'Junk DNA' Darwinism News

Non-coding RNAs undermining the junk DNA concept?

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We thought the concept of junk DNA (noncoding DNA) was dead. But Darwin’s followers keep reanimating the corpse. Maybe they’ll reanimate junk RNA too.

Meanwhile, there is an issue of Nature Structural & Molecular Biology, devoted mainly to the uses of noncoding RNAs—the noncoding explosion:

The long-held view that the primary role of RNA is to code for proteins has been severely undermined. This Focus explores the remarkable functional diversity of RNA in light of recent breakthroughs in noncoding-RNA biology. More.

The editorial (mostly exculpatory blather about the wrong ideas) is free, but the rest is paywalled.

See also: Jonathan Wells and the junk DNA myth

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17 Replies to “Non-coding RNAs undermining the junk DNA concept?

  1. 1
    wd400 says:

    We thought the concept of junk DNA (noncoding DNA) was dead.

    Junk DNA and non-codoing DNA are not the same thing. If you don’t realise that much then I’m afraid what you think about Junk DNA is pretty much worthless.

  2. 2
    rvb8 says:

    A great deal of non-coding DNA has remained in our genome unchanged for many millions of years suggesting there is strong evolutionary pressure for its retention. Why this should be is unknown, all that is known is that it does not function, transcribe proteins.

    I agree wd400, a couple of hundred words by NEWS on a subject which is fiercely researched, and continues to open up new areas of research, is glib at best, tiresome at worst.

  3. 3
    Seversky says:

    We thought the concept of junk DNA (noncoding DNA) was dead.

    What do junk DNA and Mark Twain have in common? The reports of death are greatly exaggerated.

    And what is it with the royal “we” around here? Delusions of plurality?

    You – all of you – are right to draw attention to the research on non-coding DNA, although you have missed its real significance. These papers threaten to undermine or overturn a core concept of evolutionary biology. According to neo-Paleyist belief such dissenting views should have been suppressed by the Darwinist Cabal long before they reached publication in a major peer-reviewed journal. Yet here they are. What can this mean?

  4. 4
    DavidD says:

    rvb8 “A great deal of non-coding DNA has remained in our genome unchanged for many millions of years . . . ”

    The only truly evolving thing here is the theory of evolution. Years ago humans were around 60,000, then 100.000, then 200,000, then 200,000 and now millions of years ?

    ” . . suggesting there is strong evolutionary pressure for its retention.”

    The only pressure here is from the Scientific Orthodoxy to encourage it’s worshippers to invent such asinine quips to defend Junk DNA which was pushed for a few decades as a major dogmatic proof for the faith, especially by most of the main stream clerics like Dawkins, Moran etc. Now with egg on their faces, they are force to make things up as they go along.

  5. 5
    Dionisio says:

    In vivo functions of long non-coding RNAs
    http://www.uncommondescent.com.....ent-541634

    Epigenetic coordination of embryonic heart transcription by dynamically regulated long noncoding RNAs
    http://www.uncommondescent.com.....ent-541636

    Long Non-Coding RNAs Involved in Immune Responses.
    http://www.uncommondescent.com.....ent-541629

    Developmental Programming of Long Non-Coding RNAs during Postnatal Liver Maturation…
    http://www.uncommondescent.com.....ent-541625

    Roles of long noncoding RNAs in brain development, functional diversification and neurodegenerative diseases
    http://www.uncommondescent.com.....ent-541623

    Revealing long noncoding RNA architecture and functions using domain-specific chromatin isolation by RNA purification.
    http://www.uncommondescent.com.....ent-541617

    In Situ Dissection of RNA Functional Subunits by Domain-Specific Chromatin Isolation by RNA Purification (dChIRP).
    http://www.uncommondescent.com.....ent-541617

    RNA-mediated epigenetic regulation of gene expression.
    http://www.uncommondescent.com.....ent-541605

  6. 6
    Dionisio says:

    Nuclear lncRNAs as epigenetic regulators-beyond skepticism.

    doi: 10.1016/j.bbagrm.2013.10.009.

    Systematic transcriptome analysis has revealed that a vast majority of the mammalian genome is transcribed into RNA, thus establishing the concept of “pervasive transcription.”

    More than half of these RNAs do not encode proteins, and they are collectively called noncoding RNAs.

    Although the physiological relevance of the transcription of these noncoding RNAs has remained unclear, it was recently proposed that one of the major roles of long noncoding RNAs (lncRNAs) in the nucleus is the regulation of gene expression at the transcriptional level via histone or DNA modification.

    In this review, we will summarize the advancement of our understanding of the molecular mechanisms of lncRNAs.

