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(University of Washington)   Second code found in DNA. First reports have it as ↑↑↓↓←→←→ B A   (washington.edu) divider line 64
    More: Cool, First Report, DNA, genetic code, code, genes control, National Human Genome Research Institute  
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4603 clicks; posted to Geek » on 13 Dec 2013 at 7:56 AM (36 weeks ago)   |  Favorite    |   share:  Share on Twitter share via Email Share on Facebook   more»



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2013-12-12 11:55:09 PM
Mind... blown.
 
2013-12-12 11:58:13 PM
A research team led by Dr. John Stamatoyannopoulos, University of Washington associate professor of genome sciences and of medicine, made the discovery.

Damn, Greece, WTF?
 
2013-12-13 12:20:28 AM
IT'S A COOKBOOK!

/wait... what?
 
2013-12-13 04:13:43 AM
What if it turns out that genetics is a bit like breathing, whereby if you don't think about it it's automatic, but think about it and you go into manual mode. Maybe that's why cancer is on the up. People don't know how to properly genet. You're now on manual breathing mode, and manual genetic mode.
 
2013-12-13 06:07:15 AM
One would be even further "stunned" to discover a blog writer who actually understands what he is talking about and can express it in plain language.
 
2013-12-13 07:13:21 AM
Based on my understanding from reading the abstract of the actual paper, this is not a new second code. That doesn't seem to be what the abstract is saying at all. Here is my take. If anyone does have access to the actual paper from Science, please feel free to correct me if I'm wrong.

1.) The idea of regulatory DNA is not new, nor is it really a secret code. I'm pretty sure just about everyone who has passed a reasonable high school biology class has been taught the basics of transcription regulation (even if you don't remember it), probably using the lac operon of E. coli as an example (it's the one in most textbooks).

2.) It is not surprising that some regulatory sequences which are binding sites for transcription factors (proteins which bind to DNA to affect gene expression) would also appear among the codons of coding sequences. Regulatory sequences tend to be short, and with only 4 DNA bases to work with, you would expect some to share sequences with coding sequences. Transcription factors, if they are present, will bind wherever they find the matching sequence.

3.) What the article really appears to be saying is that when this happens and you have a binding site for a transcription factor in the coding sequence of a gene (presumably to control a different gene, though it could act to repress the gene it is in, I guess) then sequence evolution is constrained because any mutation which changes that sequence will have multiple affects, possibly not only altering the amino acid sequence coded by that gene but the regulation of the other gene. That is what Dr John Stamatoyannopoulos is talking about in the quote, "Many DNA changes that appear to alter protein sequences may actually cause disease by disrupting gene control programs or even both mechanisms simultaneously."

At least that is what I gather from it. Please correct me if I'm wrong (and if anyone has access and would like to share the paper, I'd love to read it; EIP). :)
 
2013-12-13 07:20:25 AM
Actually, the extra sequence is this:

AA AC AG AT CA AC CC CG CT CA GA GC GG GT CG AT CA CG TA TC TG CC TT GC AC
 
2013-12-13 07:49:53 AM
i148.photobucket.com

dittybopper: Actually, the extra sequence is this:

AA AC AG AT CA AC CC CG CT CA GA GC GG GT CG AT CA CG TA TC TG CC TT GC AC

 
2013-12-13 07:58:02 AM

libranoelrose: [i148.photobucket.com image 475x337]


Need a hint?  Polybius.
 
2013-12-13 08:01:02 AM
Just wait, we'll be seeing "DNA 2.0" show up on developer job listings, they'll also be wanting a decade of experience with it.
 
2013-12-13 08:03:22 AM
Oh man, the Creationists are going to be all over this one.
 
2013-12-13 08:04:20 AM

Slaxl: What if it turns out that genetics is a bit like breathing, whereby if you don't think about it it's automatic, but think about it and you go into manual mode. Maybe that's why cancer is on the up. People don't know how to properly genet. You're now on manual breathing mode, and manual genetic mode.


What someone properly geneting looks like:

www.steynsafari.com
 
2013-12-13 08:12:32 AM
I thought it would be "Hello, Sweetie!"
 
2013-12-13 08:13:52 AM

turboke: I thought it would be "Hello, Sweetie!"


Lol!
 
2013-12-13 08:15:21 AM
Be sure to drink your Ovaltine!
 
2013-12-13 08:19:05 AM
readmefirst.txt
 
2013-12-13 08:33:07 AM
Wow.  Fifty-year-old news is so exciting.

Indeed a Nobel Prize was awarded in 1965 for it.   Whatever ENCODE found, it is not what was in the article.

