This sounds really neat, from the layman’s perspective. Are they saying that the neighboring non coding genes are acting as a kind of entropy source for the coding genes? If so, are there other known examples?
you and Oarch both get the idea, its not a pattern for butterfly wings, its a pattern. the pattern is conserved across species, and reused to direct morphogenesis.
Don't we have similar terminology for some of human organs. Appendix or some other organs are assumed useless. Personally I feel it's insane to call DNA or organs useless instead of acknowledging that we don't yet understand there true purpose.
Iirc appendix is now known to harbour gut microflora/bacteria when you have diarrhea, to keep them safe etc while your body clears whatever it deems unwanted
I'm not a biologist but the whole term "junk DNA" always felt a bit off to me. Millions of years of evolution and having a significant portion of DNA in all living organisms being "junk" doesn't make sense at all.
It's all 'junk' from a scientific materialist perspective.
It's a chemical reaction just like any other - it's random noise.
There's no (scientific materialist) reason to attribute 'junk' or 'not junk' to a sequence of random bits of information. There can be no 'purpose' to random noise.
Now, it is a bit odd that the most ardent secular scientific materialists do, truly in their own living experiences, tend strongly to attribute such anthropological attributes to such things, by calling some of these processes 'life', using terms such as 'evolution' instead of what is just 'random changes some of which persist in time', isn't it? It's almost like they 'believe' in some metaphysical orientation or principle which is a bit different than their stated 'belief' of materialism and the odd bunch of equations we posit to govern 'everything'?
Perhaps we can avoid going all the way down the intellectual rabbit hole by shifting these kinds of discussions into the evolving (pun intended) field of 'emergence' ...
Why? If it can copy, junk just sits there for eons. Think of free-again sectors on your old hdd that were not overwritten due to how fs driver allocates them.
Pretty ingenious, reminds me a bit about how Elite double used its own program code as a lookup table for building a procedurally generated universe in order to conserve memory.
I figured it was ingenious back then but I had no clue it‘s biomimetic :)
True enlightenment is when you realize that junk DNA is actually a great term, because evolution is great at building things out of junk and repurposing them.
The "junk" areas of repetitive DNA were actually identified as cauldrons of evolution in the early days of research, so we have known since the beginning that the junk was actually crucial.
Barbara McClintock's Nobel for this was awarded way back in 1983
This is a pet peeve of mine - the common misconceptions that "junk DNA" is just DNA with an unknown function.
By far most junk DNA really is junk. We know this because we know its nonfunctional origin (transposons, pseudogenes and similar), because we can do studies of conservation between species, and because there is a huge range of junk DNA content in otherwise similar species.
The misconception come from media bias: You'll never hear a story about "junk DNA really is junk, researchers find"
Not knowing much about DNA, it seems weird to me that it's assumed the primary purpose of DNA is to encode for proteins. Sure, that's one of its functions, but it would be just as misguided as assuming that bits only exist to encode text, and when they encode anything else, it's seen as some extraordinary exception to the norm.
people like to forget DNA has a 3D structure. A lot of the DNA that doesnt encode proteins might be involved, for example, in the association of 3D topological domains or conformational switches that impact chromatin accessibility. Interesting also is when sufficient factors bind to a local region of DNA to change the local chemistry and initiate phase separated domains where regulatory factors might preferrentially bind and thus drive the transcription of the few coding regions, and that's pretty cool too. Just to add some context to your bits-analogy.
we kind of do that to an extent but that confuses things.
for example tumor suppressor genes, actually produce a product that, among many other things, leads to suppression of tumor activity or viability.
the gene function [depending on the gene] would really be something hypothetically like -immuno signaling factor modulator gene number 9-
this makes things harder to mentally catalog for a lot of people, so we use name like SONIC; KRUPPEL; HEDGEHOG; SONIC HEDGHOG.
these are developmental pattern genes, and the names are subjective based on phenotype appearance, or what a researcher was doing when they observed it, etc.
You want Wnt to be named after butterfly stripes? Last sentence below gives away wnt and lack of it leading to colon polyps/cancer. It does a million other things though. Might as well call it signaling molecule 145626.
