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Breaking: A “junk DNA” jumping gene is critical for embryo cell development

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Not junk: 'Jumping gene' is critical for early embryo
Two-cell mouse embryo stained for LINE1 RNA (magenta/Ramalho-Santos lab, UCSF

This was discovered by someone who was skeptical of the idea that our geomes are largely useless junk. From Nicholas Weiler at Phys.Org:

A so-called “jumping gene” that researchers long considered either genetic junk or a pernicious parasite is actually a critical regulator of the first stages of embryonic development, according to a new study in mice led by UC San Francisco scientists and published June 21, 2018 in Cell.

Only about 1 percent of the human genome encodes proteins, and researchers have long debated what the other 99 percent is good for. Many of these non–protein coding regions are known to contain important regulatory elements that orchestrate gene activity, but others are thought to be evolutionary garbage that is just too much trouble for the genome to clean up.

For example, fully half of our DNA is made up of “transposable elements,” or “transposons,” virus-like genetic material that has the special ability of duplicating and reinserting itself in different locations in the genome, which has led researchers to dub them genetic parasites. Over the course of evolution, some transposons have left hundreds or thousands of copies of themselves scattered across the genome. While most of these stowaways are thought to be inert and inactive, others create havoc by altering or disrupting cells’ normal genetic programming and have been associated with diseases such as certain forms of cancer.

Now UCSF scientists have revealed that, far from being a freeloader or parasite, the most common transposon, called LINE1, which accounts for fully 24 percent of the human genome, is actually necessary for embryos to develop past the two-cell stage. More.

“evolutionary garbage that is just too much trouble for the genome to clean up”?  Yes, because Darwinism has predicted that.

Hat tip: PaV. He sent us this while travelling, adding,

LINE1, which makes up 24% of the genome is NOT “junk,” but an essential part of embryonic development.

The Darwinists are now just completely wrong. IDists predicted this. They pooh-poohed it. Well, they have five tons of egg on their face right now.

NOTA BENE: regarding the “transposons,” it’s quite interesting that it is involved with embryonic development since they are finding that “pseudogenes” are involved in brain (embryonic) development.

IOW, what’s “essential” is what the Darwinists called “junk” (And IDists called fundamental), and what was considered “essential” is only secondarily so.

Alas, no, PaV. Darwinists will simply say that Darwinism predicts this too. It’s all part of the non-falsification package. All that is lacking is a believing public.

From Richard Harris at NPR:

The noted biologist Barbara McClintock, who died in 1992, discovered these odd bits of DNA decades ago in corn, and dubbed them “jumping genes.” (She won a Nobel prize for that finding in 1983.) McClintock’s discovery stimulated generations of scientists to seek to understand this bizarre phenomenon.

Some biologists have considered these weird bits of DNA parasites, since they essentially hop around our chromosomes and infect them, sometimes disrupting genes and leaving illness in their wake. But Miguel Ramalho-Santos, a biologist at the University of California, San Francisco, doesn’t like that narrative.

“It seemed like a waste of this real estate in our genome — and in our cells — to have these elements and not have them there for any particular purpose,” Ramalho-Santos says. “So we just asked a very simple question: Could they be doing something that’s actually beneficial?” More.

“Could they be doing something that’s actually beneficial?” To understand why no one wondered before, one must understand the power of Darwinian groupthink, enforced by wrecking careers. In short, ID guys Jonathan Wells was right and Richard Dawkins was wrong. So was Jerry Coyne. And Michael Shermer.

See also: Note: One junk DNA defender just isn’t doing politeness anymore. In a less Darwinian science workplace, that could become more a problem for him than for his colleagues.

See also: Junk DNA can actually change genitalia.

Junk DNA: Darwinism evolves swiftly in real time

At Quanta: Cells need almost all of their genes, even the “junk DNA”

“Junk” RNA helps regulate metabolism

Junk DNA defender just isn’t doing politeness any more.

