on a Smartphone is Non-Coding simply because it does not run on a larger computer. Or a sub-routine embedded in a modem for communications is Non-Coding because it does not exist on a Communications Hub.

    Non-sense.

    Code is Code whether large or small. And sometimes the best code is the smallest of all 😉

  14. 14
    DATCG says:

    This is interesting Epigenetics research. The field will expand rapidly…

    “piRNAs had been classically known to regulate transposons in the germ cells. However, piRNAs have been, recently, found to be expressed in the brain and possibly function by imparting epigenetic changes by DNA methylation. piRNAs are known to be maternally inherited and we assume that they may play a role in early development.”

    Non-coding RNA interact to regulate neuronal development and function

  15. 15
    gpuccio says:

    DATCG:

    Thank you for the kind words! 🙂

    You are right, “non coding” means nothing in the light of what we know today. It would be better to call it “non protein coding”, or “non translated”.

    I see the same problem for the word “gene”, which was traditionally used for protein coding genes, while it is now used for many genes which only code for nuclear regulatory RNA.

    Moreover, the distinction between protein coding genes and non protein coding genes is not so clear as it could seem, given that protein coding genes are often also part of regulatory transcripts which are not translated into proteins.

    By the way, thank you for the very interesting link.

  16. 16
    Axel says:

    But now that they’ve been exposed as inadvertent lies, it’s much more fun to continue with deliberate lies. You know.. infotainment.

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