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Paper at Nature Reviews Genetics demands some respect for junk DNA

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Abstract: Pseudogenes are defined as regions of the genome that contain defective copies of genes. They exist across almost all forms of life, and in mammalian genomes are annotated in similar numbers to recognized protein-coding genes. Although often presumed to lack function, growing numbers of pseudogenes are being found to play important biological roles. In consideration of their evolutionary origins and inherent limitations in genome annotation practices, we posit that pseudogenes have been classified on a scientifically unsubstantiated basis. We reflect that a broad misunderstanding of pseudogenes, perpetuated in part by the pejorative inference of the ‘pseudogene’ label, has led to their frequent dismissal from functional assessment and exclusion from genomic analyses. With the advent of technologies that simplify the study of pseudogenes, we propose that an objective reassessment of these genomic elements will reveal valuable insights into genome function and evolution. – Cheetham, S.W., Faulkner, G.J. & Dinger, M.E. Overcoming challenges and dogmas to understand the functions of pseudogenes. Nat Rev Genet (2019) doi:10.1038/s41576-019-0196-1 Published: 17 December 2019

The friend who sent us the abstract also quotes from the paywalled paper:

In addition to the untested hypothesis that evolution has left us with a dichotomy between genes and pseudogenes, the term pseudogene itself asserts a paradigm of non-functionality through its taxonomic construction. Pseudogenes are defined as defective and not genes. This point is highlighted because impartial language in science is known to inherently restrict the neutral investigation between conflicting paradigms[119]. In the case of pseudogenes, the term itself is constructed to support the dominant paradigm and therefore limit, consciously or unconsciously, scientific objectivity in their investigation.

It was in fact Darwinism that prevented the role of pseudo genes from being properly recognized.

As another friend puts the matter, “This is an important paper for documenting that not only is pseudogene function is far more prevalent than we often recognize but also that evolutionary “dogma” has prevented investigation into the function of pseudogenes. The paper’s message is that pseudogenes probably have many more functions than we think and only the false view that they are “junk” prevents us from finding them.”

Remember how important pseudogenes (evolution’s huge library of useless junk) once were?

By now, Darwin could paper his study with goodbye notes.