Anyone remember ENCODE? Not much junk DNA? Still not much. (Paper is open access.)

Yes, Darwin’s followers did use junk DNA as an argument for their position.

Another response to Darwin’s followers’ attack on the “not-much-junk-DNA” ENCODE findings

Comments
gpuccio: What you wrote makes sense and answers my posted questions satisfactorily. Thank you. Still I think your short answer “they don’t” is easily falsifiable. However, it may never get falsified because it’s true. In order to falsify it all one would have to do is point to a valid paper containing the Darwinian explanation.PeterA
July 17, 2018
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OLV at #131: I think PeterA is probably kidding. :) Of course, if that paper made any serious attempt at explaining those things from a darwinian point of view, that would be mentioned in the abstract. However, starting to study chinese could not be a bad idea: the chinese really seem to be leaders in this field (and probably in many others). :)gpuccio
July 17, 2018
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OLV at #130: Of course it is pertinent. The functions of lncRNAs are just starting to be discovered. The simple truth is that we already know about 15000 such structures in humans, and we ignore almost everything about what they do and how they do it. At present, most of the new information is coming from studies about specific human diseases, especially cancer. That's what usually happens: the behaviour of specific molecules in cancer is often the way to understand what they really do in normal conditions. But again, the task is not easy: lncRNAs, and other forms of non coding RNAs, are most likely involved in important regulatory functions, often species-specific. Moreover, there are many potential ways they can work, by interacting with chromatin, with other RNAs, with proteins, and so on. It's a wonderful new field, and I am looking forward to important advances.gpuccio
July 17, 2018
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PeterA: Do you really think that paper has the explanation ? Really?OLV
July 17, 2018
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Not sure if this off topic here: https://www.tandfonline.com/doi/full/10.1080/03008207.2017.1412432 Regulation of osteogenesis by long noncoding RNAs: An epigenetic mechanism contributing to bone formation Long noncoding RNAs (lncRNAs) have recently emerged as novel regulators of lineage commitment, differentiation, development, viability, and disease progression. Few studies have examined their role in osteogenesis; however, given their critical and wide-ranging roles in other tissues, lncRNAs are most likely vital regulators of osteogenesis. In this study, we extensively characterized lncRNA expression in mesenchymal cells during commitment and differentiation to the osteoblast lineage using a whole transcriptome sequencing approach (RNA-Seq). Using mouse primary mesenchymal stromal cells (mMSC), we identified 1438 annotated lncRNAs expressed during MSC differentiation, 462 of which are differentially expressed. We performed guilt-by-association analysis using lncRNA and mRNA expression profiles to identify lncRNAs influencing MSC commitment and differentiation. These findings open novel dimensions for exploring lncRNAs in regulating normal bone formation and in skeletal disorders.OLV
July 17, 2018
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OLV:
How do scientists explain the appearance of such “species-specific epigenetic regulation” through Darwinian processes?
gpuccio:
They don’t.
Well, that's a strong affirmation that can be easily falsified. Actually, could it be that the paper written in Chinese contains that explanation? Does any of the readers here know Chinese language to tell us?PeterA
July 16, 2018
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DATCG, OLV: What about this? (2018): Identification of Transposable Elements Contributing to Tissue-Specific Expression of Long Non-Coding RNAs https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5793176/
Abstract: It has been recently suggested that transposable elements (TEs) are re-used as functional elements of long non-coding RNAs (lncRNAs). This is supported by some examples such as the human endogenous retrovirus subfamily H (HERVH) elements contained within lncRNAs and expressed specifically in human embryonic stem cells (hESCs), as required to maintain hESC identity. There are at least two unanswered questions about all lncRNAs. How many TEs are re-used within lncRNAs? Are there any other TEs that affect tissue specificity of lncRNA expression? To answer these questions, we comprehensively identify TEs that are significantly related to tissue-specific expression levels of lncRNAs. We downloaded lncRNA expression data corresponding to normal human tissue from the Expression Atlas and transformed the data into tissue specificity estimates. Then, Fisher’s exact tests were performed to verify whether the presence or absence of TE-derived sequences influences the tissue specificity of lncRNA expression. Many TE–tissue pairs associated with tissue-specific expression of lncRNAs were detected, indicating that multiple TE families can be re-used as functional domains or regulatory sequences of lncRNAs. In particular, we found that the antisense promoter region of L1PA2, a LINE-1 subfamily, appears to act as a promoter for lncRNAs with placenta-specific expression.