    This article is part of a Special Issue entitled: Chromatin and epigenetic regulation of animal development.

    http://www.ncbi.nlm.nih.gov/pubmed/24200874

  7. 7
    hrun0815 says:

    The only truly evolving thing here is the theory of evolution. Years ago humans were around 60,000, then 100.000, then 200,000, then 200,000 and now millions of years ?

    Have you considered that the exact answer depends simply on exactly at what stage you separate humans from their ancestors?

  8. 8
    Dionisio says:

    RNAs – physical and functional modulators of chromatin reader proteins.

    doi: 10.1016/j.bbagrm.2014.03.015

    The regulatory role of histone modifications with respect to the structure and function of chromatin is well known.

    Proteins and protein complexes establishing, erasing and binding these marks have been extensively studied.

    RNAs have only recently entered the picture of epigenetic regulation with the discovery of a vast number of long non-coding RNAs.

    Fast growing evidence suggests that such RNAs influence all aspects of histone modification biology.

    Here, we focus exclusively on the emerging functional interplay between RNAs and proteins that bind histone modifications.

    We discuss recent findings of reciprocally positive and negative regulations as well as summarize the current insights into the molecular mechanism directing these interactions.

    This article is part of a Special Issue entitled: Molecular mechanisms of histone modification function.

    http://www.ncbi.nlm.nih.gov/pubmed/24704208

  9. 9
    Dionisio says:

    Histone-binding domains: strategies for discovery and characterization.

    doi: 10.1016/j.bbagrm.2014.01.007.

    Chromatin signaling dynamics fundamentally regulate eukaryotic genomes.

    The reversible covalent post-translational modification (PTM) of histone proteins by chemical moieties such as phosphate, acetyl and methyl groups constitutes one of the primary chromatin signaling mechanisms.

    Modular protein domains present within chromatin-regulatory activities recognize or “read” specifically modified histone species and transduce these modified species into distinct downstream biological outcomes.

    Thus, understanding the molecular basis underlying PTM-mediated signaling at chromatin requires knowledge of both the modification and the partnering reader domains.

    Over the last ten years, a number of innovative approaches have been developed and employed to discover reader domain binding events with histones.

    Together, these studies have provided crucial insight into how chromatin pathways influence key cellular programs.

    This article is part of a Special Issue entitled: Molecular mechanisms of histone modification function.

    http://www.ncbi.nlm.nih.gov/pubmed/24525102

  10. 10
    Dionisio says:

    Sensing core histone phosphorylation – a matter of perfect timing.

    doi: 10.1016/j.bbagrm.2014.04.013.

    Systematic analysis of histone modifications has revealed a plethora of posttranslational modifications that mediate changes in chromatin structure and gene expression.

    Histone phosphorylation is a transient histone modification that becomes induced by extracellular signals, DNA damage or entry into mitosis.

    Importantly, phosphorylation of histone proteins does lead not only to the binding of specific reader proteins but also to changes in the affinity for readers or writers of other histone modifications.

    This induces a cross-talk between different chromatin modifications that allows the spatio-temporal control of chromatin-associated events.

    In this review we will summarize the progress in our current knowledge of factors sensing reversible histone phosphorylation in different biological scenarios.

    This article is part of a Special Issue entitled: Molecular mechanisms of histone modification function.

    http://www.ncbi.nlm.nih.gov/pubmed/24747175

  11. 11
    Dionisio says:

    Chromatin dynamics: interplay between remodeling enzymes and histone modifications.

    doi: 10.1016/j.bbagrm.2014.02.013.

    Chromatin dynamics play an essential role in regulating the accessibility of genomic DNA for a variety of nuclear processes, including gene transcription and DNA repair.

    The posttranslational modification of the core histones and the action of ATP-dependent chromatin remodeling enzymes represent two primary mechanisms by which chromatin dynamics are controlled and linked to nuclear events.

    Although there are examples in which a histone modification or a remodeling enzyme may be sufficient to drive a chromatin transition, these mechanisms typically work in concert to integrate regulatory inputs, leading to a coordinated alteration in chromatin structure and function.

    Indeed, site-specific histone modifications can facilitate the recruitment of chromatin remodeling enzymes to particular genomic regions, or they can regulate the efficiency or the outcome of a chromatin remodeling reaction.

    Conversely, chromatin remodeling enzymes can also influence, and sometimes directly modulate, the modification state of histones.

    These functional interactions are generally complex, frequently transient, and often require the association of myriad additional factors.