This is not the first time for this project.  ENCODE has a history of extremely misleading press releases.  As if they care more about blowing their own horn then keeping the public informed about their work.
 
2013-12-13 08:33:22 AM
GATTACA!


GATTACA!


GATTACA!
 
2013-12-13 08:34:19 AM

mamoru: Based on my understanding from reading the abstract of the actual paper, this is not a new second code. That doesn't seem to be what the abstract is saying at all. Here is my take. If anyone does have access to the actual paper from Science, please feel free to correct me if I'm wrong.

1.) The idea of regulatory DNA is not new, nor is it really a secret code. I'm pretty sure just about everyone who has passed a reasonable high school biology class has been taught the basics of transcription regulation (even if you don't remember it), probably using the lac operon of E. coli as an example (it's the one in most textbooks).

2.) It is not surprising that some regulatory sequences which are binding sites for transcription factors (proteins which bind to DNA to affect gene expression) would also appear among the codons of coding sequences. Regulatory sequences tend to be short, and with only 4 DNA bases to work with, you would expect some to share sequences with coding sequences. Transcription factors, if they are present, will bind wherever they find the matching sequence.

3.) What the article really appears to be saying is that when this happens and you have a binding site for a transcription factor in the coding sequence of a gene (presumably to control a different gene, though it could act to repress the gene it is in, I guess) then sequence evolution is constrained because any mutation which changes that sequence will have multiple affects, possibly not only altering the amino acid sequence coded by that gene but the regulation of the other gene. That is what Dr John Stamatoyannopoulos is talking about in the quote, "Many DNA changes that appear to alter protein sequences may actually cause disease by disrupting gene control programs or even both mechanisms simultaneously."


Back in the '90s, I had a genetics research professor who believed exactly this, so I don't see anything new in this paper. At the time, they weren't sure which sequences were only coding related and which were only regulation, but they were pretty certain that overlap had to occur, so any mutation could affect both functions. I may be missing something, but this appears to be a confirmation study more than anything about breaking new ground.
 
2013-12-13 08:36:53 AM
Well there's Dan Brown's next book plot.
 
2013-12-13 08:50:44 AM
Wow, is there anything that Stephen Fry can't do?
 
2013-12-13 08:53:41 AM

mamoru: Based on my understanding from reading the abstract of the actual paper, this is not a new second code. That doesn't seem to be what the abstract is saying at all. Here is my take. If anyone does have access to the actual paper from Science, please feel free to correct me if I'm wrong.

1.) The idea of regulatory DNA is not new, nor is it really a secret code. I'm pretty sure just about everyone who has passed a reasonable high school biology class has been taught the basics of transcription regulation (even if you don't remember it), probably using the lac operon of E. coli as an example (it's the one in most textbooks).

2.) It is not surprising that some regulatory sequences which are binding sites for transcription factors (proteins which bind to DNA to affect gene expression) would also appear among the codons of coding sequences. Regulatory sequences tend to be short, and with only 4 DNA bases to work with, you would expect some to share sequences with coding sequences. Transcription factors, if they are present, will bind wherever they find the matching sequence.

3.) What the article really appears to be saying is that when this happens and you have a binding site for a transcription factor in the coding sequence of a gene (presumably to control a different gene, though it could act to repress the gene it is in, I guess) then sequence evolution is constrained because any mutation which changes that sequence will have multiple affects, possibly not only altering the amino acid sequence coded by that gene but the regulation of the other gene. That is what Dr John Stamatoyannopoulos is talking about in the quote, "Many DNA changes that appear to alter protein sequences may actually cause disease by disrupting gene control programs or even both mechanisms simultaneously."

At least that is what I gather from it. Please correct me if I'm wrong (and if anyone has access and would like to share the paper, I'd love to read it; EIP). :)


I'll take a look at the paper later, but that sounds like a pretty good summary.  The complexity of life continues to amaze me.
 
2013-12-13 08:54:53 AM
Zoanoids?
 
2013-12-13 09:15:59 AM
Is it A,B,A,C,A,B,B?  Everyone knows that's how blood is made.
 
2013-12-13 09:20:49 AM

Fun Dumpster: Is it A,B,A,C,A,B,B?  Everyone knows that's how blood is made.


oh my god, i can't believe i immediately knew what that was before reading everything after the question mark.
 
2013-12-13 09:22:46 AM
"And then what?"
"Checkmate."

img43.imageshack.us
 
2013-12-13 09:25:19 AM

mamoru: Based on my understanding from reading the abstract of the actual paper, this is not a new second code. That doesn't seem to be what the abstract is saying at all. Here is my take. If anyone does have access to the actual paper from Science, please feel free to correct me if I'm wrong.

