Butterfly wing patterns emerge from ancient ‘junk’ DNA
news.cornell.edu
news.cornell.edu
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' ...
I figured it was ingenious back then but I had no clue it‘s biomimetic :)
One of the worst names I've come across for a concept
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
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"
"While some TEs confer benefits on their hosts, most are regarded as selfish DNA parasites" (https://en.wikipedia.org/wiki/Transposable_element#Evolution)
"Pseudogene sequences may be transcribed into RNA at low levels, due to promoter elements inherited from the ancestral gene or arising by new mutations. Although most of these transcripts will have no more functional significance than chance transcripts from other parts of the genome, some have given rise to beneficial regulatory RNAs and new proteins." (https://en.wikipedia.org/wiki/Pseudogene)
I would define truly junk DNA as any DNA that if removed would be beneficial or not harmful to the majority of organisms in a species, and be beneficial or not harmful to the ability of a species to adapt and evolve its genome.
Ok, but by that definition, nothing is really junk: Even our own junkyards are still home to all sorts of animals and microorganisms which feed on the junk.
Not even starting with the recycling/upcycling movement.
Doesn't change the fact that it's junk in the sense of its original purpose and immediate utility to us.
In the same way, if junk DNA really has no effect on the body it's currently part of (like freed but uncleared memory in RAM), then I think the name is appropriate.
What I'm really missing in popular reporting about genetics though is more focus on the "regulatory elements". The understanding of DNA as given by pop-science articles is mostly that DNA is either instructions for building proteins or "junk", nothing else. This completely leaves out the question how the cell decides when/if a particular protein should be built - which is of course integral for understanding how a number of protein building instructions can result in a complex organism.
It's like describing a programming language as consisting only of instructions and comments but completely leaving out branches and loops.
(even though gene regulation does not happen through branches and loops)
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.
As I see, the answer still cryptic name, and lookup table.
I just think we can do better than the first system we came up with, and improving the system would open the whole thing up to more people and possibility.
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
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.
On your digital bookshelves in 2074.
The whole saga of 'junk' DNA is pretty interesting, and serves as a cautionary tale for those who want to use science to prop up their metaphysical ideologies. These non-coding regions of the genome were long thought to be the detritus of evolution, nothing but extra baggage carried around by the genome. Richard Dawkins and others famously settled on this as a means of discrediting the ideology of 'intelligent design' because, as they saw it, an intelligent designer wouldn't leave all this junk sitting in the genome. The later realization that this junk was actually playing all kinds of roles in large-scale regulation, cell differentiation, three-dimensional structure of the genome, and was often being actively transcribed (to regulatory RNA), etc. tossed that whole notion out the window and then it became (for a few years) something the intellectual creationists tried to use to discredit Dawkins and co. There was something called the 'Encode controversy' over a decade ago which featured centrally and which is well described here:
https://www.science20.com/adaptivecomplexity/our_genomes_enc...
Most people seem to have forgotten all that and accepted that large non-protein-gene-coding regions of eukaryotic genomes have various essential functional roles.
Moving on to biology, we have ~2500 smell receptor genes in various states of decay. We also have a lot of deactivated smell receptor genes, with a lot of polymorphism across humans.. as it's in free drift. Perhaps a long time ago when we shared a common ancestor with rats, many of these were far more useful, with strong selection pressure to preserve working copies, but not so much anymore.. Perhaps the trash man didn't come yet, but it's definitely stored away in our basements.
A more concrete example would be the roughly 40% of our genome that consists of repetitive elements, transposons, and retrotransposons. One of them, the ALU sequence, is 300 basepairs long, and yet is about %10 of our genome. There are about ~1 million copies of this sequence across our genome. It's spread has slowed down recently. Out of about a million copies, most of them are "inert", with no further ability to copy themselves. Sure, given just how much of our genome is this one thing being repeated over and over again, it has some function in some places - causes various splicing events here and there, helps shuffle genes (which is a bit of a meta function across evolutionary timescales), but overall, if you had children with these parts mutated, 99.9% of the time nothing of significance would happen. 10% is huge, given the protein coding region is about 1%, and the regulatory regions influencing transcription & RNA expression with some sort of identifiable action is about ~10% (if we're being very, very generous). DNA is promiscuously transcribed, but this doesn't mean much of that has any particular function. A lot of is transcribed at very low copy numbers, and degraded as fast as possible. A lot of things are stochastic, so there is a "long tail" of what gets transcribed, and at very low numbers at that.
Another good chunk of that 40% of repetitive sequence is is old retroviruses we got infected with (not dissimilar to HIV) that totally raided our DNA and became endogenous - in fact they're called HERVs - human endogenous retroviruses. These mostly stopped spreading in our DNA as well. Also, large streches of our DNA is the same couple of bases repeated ad nauseam for no particular reason.. let's say AT... there are these massive streches that go ATATATATATATA and you find people are highly polymorphic and tolerate a lot of mutations in these sequences. Some people have it deleted with no ill effect. There are rare examples of this occuring inside a gene, where having the repeat go on for too long is bad for you ("Huntingtin" (no it's not a mis-spelling) is the paradigmatic example). This is the exception rather than the rule, considering we have more repeats than the entire % of coding regions in the genome.
Junk is a bad word, but it's not like there is a "clean rewrite", or "clean refactor" either... so things accumulate, get shuffled around, get forgotten.. randomly get deleted in snippets... most mutations are either neutral or detrimental, with happy accidents happening here and there.
Overall, it is nonsensical to force things into this binary of "junk", "not junk", but beware of thinking of the genome as one would a design schematic for a microprocessor, or an aircraft for that matter. There is a lot of stuff in it that's like meh... doesn't really matter if it's there or not.
picture if you will, a big mass of magtape, no spool just a disaster, and you have to scan accross this mess until you find an accessible loop of it with a particular flag or type readable- likehow magtape works, except you have the mechanical challange of reading the tape in the form of a quivering, dynamic mass of spaggetti being read at mutiple locations and having to remain undamaged.
some of these regions make the biggest contribution by simply allowing mechanical slack and positioning of contact sites.
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.
At least until it gets repurposed.
Apologies for getting too meta.
Junk gene is a junk meme? Yeah, that's about right.
> At least until it gets repurposed.
Like all memes do. And genes, for that matter.
the system is legacy dependent for early boot configurations then changes mode to runtime with recently versioned modules and libraries
(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.)
(paper is not yet available on scihub)