Emphasis mine.gpuccio
July 16, 2018
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DATCG, OLV: This is a little bit older (2015), but interesting: Transposable elements at the center of the crossroads between embryogenesis, embryonic stem cells, reprogramming, and long non-coding RNAs. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4624819/
Abstract: Transposable elements (TEs) are mobile genomic sequences of DNA capable of autonomous and non-autonomous duplication. TEs have been highly successful, and nearly half of the human genome now consists of various families of TEs. Originally thought to be non-functional, these elements have been co-opted by animal genomes to perform a variety of physiological functions ranging from TE-derived proteins acting directly in normal biological functions, to innovations in transcription factor logic and influence on epigenetic control of gene expression. During embryonic development, when the genome is epigenetically reprogrammed and DNA-demethylated, TEs are released from repression and show embryonic stage-specific expression, and in human and mouse embryos, intact TE-derived endogenous viral particles can even be detected. A similar process occurs during the reprogramming of somatic cells to pluripotent cells: When the somatic DNA is demethylated, TEs are released from repression. In embryonic stem cells (ESCs), where DNA is hypomethylated, an elaborate system of epigenetic control is employed to suppress TEs, a system that often overlaps with normal epigenetic control of ESC gene expression. Finally, many long non-coding RNAs (lncRNAs) involved in normal ESC function and those assisting or impairing reprogramming contain multiple TEs in their RNA. These TEs may act as regulatory units to recruit RNA-binding proteins and epigenetic modifiers. This review covers how TEs are interlinked with the epigenetic machinery and lncRNAs, and how these links influence each other to modulate aspects of ESCs, embryogenesis, and somatic cell reprogramming.
gpuccio
July 16, 2018
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DATCG, OLV: Let's go back to transposons. This is about plants: Transposon-Derived Non-coding RNAs and Their Function in Plants. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5943564/
Abstract: Transposable elements (TEs) are often regarded as harmful genomic factors and indeed they are strongly suppressed by the epigenetic silencing mechanisms. On the other hand, the mobilization of TEs brings about variability of genome and transcriptome which are essential in the survival and evolution of the host species. The vast majority of such controlling TEs influence the neighboring genes in cis by either promoting or repressing the transcriptional activities. Although TEs are highly repetitive in the genomes and transcribed in specific stress conditions or developmental stages, the trans-acting regulatory roles of TE-derived RNAs have been rarely studied. It was only recently that TEs were investigated for their regulatory roles as a form of RNA. Particularly in plants, TEs are ample source of small RNAs such as small interfering (si) RNAs and micro (mi) RNAs. Those TE-derived small RNAs have potentials to affect non-TE transcripts by sequence complementarity, thereby generating novel gene regulatory networks including stress resistance and hybridization barrier. Apart from the small RNAs, a number of long non-coding RNAs (lncRNAs) are originated from TEs in plants. For example, a retrotransposon-derived lncRNA expressed in rice root acts as a decoy RNA or miRNA target mimic which negatively controls miRNA171. The post-transcriptional suppression of miRNA171 in roots ensures the stabilization of the target transcripts encoding SCARECROW-LIKE transcription factors, the key regulators of root development. In this review article, the recent discoveries of the regulatory roles of TE-derived RNAs in plants will be highlighted.
Emphasis mine.gpuccio
July 16, 2018
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OLV: "How do scientists explain the appearance of such “species-specific epigenetic regulation” through Darwinian processes?" They don't.gpuccio