1.) The idea of regulatory DNA is not new, nor is it really a secret code. I'm pretty sure just about everyone who has passed a reasonable high school biology class has been taught the basics of transcription regulation (even if you don't remember it), probably using the lac operon of E. coli as an example (it's the one in most textbooks).

2.) It is not surprising that some regulatory sequences which are binding sites for transcription factors (proteins which bind to DNA to affect gene expression) would also appear among the codons of coding sequences. Regulatory sequences tend to be short, and with only 4 DNA bases to work with, you would expect some to share sequences with coding sequences. Transcription factors, if they are present, will bind wherever they find the matching sequence.

3.) What the article really appears to be saying is that when this happens and you have a binding site for a transcription factor in the coding sequence of a gene (presumably to control a different gene, though it could act to repress the gene it is in, I guess) then sequence evolution is constrained because any mutation which changes that sequence will have multiple affects, possibly not only altering the amino acid sequence coded by that gene but the regulation of the other gene. That is what Dr John Stamatoyannopoulos is talking about in the quote, "Many DNA changes that appear to alter protein sequences may actually cause disease by disrupting gene control programs or even both mechanisms simultaneously."

At least that is what I gather from it. Please correct me if I'm wrong (and if anyone has access and would like to share the paper, I'd love to read it; EIP). :)


Here is a link to the paper  https://dl.dropboxusercontent.com/u/51521446/Science-2013-Stergachis- 1 367-72.pdf

TheMysteriousStranger: Wow.  Fifty-year-old news is so exciting.

Indeed a Nobel Prize was awarded in 1965 for it.   Whatever ENCODE found, it is not what was in the article.

This is not the first time for this project.  ENCODE has a history of extremely misleading press releases.  As if they care more about blowing their own horn then keeping the public informed about their work.


This is also true.  ENCODE is better at selling their science than anyone I have ever seen.

/now off to read the paper
 
2013-12-13 09:31:22 AM
cltampa.com

Konami!
 
2013-12-13 09:35:58 AM

mamoru: Based on my understanding from reading the abstract of the actual paper, this is not a new second code. That doesn't seem to be what the abstract is saying at all. Here is my take. If anyone does have access to the actual paper from Science, please feel free to correct me if I'm wrong.

1.) The idea of regulatory DNA is not new, nor is it really a secret code. I'm pretty sure just about everyone who has passed a reasonable high school biology class has been taught the basics of transcription regulation (even if you don't remember it), probably using the lac operon of E. coli as an example (it's the one in most textbooks).

2.) It is not surprising that some regulatory sequences which are binding sites for transcription factors (proteins which bind to DNA to affect gene expression) would also appear among the codons of coding sequences. Regulatory sequences tend to be short, and with only 4 DNA bases to work with, you would expect some to share sequences with coding sequences. Transcription factors, if they are present, will bind wherever they find the matching sequence.

3.) What the article really appears to be saying is that when this happens and you have a binding site for a transcription factor in the coding sequence of a gene (presumably to control a different gene, though it could act to repress the gene it is in, I guess) then sequence evolution is constrained because any mutation which changes that sequence will have multiple affects, possibly not only altering the amino acid sequence coded by that gene but the regulation of the other gene. That is what Dr John Stamatoyannopoulos is talking about in the quote, "Many DNA changes that appear to alter protein sequences may actually cause disease by disrupting gene control programs or even both mechanisms simultaneously."

At least that is what I gather from it. Please correct me if I'm wrong (and if anyone has access and would like to share the paper, I'd love to read it; EIP). :)


About the only thing I saw in the abstract of the Science paper that piqued my interest was the ability of this "dual use" of codons to explain biased codon selection, which (at least to me) seems pretty interesting. Otherwise I agree with whoever said it upstream: what ENCODE seems to do best is publicize ENCODE. They're not quite to Venterian levels, but getting there.
 
2013-12-13 09:40:41 AM
WorkingInParadise:

"Nature will find a way"
i.imgur.com
 
2013-12-13 09:53:57 AM
Damn, I had higher hopes when I started this article. I was expecting some other region of the neucleotide to have a "coding area" similar to the 2/3 H-bonding positions on the purine/pyrimidines that we currently know of. Or something akin to methylation/acetylation, where regions of DNA/chomatin are "flagged" for up or down regulation.

This is basically saying the existing code can have multiple applications, which, as has been said, is fairly well known already (promoters, operons, etc).

Still cool, but I was hoping for another parallel, discrete code, not an extra layer/use to the existing one.
 