    This article is part of a Special Issue entitled: Molecular mechanisms of histone modification function.

    http://www.ncbi.nlm.nih.gov/pubmed/24583555

  12. 12
    Dionisio says:

    Chromatin and oxygen sensing in the context of JmjC histone demethylases.

    doi: 10.1042/BJ20140754.

    Responding appropriately to changes in oxygen availability is essential for multicellular organism survival.

    Molecularly, cells have evolved [how?] intricate gene expression programmes to handle this stressful condition.

    Although it is appreciated that gene expression is co-ordinated by changes in transcription and translation in hypoxia, much less is known about how chromatin changes allow for transcription to take place.

    The missing link between co-ordinating chromatin structure and the hypoxia-induced transcriptional programme could be in the form of a class of dioxygenases called JmjC (Jumonji C) enzymes, the majority of which are histone demethylases.

    In the present review, we will focus on the function of JmjC histone demethylases, and how these could act as oxygen sensors for chromatin in hypoxia.

    The current knowledge concerning the role of JmjC histone demethylases in the process of organism development and human disease will also be reviewed.

    http://www.ncbi.nlm.nih.gov/pubmed/25145438

  13. 13
    Joe says:

    Have you considered that the exact answer depends simply on exactly at what stage you separate humans from their ancestors?

    There was never any non-human ancestors of humans.

  14. 14
    DavidD says:

    Joe “There was never any non-human ancestors of humans.”

    It’s yet another example of religiously driven ideological blind faith, backed by the “But We Have the Consensus” argument. Looking around at the messed up condition of the world around us, I’d say the Consensus gang has been screwing up big time.

  15. 15
    JoeCoder says:

    Humans get 60 to 160 new mutations every generation. Population genetics tells us that the deleterious mutation rate must be very low in order for a species to survive at all, let alone evolve. As Larry Moran explained:

    if the deleterious mutation rate is too high, the species will go extinct… It should be no more than 1 or 2 deleterious mutations per generation.

    That means at most only 2 of those 60 to 160 mutations could be deleterious. And in turn only 2/160th to 2/60th of the genome (1.25% to 3.3%) can be functional, in the strictest sense of the word. The rest would have to be able to endure substitution mutations free of any consequence on evolutionary fitness.

    The problem for evolutionary theory is that we already know that far more than 1.25 to 3.33% of the genome is strictly, nucleotide-specific functional.

    Pheasant and Mattick, 2007 tell us that “the functional portion of the genome may exceed 20%” based on conserved sequences and those under purifying selection. Meaning that even if common descent were true, whatever mutated those sequences didn’t live to tell about it.

    ENCODE 2012 estimated “that at a minimum 20% (17% from protein binding and 2.9% protein coding gene exons) of the genome participates in… specific functions, with the likely figure significantly higher”

    ENCODE 2014 estimated that “12-15%” of DNA is evolutionarily conserved.

    Martin Smith et al, 2013 estimated that at least 13.6 – 30% of DNA is conserved in its RNA structure. This means that animals with different DNA sequences still produce RNA molecules that have the same shape. They report of their conserved RNA’s that “88% of which fall outside any known sequence-constrained element, suggesting that a large proportion of the mammalian genome is functional.”

    All of these are lower-bound estimates.

    Even if we take ENCODE 2014’s lower estimate of 12% DNA conservation, plus Martin Smith et al’s lower estimate of 13.6% * 88% = 12% conserved at the RNA level, that means at least 24% is strictly, nucleotide-specific functional as a minimum lower bound. That’s already 10 times too high for evolution to even prevent degeneration. And what evolution can’t preserve, it certainly can’t create.

    In addition to this lower bound, we also know that:

    1. At least 85% of DNA is transcribed to RNA (Matthew Hangauer et al, 2013)
    2. That “the nucleic acids that make up RNA connect to each other in very specific ways, which force RNA molecules to twist and loop into a variety of complicated 3D structures”
    3. “Where tested, these noncoding RNAs usually show evidence of biological function in different developmental and disease contexts, with, by our estimate, hundreds of validated cases already published and many more en route, which is a big enough subset to draw broader conclusions about the likely functionality of the rest.” (John Mattick, 2013,)

    So it appears these new papers are fulfilling Mattick’s projection that functionality will continue to be found for the rest.

  16. 16
    Zachriel says:

    JoeCoder: As Larry Moran explained

    You didn’t read Larry Moran very carefully. Most of the functional genome doesn’t code for proteins so is much less constrained.

  17. 17
    Joe says:

    Most of the functional genome doesn’t code for proteins so is much less constrained.

    You didn’t read what JoeCoder posted very carefully. And a mutation can be deleterious even when it happens in a non-protein coding sequence.

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