July 16, 2018
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gpuccio (122): That article is very interesting indeed. Thanks. “species-specific epigenetic regulation greatly contributes to the differences between humans and mice.” How do scientists explain the appearance of such “species-specific epigenetic regulation” through Darwinian processes?OLV
July 16, 2018
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DATCG (121): “all these disparate systems must coordinate together, signal and make orderly processing together in tight control windows of time. Or kaput, tagged for recycling, maybe modification if fortunate. Amazing! “ Amazing seems like an understatement in this case. In that thread, which seems utterly relevant, gruccio, Dionisio and you posted so many references to interesting papers that it’s very difficult to keep track of them. It’s practically insane. Please, don’t take it wrong, no offense intended. You’re all doing a magnificent job. Keep it up! Thanks.OLV
July 16, 2018
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DATCG and OLV: This seems really interesting: Analysis of orthologous lncRNAs in humans and mice and their species-specific epigenetic target genes https://www.ncbi.nlm.nih.gov/pubmed/29997097
Abstract OBJECTIVE: To identify orthologous lncRNAs in human and mice and the species specificity of their epigenetic regulatory functions. METHODS: The human/mouse whole-genome pairwise alignment (hg19/mm10, genome.UCSC.edu) was used to identify the orthologues in 13 562 and 10 481 GENCODE-annotated human and mouse lncRNAs. The Infernal program was used to search the orthologous sequences of all the exons of the 13562 human lncRNAs in mouse genome (mm10) to identify the highly conserved orthologues in mice. LongTarget program was used to predict the DNA binding sites of the orthologous lncRNAs in their local genomic regions. Gene Ontology analysis was carried out to examine the functions of genes. RESULTS: Only 158 orthologous lncRNAs were identified in humans and mice, and many of these orthologues had species-specific DNA binding sites and epigenetic target genes. Some of the epigenetic target genes executed important functions in determining human and mouse phenotypes. CONCLUSIONS: Only a few human and mouse lncRNAs are orthologues, and most of lncRNAs are species-specific. The orthologous lncRNAs have species-specific epigenetic target genes, and species-specific epigenetic regulation greatly contributes to the differences between humans and mice.
Article in chinese. Emphasis mine.gpuccio
July 15, 2018
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OLV @117, interesting! That will take some time to get through for me :) And I've yet to read the papers Gpuccio recommended earlier. Not sure if you were interested in general definitions or examples and diagrams. I enjoy researching NCBI when I have the time. But when in a hurry use Wiki. Signaling cascades are cool, included in links below. Quick crosstalk link... https://en.wikipedia.org/wiki/Crosstalk_(biology) I may be overstating the case, but have long thought signal cascades are one more good case for Design, finely tuned communications system that cannot be allowed to blindly form without monitoring and error correction. If a signal is wrong, late, unrecognized, or a receptor mutates and cannot function, it's over, or leads to disease. Signaling is critical to survival. Youtube is also a great tool for video 3D type reviews. The paper you linked is full of Design criteria in just the first few paragraphs that must meet stringent criteria.
Given that so many kinases and phosphatases converge onto two key mitotic processes, it is perhaps not surprising to learn that they are, quite literally, entangled in cross-talk. Inhibition of any one of these enzymes produces secondary effects on all the others, which results in a complicated picture that is very difficult to interpret.
When you tell me they're "entagled" to me it indicates the complexity is so tightly controlled together a mutatoin in the wrong place can degenerate the overall systems performance. I see you've commented on Gpuccio's Ubiquitin post. There's an interesting reference by one of Dionisio's comments on the Kinetochore and Ubiquitin at comment #22 as well. Kinetochore and fine-tuning So, all these disparate systems must coordinate together, signal and make orderly processing together in tight control windows of time. Or kaput, tagged for recycling, maybe modification if fortunate. Amazing! :)DATCG
July 13, 2018
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Gpuccio @116, Thank you! :)DATCG
July 13, 2018
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gpuccio: Thank you for the clarifying explanation.OLV