The activation of the pathway occurs at the cellular membrane, where Wnt ligands bind to the seven transmembrane-domain protein receptors Frizzled (Fzd) and/or to the low-density lipoprotein receptor-related protein (LRP) 5/6. This interaction leads to the inhibition of the axin degradasome destruction complex, which is a multiprotein complex that controls the cytoplasmic amount of β-catenin via phosphorylation, and, thereby, triggers β-catenin degradation by the proteasome in the absence of Wnt [10]. The destruction complex comprises the tumor suppressor adenomatous polyposis coli (APC), the axin scaffold protein, and two Ser/Thr kinases: glycogen synthase kinase 3 (GSK3) β and casein kinase 1 (CK1). In the absence of Wnt ligands, CK1 phosphorylates β-catenin at Ser45 residue and GSK3β at Ser33/Ser37/Thr41 residues. Then, the β-transducin repeats-containing protein (β-TrCP), an E3-ubiquitin ligase, ubiquitinates phosphorylated β-catenin, which becomes a target for proteasomal degradation [10].
When Wnt binds to Fzd and/or LRP5/6 receptors, the Wnt/β-catenin pathway is activated and the axin degradasome is inhibited [9]. As a consequence, Dishevelled (Dvl) is activated and recruits the degradasome complex to the plasma membrane, and, thereby, promotes the interaction between LRP5/6 and axin [11,12]. Consequently, LRP5/6 is phosphorylated at specific amino acidic residues (Ser1490, Thr1530, Thr1572, Ser1590, Ser1607) [13], acting as a direct competitive inhibitor of GSK3β [14].
Moreover, inactivation of GSK3β through Akt-dependent Ser9 phosphorylation prevents the phosphorylation of β-catenin, which allows its stabilization and accumulation in the cytoplasm. Stabilized β-catenin translocates to the nucleus where it binds to transcription factors, notably T-cell factor (TCF) and lymphoid enhancing factor (LEF), TCF/LEF. This interaction displaces the co-TCF/LEF repressor Groucho, whose function under basal conditions is to compact chromatin [15]. Groucho and TCF/LEF form a multiprotein complex, which is also termed Wnt enhanceosome, that recruits transcriptional co-activators and histone modifiers such as the ATP-dependent helicase Brahma-related gene 1 (BRG1, also known as SMARCA4), cyclic adenosine mono phosphate response element (CREB)-binding protein (CBP), p300, B-cell lymphoma 9 (BCL9), and pygo [15,16]. The Wnt enhanceosome regulates chromatin remodeling and activates the transcription of β-catenin-dependent genes involved in cell growth and survival, including C-MYC, CCND1, BIRC5, and CDKN1a [9]. C-myc is a proto-oncogene that activates cyclin D1 and simultaneously inhibits p21 and p27, which leads to uncontrolled cell proliferation
Thinking of DNA as code, with the particularity that outdated versions of the code are kept in "binaries", it's a creative use to recycle them as a random pattern generator!
We need to stop using the term “junk” DNA - it’s an outmoded term based on the wrongheaded assumption that DNA directly encoding proteins was the be all end all.
To add to the stash of dangerously simplifying computer analogies, this almost sounds like separate "code" and "data" sections: The coding DNA sort of interpreting the non-coding part as "data".
The advantage is the same: The coding parts can evolve only slowly, because a wrong mutation can mess up the entire functioning of the wings and would seriously reduce the individual's chance of survival. Meanwhile, a mutation in the non-coding part can only change the color pattern and nothing else. Therefore, the non-coding part can evolve a lot faster.
The problem isn't classification, as much as undoing the effect of a generation of academic and pop-sci publishing, which popularized the term "junk DNA" - and groups that perpetuate this term today, e.g. creationist/anti-evolution groups that use it to argue biologists are full of hubris (and thus wrong about evolution), and inadvertently keep the term itself alive.
It would've been nice if the article could have even shown a single image of how knocking out a certain sequence caused some wing pattern to disappear. But I guess that's hidden behind a paywall.
The first image, before the text of the article, has this caption: "Wings of the painted lady butterfly – Vanessa cardui, modified by deletion of non-coding DNA sequence."
