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Cell Requires Hundreds of Kilobases for Mature Micro-RNA

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Here’s todays headscratcher from Phys.Org.

It appears that to contrive a “mature” micro-RNA (mi-RNA), involved in gene regulation, the cell requires hundreds of kilobases of sequence. How odd. “Mature” mi-RNA’s are ~22 bases in length, and hundreds of thousand of nucleotide bases are needed (of primary-mi-RNA) to effect this ~22-nucleotide regulatory element?

Here’s what they say:

MicroRNAs are short noncoding RNAs that play critical roles in regulating gene expression in normal physiology and disease. . . .

Although mature miRNAs are only ~22 nucleotides, their transcripts are up to hundreds of kilobases long. Primary miRNA transcripts, or pri-miRNAs, are quickly processed into mature miRNAs from hairpin structures located in the exons or introns of pri-miRNA transcripts.

One remarkable feature of primary miRNAs is their extreme length, even in cases where they function only to produce a single ~22 nucleotide miRNA,” said Joshua Mendell, corresponding author of the study. “Although it seems wasteful to produce such long RNAs, most of which will be immediately degraded, this organization may have arisen to allow complex mechanisms of regulation of the encoded miRNA.

As usual, they’re “surprised” about their findings (very likely they are ‘surprised’ because they weren’t expecting things to turn out so complex). And, as usual, the pro forma reaching out to “evolution” as the explanatory mechanism, when, in fact, no explanation is given at all: . . . this organization may have arisen to allow complex mechanism of regulation of the encoded mi-RNA.”

It may have; but, it may have not. Is this scientist willing to consider this other possibility, or is it simply an article of faith that “evolution-did-it”? One wonders.