July 13, 2018
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OLV: "Cross talk" seems to mean that there are complex, ordered interactions between those proteins. I have looked into some of them. Aurora B: 344 AAs in humans. Best hit in prokaryotes: 145 bits Best hit in single celled eukaryotes: 401 bits Well conserved in all metazoa. No significant information jump in vertebrates. This seems to be essentially a new eukaryotic protein, sharing low homology with different prokaryotic serine/threonine kinases. MPS1: 857 AAs in humans. The human sequence has very limited homology in pre-vertebrates, and undergoes a gradual information jump in vertebrates, from cartilaginous fish to reptiles. BUB1: 1085 AAs in humans The human sequence has very limited homology in pre-vertebrates, and undergoes two major jumps, one (smaller) in cartilaginous fish, the second and bigger one in mammals. BUBR1: 1050 AAs in humans: Similar to BUB1. PLK1: 603 AAs in humans Similar to Aurora B: Information jump from prokaryotes (132 bits) to single celled eukaryotes (491 bits). Well conserved in metazoa, no big jumps there. As you can see, there are two different patterns here. Some proteins are essentially engineered in single celled eukaryotes, and their evolutionary history is rather smooth after that, in Metazoa (Aurora B, PLK1). These are essentially new proteins in eukaryotes, even is some low homology can be detected with prokaryotic serine/threonine kinases. Another group of proteins, instead, is essentially engineered in its human-conserved sequence in vertebates, but gradually, with discrete jumps in cartilaginous fish, bony fish, amphibians and reptiles, then undergoes a final jump in mammals (BUB1, BUBR1). These different evolutionary behaviours could certainly point to different functional specificities.gpuccio
July 12, 2018
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gpuccio and DATCG: do you guys understand this cross-talk topic? are these cross-talks between a bunch of proteins present in prokaryotes and eukaryotes? basically at which point did this appear in the biological cells? it's mindboggling either way I look at it. do any of these proteins show significant functional information jump at some point? Thanks. Kinase and Phosphatase Cross-Talk at the Kinetochore
it is perhaps not surprising to learn that they are, quite literally, entangled in cross-talk.
OLV
July 12, 2018
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DATCG: Here it is: https://uncommondescent.com/intelligent-design/bioinformatics-tools-used-in-my-ops-some-basic-information/gpuccio
July 12, 2018
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Gpuccio @111, "Again, the problem of control levels arises: if, as it seems, m6A contributes significantly to regulate transcription differently in different contexts, using introns as a parallel level of information, what tells the system of proteins that implement m6A what and when and how to methylate?" Smiles great insight and question! Might I speculate a bit for the "what and when" that previously heretofore named "JUNK" elements and designed feedback loops? Dependent upon internal and/or external signal processing whereby decision trees, "if-then" type logic "funnels" information(for lack of better words) to appropriate "levels" of reactionary code interfaces? For lack of better term, a checking mechanism and/or cascade of pre-determined sets and switches.DATCG
July 10, 2018
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Gpuccio @111-112, Ooooo... thanks for that info! By the way, your post on utilizing BLAST. I used it some time ago, but unable to locate it again. Maybe, if OK with UD, think we should post your BLAST instructions at least as a Comment under Resources link? Or add it to the current list. I'd saved those links in the past of your initial Blast posting(s), but moved around since and lost them.DATCG
July 10, 2018
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Thanks Gpuccio for your summation @110. And your always magnanimous attitude in an area I'm still learning and will for life. :)DATCG
July 10, 2018
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DATCG: By the way, Protein virilizer homolog is also the protein in the group that undergoes the biggest information jump at the vertebrate transition: 0.7621413 baa 1381 bitsgpuccio
July 10, 2018
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DATCG: Very interesting paper about m6A. Now, the process is only one of more than a hundred similar modifications. From the paper:
The RNA nucleotide code is supplemented by more than a hundred chemical modifications, greatly extending the functionality and information content of RNA (Fu et al., 2014, Harcourt et al., 2017).