(I'm definitely not paying for this content, and it is available in a fresh incognito browser session, so I suppose it should be available to all readers.)
Man, butterflies relying on all this old shit smh.... [ indiscriminate murmuring.... ] Yo hey [hallway scuffling] Yo PM, can't we just deprecate butterflies already? Ah he- I know I kno- yes I understand the boss likes butterflies, pretty and what no- no stop. Butterflies are a cost center, can we just deprecate and phase them out? Deprecation Plan? Cost Center Optimization? Ah shit ah- yeah, we keep the butterflies....
[+] [-] haimez|3 years ago|reply
[+] [-] Oarch|3 years ago|reply
[+] [-] rolph|3 years ago|reply
[+] [-] smusamashah|3 years ago|reply
[+] [-] RugnirViking|3 years ago|reply
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[+] [-] melagonster|3 years ago|reply
[+] [-] can16358p|3 years ago|reply
[+] [-] jasmer|3 years ago|reply
It's a chemical reaction just like any other - it's random noise.
There's no (scientific materialist) reason to attribute 'junk' or 'not junk' to a sequence of random bits of information. There can be no 'purpose' to random noise.
Now, it is a bit odd that the most ardent secular scientific materialists do, truly in their own living experiences, tend strongly to attribute such anthropological attributes to such things, by calling some of these processes 'life', using terms such as 'evolution' instead of what is just 'random changes some of which persist in time', isn't it? It's almost like they 'believe' in some metaphysical orientation or principle which is a bit different than their stated 'belief' of materialism and the odd bunch of equations we posit to govern 'everything'?
Perhaps we can avoid going all the way down the intellectual rabbit hole by shifting these kinds of discussions into the evolving (pun intended) field of 'emergence' ...
[+] [-] wruza|3 years ago|reply
[+] [-] endymi0n|3 years ago|reply
I figured it was ingenious back then but I had no clue it‘s biomimetic :)
https://en.m.wikipedia.org/wiki/Elite_(video_game)
[+] [-] lmpdev|3 years ago|reply
One of the worst names I've come across for a concept
[+] [-] epistasis|3 years ago|reply
The "junk" areas of repetitive DNA were actually identified as cauldrons of evolution in the early days of research, so we have known since the beginning that the junk was actually crucial.
Barbara McClintock's Nobel for this was awarded way back in 1983
https://en.wikipedia.org/wiki/Barbara_McClintock
[+] [-] jakobnissen|3 years ago|reply
By far most junk DNA really is junk. We know this because we know its nonfunctional origin (transposons, pseudogenes and similar), because we can do studies of conservation between species, and because there is a huge range of junk DNA content in otherwise similar species.
The misconception come from media bias: You'll never hear a story about "junk DNA really is junk, researchers find"
[+] [-] Gatsky|3 years ago|reply
[+] [-] thanatos519|3 years ago|reply
[+] [-] lrhegeba|3 years ago|reply
[+] [-] pwdisswordfish9|3 years ago|reply
[+] [-] hsn915|3 years ago|reply
[+] [-] amphitoky|3 years ago|reply
[+] [-] Mizza|3 years ago|reply
Seems like the whole thing might be easier to understand if we called a gene "butterflyStripeWidth" rathern than "WntA".
It's like we're writing a new core library but only using obfuscated function names.
[+] [-] nguyenkien|3 years ago|reply
[+] [-] rolph|3 years ago|reply
for example tumor suppressor genes, actually produce a product that, among many other things, leads to suppression of tumor activity or viability.
the gene function [depending on the gene] would really be something hypothetically like -immuno signaling factor modulator gene number 9-
this makes things harder to mentally catalog for a lot of people, so we use name like SONIC; KRUPPEL; HEDGEHOG; SONIC HEDGHOG.
these are developmental pattern genes, and the names are subjective based on phenotype appearance, or what a researcher was doing when they observed it, etc.