Comments
Alicia Cartelli, you said that you would 'shoot it down'. Thus the burden is on you to provide, not your opinion (as if I care what your blowhard opinion is anymore given your dogmatic antics thus far), but the appropriate experimental evidence that, to use your words, 'shoots it down'. As to the fact that the cell is a sophisticated biological computer, programmed far above anything man has ever accomplished in his machines, do you disagree with that fact? If so you are more ignorant of biology than expected in spite of how hard you toot your own horn.bornagain77
August 24, 2015
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Born, can you give an example of the molecular information expressed and/or the computation that's being done? PLease keep the response short, to the point, and in your own words. We've all seen too much of your usual schtick already.Alicia Cartelli
August 24, 2015
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Alicia Cartelli, I say the sequences have, among other things, some type of computational purpose, perhaps quantum, in which essential molecular information is expressed at the appropriate time to allow an appropriate computation to take place at the right time. And yes, there is sufficient reason to suspect that this might be the case. When a computer operating system was compared to regulatory networks, guess which one was more efficiently organized?
(Comparing Computer Operating Systems to Regulatory Networks in E-Coli) What Is The Genome? It's Not Junk! - Dr. Robert Carter - video http://www.metacafe.com/watch/8905583/ Comparing genomes to computer operating systems - Van - May 2010 Excerpt: we present a comparison between the transcriptional regulatory network of a well-studied bacterium (Escherichia coli) and the call graph of a canonical OS (Linux) in terms of topology,,, http://www.ncbi.nlm.nih.gov/pubmed/20439753
An extremely easy way to prove the sequences are non-funcional and wasteful as you hold would be to do knockout experiments of the sequences in question and see what happens. When 'knockouts' been done in the past with supposed junk DNA sequences, the results, as usual, did not conform to neo-Darwinian expectations. I see no reason to suppose that it will be any different this time if the experiments are ever done.
Jonathan Wells on Darwinism, Science, and Junk DNA - November 2011 Excerpt: Mice without “junk” DNA. In 2004, Edward Rubin] and a team of scientists at Lawrence Berkeley Laboratory in California reported that they had engineered mice missing over a million base pairs of non-protein-coding (“junk”) DNA—about 1% of the mouse genome(actually 1mb from a mouse genome is about .03%, not 1%.)—and that they could “see no effect in them.” But molecular biologist Barbara Knowles (who reported the same month that other regions of non-protein-coding mouse DNA were functional) cautioned that the Lawrence Berkeley study didn’t prove that non-protein-coding DNA has no function. “Those mice were alive, that’s what we know about them,” she said. “We don’t know if they have abnormalities that we don’t test for.”And University of California biomolecular engineer David Haussler said that the deleted non-protein-coding DNA could have effects that the study missed. “Survival in the laboratory for a generation or two is not the same as successful competition in the wild for millions of years,” he argued. In 2010, Rubin was part of another team of scientists that engineered mice missing a 58,000-base stretch of so-called “junk” DNA. The team found that the DNA-deficient mice appeared normal until they (along with a control group of normal mice) were fed a high-fat, high-cholesterol diet for 20 weeks. By the end of the study, a substantially higher proportion of the DNA-deficient mice had died from heart disease. Clearly, removing so-called “junk” DNA can have effects that appear only later or under other circumstances. https://uncommondescent.com/intelligent-design/jonathan-wells-on-darwinism-science-and-junk-dna/
. Also Alicia, I noticed that you did not answer my question on the modern synthesis. Are you still a believer? Or are you among the growing number of 'heretics' who reject neo-Darwinian explanations?bornagain77
August 24, 2015
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Like I said, there is simply too much working against your hunt for unknown regulatory mechanisms. Thousands of bases to reconcile, the efficiency of Drosha leaves little time for regulatory processes to even occur(even on a molecular scale), and the unprotected strands that have been excised out are degraded by nucleases. That's my argument. When someone has an idea or two with actual biological relevance, I will do my best to shoot them down. I'm not here to argue about arguing. =)Alicia Cartelli
August 24, 2015
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I have no problem admitting “we simply don’t know,” when necessary.
WHEN NECESSARY ... when the (fine-tuned) universe needs to be explained from nothing, morality from indifference, consciousness from unaware particles, freedom from determinism, rationality from nonrationality, the unity we call "organism" from chaos and the information in life from ... chance. "When necessary" means: when we cannot allow a divine foot in the door.Box
August 24, 2015
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So an appeal to future discoveries is only allowed as long as it justifies the materialist position, and Is absolutely not allowed if it props up something that is anti-ID. No evidence for abiogenesis? Give us time, it's only been 50 years. This study appears to show a waste in energy? Done deal... The designer would not have done it like that. Highly unlikely any future test will show anything different.scottH
August 24, 2015
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AC
I have no problem admitting “we simply don’t know,” when necessary.
It is necessary in this case because you don't know how it works and you don't know the origin of any of it - so you can't know that is has no function. Your resistance to that fact is telling, as I see it.Silver Asiatic
August 24, 2015
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"I have no problem admitting “we simply don’t know,” when necessary." Apparently you have a huge problem with admitting 'you simply don't know' since you insist on making the same mistake, (i.e. I think its junk therefore its junk), over again that Darwinists have been making for decades, going all the way back to their original vestigial organ argument.