Comments
Sven
the machine-replication system is irreducibly complex
That's a good step forward. Now, we're talking about an information processing network. It's irreducibly complex. Code, sender, translation, receiver, confirmation.Silver Asiatic
December 31, 2019
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Sven Mil:
Biological systems are not anything like machines or computers.
Except when there are, right? Information processing and coded systems. Rotary engines.
Just because the machine-replication system is irreducibly complex, does not mean the biological system is irreducibly complex.
True. The fact that biological systems and structures meet the definition of irreducible complexity is a hint, though.
I hate to break it to you, but there is nothing irreducibly complex in all of biology.
And yet a very long list of IC in biology exists. You don't even have a mechanism capable of producing biologically relevant molecular replicators. And you expect us to believe that nature produced coded systems from the bottom up? Meaning the codes emerged only once the system was up and running. Talk about saying anything...ET
December 31, 2019
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No, you avoided the question, as you are doing now. Probably because you know that machine-biology analogies are extremely superficial. Von Neumann's automaton system was an accurate prediction of the basic components and their general functions, which was an incredible feat at the time, but it is not useful beyond that. Biological systems are not anything like machines or computers. Just because the machine-replication system is irreducibly complex, does not mean the biological system is irreducibly complex. I hate to break it to you, but there is nothing irreducibly complex in all of biology. The only way you can portray things in biology as irreducibly complex is by drawing poor analogies which always breakdown at the molecular level. I believe you know this, but as I have said, you will say anything to support your own ideas and worldview.Sven Mil
December 31, 2019
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. Sorry for the long holiday delay. Merry Christmas and Happy New Year to all.
I’m asking if you think von Neumann’s automaton system of machines and tape are a perfect analogy to biological systems.
I think I’ve already answered this question, and even clarified with a short summary of some of the critical conditions involved. You are welcome to make whatever point you have in mind.
Is it possible that this system is irreducibly complex only when constrained by the principles of computers/machines?
These systems are irreducibly complex because they have to be. They have to perform the real-world task of freely specifying things among alternatives, and they must accomplish this task (dynamic freedom) under real-world physical conditions (invariant law). A system of discontinuous association is the means to accomplish this task, and the type of physical arrangement that makes discontinuous association possible is irreducibly complex. That is, each individual object to be specified by the system requires one arrangement of matter to serve as a token of memory and a second arrangement of matter to independently establish what is being specified by the token. This organization forms Peirce’s famous triadic relationship (object-symbol-interpretant) and is not only found at the very heart of von Neumann’s prediction, but was experimentally confirmed and described in the gene system as well (amino acid-codon-aaRS).
Biology and computers play by very different rules.
It is interesting that you say that. One of the defining issues is that they both have rules that they play by (i.e. there are no rules in physics … laws are universal, time-dependent, and reversible; rules are local, time-independent, and irreversible). Let me say a couple of things about the desire to separate protein synthesis from genuine semiosis (as exemplified by von Neumann’s prediction of open-ended self-replication). The attempt will fail. These conditions have been subject to a great deal of interest over decades and generations. The intellectual feelers from this issue spread out into a wide range of disciplines, questions, and areas of interest. Consequently, the material conditions involved here (and there are many of them) have been very (very) carefully recorded in the scientific literature, particularly since the discovery of DNA. The issue here is not “Is protein synthesis a semiotic process?” That question has already been answered, fully and completely. What we refer to as “protein synthesis” was predicted to be enabled by a genuine symbol system, and subsequently, a genuine symbol system was found inside the cell and has been thoroughly described as such. The question today, at least for me, is “Are there any ID critics visiting UD, claiming to be led by the virtues of empirical science, who are prepared to acknowledge the reality?”Upright BiPed
December 26, 2019
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Sven Mil:
Is it possible that this system is irreducibly complex only when constrained by the principles of computers/machines?
Basic biological reproduction is irreducibly complex: Peering into Darwin's Black Box: The cell division processes required for bacterial life But that is moot as you need to go from biologically relevant replicating molecules to producing coded systems from the ground up. Too bad Spiegelman's Monster says that ain't happening.
Biology and computers play by very different rules.
They also play by different codes. Rules and codes that, by all evidence and knowledge, were intelligently designed.ET
December 23, 2019
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Im asking if you think von Neumann's automaton system of machines and tape are a perfect analogy to biological systems. Is it possible that this system is irreducibly complex only when constrained by the principles of computers/machines? Biology and computers play by very different rules.Sven Mil
December 23, 2019
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Sven
And you think von Nuemann’s system is a perfect analogy to biological systems?