[+] [-] Pigalowda|3 years ago|reply
The activation of the pathway occurs at the cellular membrane, where Wnt ligands bind to the seven transmembrane-domain protein receptors Frizzled (Fzd) and/or to the low-density lipoprotein receptor-related protein (LRP) 5/6. This interaction leads to the inhibition of the axin degradasome destruction complex, which is a multiprotein complex that controls the cytoplasmic amount of β-catenin via phosphorylation, and, thereby, triggers β-catenin degradation by the proteasome in the absence of Wnt [10]. The destruction complex comprises the tumor suppressor adenomatous polyposis coli (APC), the axin scaffold protein, and two Ser/Thr kinases: glycogen synthase kinase 3 (GSK3) β and casein kinase 1 (CK1). In the absence of Wnt ligands, CK1 phosphorylates β-catenin at Ser45 residue and GSK3β at Ser33/Ser37/Thr41 residues. Then, the β-transducin repeats-containing protein (β-TrCP), an E3-ubiquitin ligase, ubiquitinates phosphorylated β-catenin, which becomes a target for proteasomal degradation [10]. When Wnt binds to Fzd and/or LRP5/6 receptors, the Wnt/β-catenin pathway is activated and the axin degradasome is inhibited [9]. As a consequence, Dishevelled (Dvl) is activated and recruits the degradasome complex to the plasma membrane, and, thereby, promotes the interaction between LRP5/6 and axin [11,12]. Consequently, LRP5/6 is phosphorylated at specific amino acidic residues (Ser1490, Thr1530, Thr1572, Ser1590, Ser1607) [13], acting as a direct competitive inhibitor of GSK3β [14]. Moreover, inactivation of GSK3β through Akt-dependent Ser9 phosphorylation prevents the phosphorylation of β-catenin, which allows its stabilization and accumulation in the cytoplasm. Stabilized β-catenin translocates to the nucleus where it binds to transcription factors, notably T-cell factor (TCF) and lymphoid enhancing factor (LEF), TCF/LEF. This interaction displaces the co-TCF/LEF repressor Groucho, whose function under basal conditions is to compact chromatin [15]. Groucho and TCF/LEF form a multiprotein complex, which is also termed Wnt enhanceosome, that recruits transcriptional co-activators and histone modifiers such as the ATP-dependent helicase Brahma-related gene 1 (BRG1, also known as SMARCA4), cyclic adenosine mono phosphate response element (CREB)-binding protein (CBP), p300, B-cell lymphoma 9 (BCL9), and pygo [15,16]. The Wnt enhanceosome regulates chromatin remodeling and activates the transcription of β-catenin-dependent genes involved in cell growth and survival, including C-MYC, CCND1, BIRC5, and CDKN1a [9]. C-myc is a proto-oncogene that activates cyclin D1 and simultaneously inhibits p21 and p27, which leads to uncontrolled cell proliferation
[+] [-] hbbio|3 years ago|reply
[+] [-] fuckstick|3 years ago|reply
[+] [-] djbusby|3 years ago|reply
[+] [-] xg15|3 years ago|reply
The advantage is the same: The coding parts can evolve only slowly, because a wrong mutation can mess up the entire functioning of the wings and would seriously reduce the individual's chance of survival. Meanwhile, a mutation in the non-coding part can only change the color pattern and nothing else. Therefore, the non-coding part can evolve a lot faster.
[+] [-] zakki|3 years ago|reply
[+] [-] JohnJamesRambo|3 years ago|reply
[+] [-] TeMPOraL|3 years ago|reply
[+] [-] unknown|3 years ago|reply
[deleted]
[+] [-] johnnylambada|3 years ago|reply
[+] [-] alrlroipsp|3 years ago|reply
[+] [-] rolph|3 years ago|reply
the system is legacy dependent for early boot configurations then changes mode to runtime with recently versioned modules and libraries
[+] [-] supernova87a|3 years ago|reply
[+] [-] olejorgenb|3 years ago|reply
(paper is not yet available on scihub)
[+] [-] taneliv|3 years ago|reply
(I'm definitely not paying for this content, and it is available in a fresh incognito browser session, so I suppose it should be available to all readers.)
[+] [-] karmaniverous|3 years ago|reply
[+] [-] daguava|3 years ago|reply