m6A is implemented by a number of important proteins: METTL3 580 AAs in humans METTL14 456 AAs in humans WTAP 396 AAs in humans Protein virilizer homolog 1812 AAs in humans Two demethylases: FTO (505 AAs in humans) and ALKB5 (394 AAs in humans) The most specific component is probably the Protein virilizer homolog, a 1812 AA long protein. From Uniprot:
Associated component of the WMM complex, a complex that mediates N6-methyladenosine (m6A) methylation of RNAs, a modification that plays a role in the efficiency of mRNA splicing and RNA processing (PubMed:24981863, PubMed:29507755). Acts as a key regulator of m6A methylation by promoting m6A methylation of mRNAs in the 3'-UTR near the stop codon: recruits the catalytic core components METTL3 and METTL14, thereby guiding m6A methylation at specific sites (PubMed:29507755)
Again, the problem of control levels arises: if, as it seems, m6A contributes significantly to regulate transcription differently in different contexts, using introns as a parallel level of information, what tells the system of proteins that implement m6A what and when and how to methylate? It's a continuous generation of new meta-levels: fascinating, and probably a little bit frustrating! :)gpuccio
July 10, 2018
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DATCG: Again, excellent points. I think we agree on almost everything! :) Regarding the general problem of derivation of metazoa, there are only three things that I am rather sure of: a) It happens (new phyla, species and so on do appear at discrete times). b) It happens by design (this is the most certain thing of all). c) In some way, existing information is physically re-used in the process, and it carries with itself the inherent degradation that has already taken place in the past (that's what I mean by "descent"). All the rest is completely open, because the facts we have are still too limited. I too hope that the future will help us understand better.gpuccio
July 10, 2018
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The paper on Introns and splicing processing speeds on Alternative Splicing... https://www.cell.com/cell-reports/fulltext/S2211-1247(18)30858-1 GPuccio, cross-posting at your original Spliceosome post... https://uncommondescent.com/intelligent-design/the-spliceosome-a-molecular-machine-that-defies-any-non-design-explanation/DATCG
July 9, 2018
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And here's the previous article mentioned from Jan 17 which offers some background and somehow I missed. Awesome! :) https://evolutionnews.org/2017/01/cornell_researc/
What we see here is another Signature in the Cell. Intelligent design advocates are not surprised to find codes and switches in irreducibly complex systems. In fact, we expect that this finding will stimulate the discovery of additional codes, such as those that decide which mRNA transcripts should be treated as more important than others. Darwinian evolution, by contrast, has a big challenge in explaining how multiple players mutated together by chance to hit upon a language convention. What do unguided, blind processes know about codes? What do they understand about information? In short, nothing.
Indeed, a blind, unguided series of Lemony Snicket events does not have a clue.DATCG
July 9, 2018
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OK, so this is from Evolution News again, Encryption System Found in Genes - Psssst Introns Inolved! ;-) https://evolutionnews.org/2018/07/encryption-system-found-in-genes/ Introns fascinated me long ago. So here's more news from our friends. A copy of some of the relevant info...
RNA is composed of four bases (abbreviated A, U, G and C), thereby disseminating its message with a fairly simple code. In recent years, research has shown an unprecedented impact of RNA modifications at all steps of the maturation process. More than a hundred RNA modifications have been identified with roles in both inhibiting and facilitating binding to proteins, DNA and other RNA molecules. This encryption by RNA modification is a way to prevent the message of the RNA in being read by the wrong recipients. The research-team has focused on the RNA-modification m6A and shown that RNA can be labeled with this modification while being copied from DNA…. The results demonstrate that an m6A positioned at an exon next to an intron increases the RNA maturation process, while m6A within the introns slows down the maturation of RNA (Figure 2).
And the reason I'm so excited about this article follows, as I've haphazardly tried to explain before in comparisons of storage media, data retrieval and modifications...
It has long been a mystery why genes code for stretches called introns that are translated but then cut out afterwards. Why are they there? Here’s where the findings get really interesting. Introns appear to help scramble the message, fulfilling the encryption role, but they do something else: they regulate how the exons will be assembled.