It's like any biological information circuit. Symbol. Sender. Medium. Translation. Receiver. It's irreducibly complex. It's not a question of trying to shoehorn design in. You have a show how mindless random effects preserve the function with parts of the process missing.Silver Asiatic
December 23, 2019
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AaronS- A person like Sven and Acartia Eddie cannot attack anyone's character and expect sane people to listen. And I make astute observations, as opposed to name calling.ET
December 23, 2019
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@ET No no the resemblance is the Unnecessary name calling you actually engage and put your reasons down Sven Mil suggest makes predictable smart ass remarks and implies everyone that doesn’t agree with him is stupid, which speaks waves about his character. At the very beginning of this he said nobody knew what they were talking about and then provided no reason why they were wrong And still hasn’t but he likes to attack your character a lotAaronS1978
December 22, 2019
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More evidences supporting ID: Gene Regulatory Logic of Sonic Hedgehog Morphogen Patterning of the Vertebrate Neural Tube Morphogen Tissue Patterning Transcriptional Networks and Cellular Decision Making  The Early Life of an Embryo: from Fertilization to the Midblastula TransitionOLV
December 22, 2019
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ID unleashed! mTORC1/AMPK responses define a core gene set for developmental cell fate switching
manipulating activities of mTORC1/AMPK in the absence of nutrient withdrawal is sufficient for a growth-to-developmental fate switch in Dictyostelium, providing a means to identify transcriptional networks and signaling pathways essential for early development.
This study indicates that rapamycin-targeted inactivation of mTORC1 with reciprocal activation of AMPK, in the absence of nutrient withdrawal, is sufficient to effect a growth-to-developmental fate switch to induce multi-cell development of Dictyostelium. Using an RNA-sequencing approach, we identified mTORC1/AMPK-regulated transcriptional networks and associated signaling pathways that are essential for early developmental induction but are regulated independently of nutrient withdrawal. We then investigated genes with unclassifiable GO and ortholog terminologies and showed that the rapamycin-induced expression group can be applied for novel gene discovery in pathways essential for early developmental induction.
   OLV
December 22, 2019
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>>>>>>>>Sven: And you think von Nuemann’s system is a perfect analogy to biological systems? Perfect? Are you asking me if von Neumann predicted aminoacyl synthetase by name? Let's be direct. Von Neumann's prediction included construction, copying, control, open-ended potential, a quiescent symbolic description, a set of state transformations (interpretive constraints) to interpret the symbols, and semantic closure. All of these have been very famously documented in the scientific literature. These fundamentals are not even in question, and have been described just as I have presented them here by acclaimed scientists over decades. Which of these would you like to take issue with? Please be specific.Upright BiPed
December 22, 2019
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Holy crap- Is it really too difficult for Sven to actually make a coherent argument? Or is flailing about the best you have?ET
December 22, 2019
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And you think von Nuemann's system is a perfect analogy to biological systems?Sven Mil
December 22, 2019
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ATF7IP regulates SETDB1 nuclear localization and increases its ubiquitination
Understanding of the appropriate regulation of enzymatic activities of histone?modifying enzymes remains poor. The lysine methyltransferase, SETDB1, is one of the enzymes responsible for the methylation of histone H3 at lysine 9 (H3K9) and plays a key role in H3K9 trimethylation?mediated silencing of genes and retrotransposons. Here, we reported that how SETDB1's enzymatic activities can be regulated by the nuclear protein, ATF7IP, a known binding partner of SETDB1. Mechanistically, ATF7IP mediates SETDB1 retention inside the nucleus, presumably by inhibiting its nuclear export by binding to the N?terminal region of SETDB1, which harbors the nuclear export signal motifs, and also by promoting its nuclear import. The nuclear localization of SETDB1 increases its ubiquitinated, enzymatically more active form. Our results provided an insight as to how ATF7IP can regulate the histone methyltransferase activity of SETDB1 accompanied by its nuclear translocation.
OLV
December 22, 2019
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Sven Mil:
Irreducible complexity is just a way to shoehorn design into something complex.
No, it's an accurate description of certain structures and systems. IC is only an instance of design once necessity and chance are eliminated. It remains that all it takes to refute any design inference with respect to any given IC structure or system, is to show how spontaneous or stochastic processes, produced it. And we all know why that upsets you.ET
December 22, 2019
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ID on steroids? :) A nuclear licence to silence transposons
Transposon silencing requires the histone methyltransferase SETDB1. In this issue of EMBO Reports, Tsusaka et al [1] and Osumi et al [2] illustrate how the cofactor ATF7IP and its fly homolog Windei (Wde) regulate the methyltransferase function of SETDB1 through its nuclear licensing. The new insight gained from these two articles will shift how we think about epigenetic regulation and its multiple layers of control.
     OLV
December 22, 2019
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Acartia Eddie:
Am I the only one who notices the similarity between the debating styles of Sven and ET?
Only you [insert any given evoTARD] could. Unlike Sven I provide the evidence and references to support what I say. But we have noticed that you and Sven have the same quote-mining and cowardly accusation- style.ET
December 22, 2019