2013-12-13 09:58:23 AM
FTA:  "Since the genetic code was deciphered in the 1960s, scientists have assumed that it was used exclusively to write information about proteins."


NO!!  That is just simply wrong.  It's not in any way true.  It's not an oversimplification, or poorly written, or one way of looking at it.  It's a lie.  Flat out, 100% wrong.

Half the reason the public is so stupid at science is because journalists can't string two sentences together without screwing something up.
 
2013-12-13 10:04:02 AM

mamoru: Based on my understanding from reading the abstract of the actual paper, this is not a new second code. That doesn't seem to be what the abstract is saying at all. Here is my take. If anyone does have access to the actual paper from Science, please feel free to correct me if I'm wrong.

1.) The idea of regulatory DNA is not new, nor is it really a secret code. I'm pretty sure just about everyone who has passed a reasonable high school biology class has been taught the basics of transcription regulation (even if you don't remember it), probably using the lac operon of E. coli as an example (it's the one in most textbooks).

2.) It is not surprising that some regulatory sequences which are binding sites for transcription factors (proteins which bind to DNA to affect gene expression) would also appear among the codons of coding sequences. Regulatory sequences tend to be short, and with only 4 DNA bases to work with, you would expect some to share sequences with coding sequences. Transcription factors, if they are present, will bind wherever they find the matching sequence.

3.) What the article really appears to be saying is that when this happens and you have a binding site for a transcription factor in the coding sequence of a gene (presumably to control a different gene, though it could act to repress the gene it is in, I guess) then sequence evolution is constrained because any mutation which changes that sequence will have multiple affects, possibly not only altering the amino acid sequence coded by that gene but the regulation of the other gene. That is what Dr John Stamatoyannopoulos is talking about in the quote, "Many DNA changes that appear to alter protein sequences may actually cause disease by disrupting gene control programs or even both mechanisms simultaneously."

At least that is what I gather from it. Please correct me if I'm wrong (and if anyone has access and would like to share the paper, I'd love to read it; EIP). :)


That's exactly what the paper says :) It is also important to stress that the idea of transcription factor binding sites sometimes being found in genes isn't new either. Some genes overlap one another after all, and some TFs bind within genes not just in the promoter region.

The work is cool because it quantifies those evolutionary constraints and shows how it helps account for codon usage bias. We know of lots of factors that contribute to it, but it is always good to have a more complete picture.

Also, unlike the original ENCODE publications, they looked not just at regions of the genome with signal for the binding of a transcription factor, which we know is full of false-positives even when you look in multiple cell lines, but they also looked for sites that were evolutionarily conserved. That really lets you make better statements about the biological significance of the finding.

satanorsanta: This is also true.  ENCODE is better at selling their science than anyone I have ever seen.

/now off to read the paper


True, but at least this paper actually requires evolutionary conservation as part of their definition. The major ENCODE data release last year was atrocious in terms of what they meant by "function."

Girl Pants: This is basically saying the existing code can have multiple applications, which, as has been said, is fairly well known already (promoters, operons, etc).


It isn't totally fair to say the "meh this is all old stuff we already knew", the idea of overlap between TF binding sites and coding regions isn't new sure, but the paper is actually quite good in terms of quantifying various features and showing the effect on codon usage bias. I really wish they hadn't gone down the bullshiat road of trying to coin a new term though. We don't need duon in the lexicon to describe this.
 
2013-12-13 10:13:56 AM
entropic_existence: It isn't totally fair to say the "meh this is all old stuff we already knew", the idea of overlap between TF binding sites and coding regions isn't new sure, but the paper is actually quite good in terms of quantifying various features and showing the effect on codon usage bias. I really wish they hadn't gone down the bullshiat road of trying to coin a new term though. We don't need duon in the lexicon to describe this.

Oh I didn't mean to imply that, sorry. I meant that I was a bit let down personally that this doesn't work by some brand new mechanism that I'd never heard of before, it works through a mechanism we knew of. I certainly didn't want to insult these people by saying they've found nothing new. I'm just being selfish and let my expectations go too far.
 
2013-12-13 10:16:06 AM
We still don't have infinite anything yet, Subby, unless you count stupidity, as other great minds have stated throughout the years, there are no limits to stupidity.

blacknite: Fun Dumpster: Is it A,B,A,C,A,B,B?  Everyone knows that's how blood is made.

oh my god, i can't believe i immediately knew what that was before reading everything after the question mark.


Me too.  The good ol' days of 16 bit Super Nintendo vs. Sega Genesis.
 
2013-12-13 10:32:57 AM
We should all calm down and drink a nice soothing yummy beverage:

www.hallme.com
 
2013-12-13 10:37:32 AM
So God practices steganography. Good for Her.
 