Yes! :) This is precisely what I've been excited about and hoping to find. Mentioned similar thoughts in the Spliceosome and maybe the Ubiquitin post you made Gpuccio. That Introns might be regulators of data. Though I'm not sure I articulated well. This is amazing design evidence! As a heuristic study, this is what I've often said, if it's designed, then reverse engineering with Design in mind may uncover more Intron function. We look at data storage a bit differently with our experiences. We see it as a solid state function embedded in hard drives for example with location information that can be directly accessed to more data in different tracks(think - domains) that eventually pulls together all the data into one long string(or associated strings) that is to be modified or sent as is to other functions within a program of sub-programs, that are eventually tied to events, creations and modifications of outcomes, whether as Documents or any kind of output today from Media to 3D printing. So, thinking of Introns as pre-designed storage tracking modules that link together, modulate and refine Exons :) continuing... "The paper in Cell Reports explains how it works:"
Here, we provide a time-resolved high-resolution assessment of m6A on nascent RNA transcripts and unveil its importance for the control of RNA splicing kinetics. We find that early co-transcriptional m6A deposition near splice junctions promotes fast splicing, while m6A modifications in introns are associated with long, slowly processed introns and alternative splicing events. In conclusion, we show that early m6A deposition specifies the fate of transcripts regarding splicing kinetics and alternative splicing.
Too cool! :) This is beeeeyeutiful... and includes If-then thinking...
Now, according to the scientists at Aarhus, the specific position of the m6a mark appears highly relevant not only to the type of messenger RNA produced — and thus the protein to be translated — but also to the rate of production. If the m6a mark is placed near a splice junction, the constitutive transcript is produced quickly (i.e., exons are arranged in the order they were transcribed). If the mark is placed on an intron, it slows down the splicing, and might produce a completely different transcript with a different protein resulting. Is this a method to achieve cell-specific regulation? Our January 2017 article spoke of the m6a process as a kind of “if-then” algorithm: i.e., if this gene is found in a muscle cell, transcribe it this way; if found in a nerve cell, transcribe it another way, and so on. For this to work, the gene must embed the key in its introns, and the associated m6a marker must know the key to arrange the transcript accordingly. The researchers found that 57 percent of the markers were found on introns, and another 9 percent are on untranslated regions. Only 22 percent were found in coding regions.
Now Gpuccio, back to our earlier discussions on macro-evolution. I'm more than willing to contemplate that Splicing could be a key, along with Introns as control factors and Key-Engrpytion variation for unlocking unfolding events. That seems feasible. My problem(s) with macro events in Metazoa have always been the Mechanisms required for such unfolding events. Sorry for "jumping" way off topic :)DATCG
July 9, 2018
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Gpuccio @109, Thank you for your patience and outlining different thoughts to mine. "I am uncertain of a lot of things. Not of design." We agree :) Absolutely! I embrace uncertainty at times, maybe to much. But after being to certain in the past, I am attempting to learn a bit of patience. "I have no idea if there is one TOL, or many. But at present I cannot accept that there are no TOL at all. Too many facts are against that idea." I'm not against TOL(s), just uncertain as to how many or how they unfolded over time. "For example, I cannot accept, with the facts we know, that metazoa were “created” from scratch, and not using existing single celled eukaryotes. And so on." I'm guessing nothing is from "scratch" per say from a Designer's point of view? I can see how seeds are easily advanced all over the earth and plants of many varieties and can vary over time. In that area I don't struggle or with others like bacteria and viruses, as much as I do with metazoa. "I do believe that prokaryotes have been used to design mitochondria and plastids. The rest? I don’t know. But it is true that a lot of information in eukaryotes seems to derive from prokaryotes too." This is where I am in the "I don't know" position and mainly I need to read more before I'm