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>>>>>>>> Sven: "von Neumann was the first to give a correct description of cellular reproduction. I have never said anything in opposition to that." Are you aware that von Neumann's description included an irreducibly complex symbol system and a set of interpretive constraints as the fundamental physical condition of the system? Have you actually ever read his paper? Truthfully, have you?Upright BiPed
December 22, 2019
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Ed, what do you think the effective difference between Sven's name-calling/refusal to engage physical evidence, and your obfuscation/refusal to engage physical evidence?Upright BiPed
December 22, 2019
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Essential roles of Windei and nuclear monoubiquitination of Eggless/SETDB1 in transposon silencing  
Eggless/SETDB1 (Egg), the only essential histone methyltransferase (HMT) in Drosophila, plays a role in gene repression, including piRNA?mediated transposon silencing in the ovaries. Previous studies suggested that Egg is post?translationally modified and showed that Windei (Wde) regulates Egg nuclear localization through protein–protein interaction. Monoubiquitination of mammalian SETDB1 is necessary for the HMT activity. Here, using cultured ovarian somatic cells, we show that Egg is monoubiquitinated and phosphorylated but that only monoubiquitination is required for piRNA?mediated transposon repression. Egg monoubiquitination occurs in the nucleus. Egg has its own nuclear localization signal, and the nuclear import of Egg is Wde?independent. Wde recruits Egg to the chromatin at target gene silencing loci, but their interaction is monoubiquitin?independent. The abundance of nuclear Egg is governed by that of nuclear Wde. These results illuminate essential roles of nuclear monoubiquitination of Egg and the role of Wde in piRNA?mediated transposon repression.
OLV
December 22, 2019
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more evidences supporting ID: Regulated nuclear accumulation of a histone methyltransferase times the onset of heterochromatin formation in C. elegans embryos
Heterochromatin formation during early embryogenesis is timed precisely, but how this process is regulated remains elusive. We report the discovery of a histone methyltransferase complex whose nuclear accumulation and activation establish the onset of heterochromatin formation in Caenorhabditis elegans embryos. We find that the inception of heterochromatin generation coincides with the accumulation of the histone H3 lysine 9 (H3K9) methyltransferase MET-2 (SETDB) into nuclear hubs. The absence of MET-2 results in delayed and disturbed heterochromatin formation, whereas accelerated nuclear localization of the methyltransferase leads to precocious H3K9 methylation. We identify two factors that bind to and function with MET-2: LIN-65, which resembles activating transcription factor 7–interacting protein (ATF7IP) and localizes MET-2 into nuclear hubs, and ARLE-14, which is orthologous to adenosine 5?-diphosphate–ribosylation factor-like 14 effector protein (ARL14EP) and promotes stable association of MET-2 with chromatin. These data reveal that nuclear accumulation of MET-2 in conjunction with LIN-65 and ARLE-14 regulates timing of heterochromatin domains during embryogenesis.
The nucleus of a young embryo undergoes major reorganization as it transitions from a fertilized egg to a multicellular embryo. As cells acquire specific fates and zygotic transcription commences, the nucleus is segregated into distinct domains of euchromatin and heterochromatin. While much has been learned about the mechanisms that control cell-fate specification and the onset of zygotic transcription, little is understood about the processes that establish chromatin domains de novo during embryogenesis.
     OLV
December 22, 2019
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von Neumann was the first to give a correct description of cellular reproduction. I have never said anything in opposition to that.Sven Mil
December 22, 2019
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Well that’s a gross misunderstanding of your irreducible complexity, but you’re not even close Irreducible complexity isn’t about the system just being complex, it’s the fact that all parts in the system HAD to evolve at once and be in the system for the system to work and be naturally selected in the first place, if it’s missing a part the system as a whole flops and stops working, there is no gradual pave way for it to evolve, it either has all its parts or it doesn’t work.AaronS1978
December 22, 2019
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Sven, do you also believe that Turing (the inspiration to von Neumann) was wrong as well? Was Brenner, (who hailed von Neumann's prediction) wrong too? Let me ask you a question, when Crick predicted that there would be a set of "adapters" (his famous "Adapter Hypothesis") found working in the gene system, was that a wild-assed guess on his part, or do you think it was a logical deduction? If its the latter, then why would you think so?Upright BiPed
December 22, 2019
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Am I the only one who notices the similarity between the debating styles of Sven and ET?Ed George
December 22, 2019
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So, is that what you think von Neumann got wrong - you believe that autonomous open-ended self-replication doesn't really need the complexity of both a medium of information and a set of constraints to successfully interpret it?Upright BiPed
December 22, 2019
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Call it whatever you want, but the nonsense you spout is no better than BA's quantum mechanics schtick. Irreducible complexity is just a way to shoehorn design into something complex. It amounts to: "look at how complex this is! It must be designed!"Sven Mil
December 22, 2019
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Good grief Sven. That was entirely incoherent. When you do that sort of thing, do you not think it shows?Upright BiPed
December 22, 2019
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Sven Mil any time you want to present anything show that they are wrong would be amazing Again attacking someone’s character unjustly doesn’t make you right, it makes you a jerk and a trollAaronS1978
December 22, 2019
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