2013-12-13 10:51:08 AM
Wait until they figure out that the code that they are looking at isn't the straight code but rather a compressed code.

/your genes have a pkzipper
 
2013-12-13 10:59:13 AM

eyeq360: We still don't have infinite anything yet, Subby, unless you count stupidity, as other great minds have stated throughout the years, there are no limits to stupidity.
blacknite: Fun Dumpster: Is it A,B,A,C,A,B,B?  Everyone knows that's how blood is made.

oh my god, i can't believe i immediately knew what that was before reading everything after the question mark.

Me too.  The good ol' days of 16 bit Super Nintendo vs. Sega Genesis.


B,A,D,L,A,X,B,A,B,Y. Forget what that does, though. I wanna say it unlocks a character like Noob Saibot on the Super Nintendo
 
2013-12-13 11:04:19 AM
The really interesting news is that the deeper parts of DNA are actually running a Bitcoin mine.
 
2013-12-13 11:32:26 AM
None of this is new. The Science article itself is demonstrating that the TFs that bind within coding regions constrain the evolution of proteins, and lead to the (already known) codon usage bias. This is not a revelation, although this paper seems to be giving more of the the exact details.

The abstract:

"Genomes contain both a genetic code specifying amino acids and a regulatory code specifying transcription factor (TF) recognition sequences. We used genomic deoxyribonuclease I footprinting to map nucleotide resolution TF occupancy across the human exome in 81 diverse cell types. We found that ~15% of human codons are dual-use codons ("duons") that simultaneously specify both amino acids and TF recognition sites. Duons are highly conserved and have shaped protein evolution, and TF-imposed constraint appears to be a major driver of codon usage bias. Conversely, the regulatory code has been selectively depleted of TFs that recognize stop codons. More than 17% of single-nucleotide variants within duons directly alter TF binding. Pervasive dual encoding of amino acid and regulatory information appears to be a fundamental feature of genome evolution."
 
2013-12-13 11:33:26 AM

bingethinker: Mind... blown.


Why? This is no big deal at all. Let me guess, you're still operating at a 1975 level of "knowledge" regarding genomics...
 
2013-12-13 11:36:39 AM
So basically, it's not just how the sentence is structured...but what its context is too.

Dammit, now you get all subtle on me...I just wanted it to be about grammar.
 
2013-12-13 11:57:17 AM
I'm not a biologist, but I'm also really excited about the emerging research in Epigenetics.

/Which I realize this isn't.
 
2013-12-13 12:16:18 PM

Girl Pants: Oh I didn't mean to imply that, sorry. I meant that I was a bit let down personally that this doesn't work by some brand new mechanism that I'd never heard of before, it works through a mechanism we knew of. I certainly didn't want to insult these people by saying they've found nothing new. I'm just being selfish and let my expectations go too far.


Fair enough. And yeah, given some of the headlines I read for the article I know what you mean.

Felgraf: I'm not a biologist, but I'm also really excited about the emerging research in Epigenetics.

/Which I realize this isn't.


Ugh, sorry as someone who works in genomics I get irritated every time epigenetics is thrown around, usually because for some reason both in the press and among researchers it became a sort of buzzword of the week deal. Talked about in the media like it was something totally new (it wasn't) and completely altering our perceptions of biological inheritance and evolution (it wasn't). Granted there is lots of cool research involving epigenetics, but really just like there is lots of cool research in, well... pretty much everything.
 
2013-12-13 12:22:11 PM
regulatory sequences? in my DNA? (it's more common than you think). now, with enhanced oversimplification for undergrads!
 
2013-12-13 12:26:43 PM
5'-TAG A GAGA CAT A TACT ACT-3'
 
2013-12-13 12:53:16 PM
Subby had no friends.  Any popular kid "select start" was added on for two player.

/the code without that always looks lacking
 
2013-12-13 01:07:57 PM

entropic_existence: Ugh, sorry as someone who works in genomics I get irritated every time epigenetics is thrown around, usually because for some reason both in the press and among researchers it became a sort of buzzword of the week deal. Talked about in the media like it was something totally new (it wasn't) and completely altering our perceptions of biological inheritance and evolution (it wasn't). Granted there is lots of cool research involving epigenetics, but really just like there is lots of cool research in, well... pretty much everything.


Ah, fair enough. It's okay, I feel that way whenever someone throws the word "Nano" around (and I'm doing my PhD in nanophysics/nanoengineering/nanotech).
 
2013-12-13 01:45:18 PM
upload.wikimedia.org
 
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