convinced. "I don’t know why so many people here in the ID filed seem to have a need to deny any form of descent. Maybe it’s only a religious position." Maybe, but I was not a believer or religious in the past and cannot speak for others. I don't think Creationist have yet to fundamentally put forth enough strong arguments for their case. Though I do follow their ideas, discussions as I do with Darwinist, IDist, etc. "However, I cannot agree. Descent is there, and it can be observed." OK, I'm thinking over long period of time with major evolutionary changes of many mechanisms that cannot be observed today or over modern era and must be inferred by evolutionist, the fossil records and genetics. For example quadroped to whale. Leaving out the initial complex stages from ocean to land as a mammal. While I've reviewed different works, papers, research and opinions, I'm not convinced yet of the sequences of events and/or the complex informational exchanges that took place over time. Time is not an answer, it's a block(unfortunately without adequate information) to our full understanding of the events that took place over millions of years, in my opinion. So we can infer as evolutionist do that certain major steps, novel functions are created and events occur. But I do not see them as fact, not so far. But I do think Design obviously can make a case for such guided, complex informational transitions whereas unguided, blind events do not and cannot. Maybe as technology progresses I can see a path forward in unfolding guided events. So, I'm not fully against it, but need more info, more evidence. Until then, I remain in the "I don't know" category. "Of course, it does not explain functional novelties. But it explains conserved functionalities, and the random degradations that can be observed in them." Oh, this is really good. Thanks Gpuccio. Yes, agree on "does not explain functional novelties." my sticking point. And I do agree about "conserved functionalities" and even "random degradations... observed in them." "That’s true. If it were not for design, functions would simply go down, r at most be conserved by some protection procedures. There is no doubt that unguided variation can only degrade function." Another area of agreement :) "But that is indeed the strongest argument for descent. We see the gradual degradation, time dependent degradation, in functional (or non functional) structures that are passed on. Neutral variation is everywhere to be seen." And I agree with all you said, with exception of first line - Again, I simply don't know, or maybe do not comprehend(?) in terms of larger macro events over time(see example of whale above). "I absolutely agree that there are a lot of difficulties with TOL, and Bechly is perfectly right to outline some of them. But that there are difficulties and contradictions does not mean that the idea is completely wrong. That happens all the time in science." I agree with your statement in that corrections are made all the time in science and yes, this does not rule out guided, or prescribed evolution by Design. I just admire Bechly's work in holding others accountable, much like Koonin, even though Koonin is an avowed Third Way evolutionist. "The only thing that I am completely sure of is the fundamental role of design in biology: the evidence for that is so overwhelming that it is really astounding for me that a lot of intelligent people can deny it." We are in complete agreement Gpuccio :) And I'm not ruling out anything else at this point, but simply remaining in "neutral" on macro events ;-) Thanks! Oh... and a follow up next post on introns!DATCG
July 9, 2018
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OLV @103, I'm but a simple coder/debugger trying to follow the deciphering of the ultimate of code(s) of "Life, the Universe and Everything" ;-) and Gpuccio to me is a great teacher along with many others here at UD past and present. I'm simply learning as I go through this "avalanche" as you term it of information overflow ;-) Gpuccio is always patient, kind even with those who often are abusive to him from the Darwinist side and has always been gracious to me as I stumble along the way. I've learned a lot from him. @104, Koonin, always enjoy his work, because he at least openly admitted some time ago the deficiency of neo-Darwinism and the problems at the base of Darwin's TOL. I wish I could find a paper he once wrote(or maybe he was a reviewer), at that time recognized the significance of the paper's findings to Darwin's TOL. He was a bit berated for saying so by the actual paper's authors. Think Doolittle or Baptiste was one of the authors with an online review and discussion. I have not been able to find it.DATCG
July 9, 2018
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