“There are, according to Wiedersheim, no less than 180 vestigial structures in the human body, sufficient to make of a man a veritable walking museum of antiquities.” -evidence submitted to the Scopes trial Vestigial Organs: Comparing ID and Darwinian Approaches - July 20, 2012 Excerpt: A favorite criticisms of ID is that it is a science stopper. The opposite is true. The Live Science article shows that the "vestigial organs" argument has not changed for over a century, since Wiedersheim coined the term and listed over a hundred examples (in 1893). Evolutionary theory, in fact, has been worse than a science stopper: its predictions have been flat out wrong. Only a handful of alleged vestigial organs remains from Wiedersheim's original list, and each of those is questionable. http://www.evolutionnews.org/2012/07/vestigial_organ062281.html “The thyroid gland, pituitary gland, thymus, pineal gland, and coccyx, … once considered useless by evolutionists, are now known to have important functions. The list of 180 “vestigial” structures is practically down to zero. Unfortunately, earlier Darwinists assumed that if they were ignorant of an organ’s function, then it had no function.” "Tornado in a Junkyard" - book - by former atheist James Perloff
Moreover, I hold that anyone who claims that they know for certain that most of what goes on in the unfathomed complexity of the cell is mostly useless noise is not looking at the evidence we now have in hand in an objective manner, but is looking at the evidence through the biased philosophical presupposition of reductive materialism.
Venter: Life Is Robotic Software - July 15, 2012 Excerpt: “All living cells that we know of on this planet are ‘DNA software’-driven biological machines comprised of hundreds of thousands of protein robots, coded for by the DNA, that carry out precise functions,” said (Craig) Venter. http://crev.info/2012/07/life-is-robotic-software/ How we could create life - The key to existence will be found not in primordial sludge, but in the nanotechnology of the living cell - Paul Davies - 11 December 2002 Excerpt: Instead, the living cell is best thought of as a supercomputer - an information processing and replicating system of astonishing complexity. DNA is not a special life-giving molecule, but a genetic databank that transmits its information using a mathematical code. Most of the workings of the cell are best described, not in terms of material stuff - hardware - but as information, or software. Trying to make life by mixing chemicals in a test tube is like soldering switches and wires in an attempt to produce Windows 98. It won't work because it addresses the problem at the wrong conceptual level. http://www.theguardian.com/education/2002/dec/11/highereducation.uk The Cell as a Collection of Protein Machines "We have always underestimated cells. Undoubtedly we still do today,,, Indeed, the entire cell can be viewed as a factory that contains an elaborate network of interlocking assembly lines, each which is composed of a set of large protein machines." Bruce Alberts: Former President, National Academy of Sciences; http://www.imbb.forth.gr/people/aeconomou/documents/Alberts98.pdf
bornagain77
August 24, 2015
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Alicia Cartelli, do you still adhere to the central dogma of the modern synthesis of neo-Darwinism? Or have you allowed your views to appropriately change now that the evidence has come in undermining that simplistic 'bottom up' gene centric view of life? If not why not?
Podcast - Richard Sternberg PhD - On Human Origins: Is Our Genome Full of Junk DNA? Part 5 (emphasis on ENCODE findings and the loss of the term 'gene' as a accurate description in biology and also how that loss directly undermines the modern synthesis of neo-Darwinism) http://www.discovery.org/multimedia/audio/2014/11/on-human-origins-is-our-genome-full-of-junk-dna-pt-5/ Why the 'Gene' Concept Holds Back Evolutionary Thinking - James Shapiro - 11/30/2012 Excerpt: The Century of the Gene. In a 1948 Scientific American article, soon-to-be Nobel Laureate George Beadle wrote: "genes are the basic units of all living things.",,, This notion of the genome as a collection of discrete gene units prevailed when the neo-Darwinian "Modern Synthesis" emerged in the pre-DNA 1940s. Some prominent theorists even proposed that evolution could be defined simply as a change over time in the frequencies of different gene forms in a population.,,, The basic issue is that molecular genetics has made it impossible to provide a consistent, or even useful, definition of the term "gene." In March 2009, I attended a workshop at the Santa Fe Institute entitled "Complexity of the Gene Concept." Although we had a lot of smart people around the table, we failed as a group to agree on a clear meaning for the term. The modern concept of the genome has no basic units. It has literally become "systems all the way down." There are piecemeal coding sequences, expression signals, splicing signals, regulatory signals, epigenetic formatting signals, and many other "DNA elements" (to use the neutral ENCODE terminology) that participate in the multiple functions involved in genome expression, replication, transmission, repair and evolution.,,, Conventional thinkers may claim that molecular data only add details to a well-established evolutionary paradigm. But the diehard defenders of orthodoxy in evolutionary biology are grievously mistaken in their stubbornness. DNA and molecular genetics have brought us to a fundamentally new conceptual understanding of genomes, how they are organized and how they function. http://www.huffingtonpost.com/james-a-shapiro/why-the-gene-concept-hold_b_2207245.html DNA is life's blueprint? No, master controller of the cell - 13 June 2015 by Claire Ainsworth Everything we thought we knew about the genome is turning out to be wrong as The Deeper Genome and The Developing Genome make clear. New metaphors, anyone? Excerpt: Take DNA. It's no simple linear code, but an intricately wound, 3D structure that coils and uncoils as its genes are read and spliced in myriad ways. Forget genes as discrete, protein-coding "beads on a string": only a tiny fraction of the genome codes for proteins, and anyway, no one knows exactly what a gene is any more. A key driver of this new view is ENCODE, the Encyclopedia of DNA Elements, which is an ambitious international project to identify the functional parts of the human genome. In 2012, it revealed not only that the protein-coding elements of DNA can overlap, but that the 98 per cent of the genome that used to be labelled inactive "junk" is nothing of the sort. Some of it regulates gene activity, some churns out an array of different kinds of RNA molecules (RNAs for short), some tiny, some large, many of whose functions are hotly debated. Parrington quotes ENCODE scientist Ewan Birney as saying at the time, "It's a jungle in there. It's full of things doing stuff." And that is one of the most apt genome metaphors I've ever read. Recent insights into what some of this "stuff" is reveal problems with another classic idea: that DNA is the master controller of the cell, with information flowing in one direction from it, via RNA, to proteins. Some of ENCODE's mystery RNAs control gene activity, others make changes that the cell remembers and passes on when it divides, and which can even be passed down generations. The RNAs may be one way the environment alters the behaviour of genes without changing their DNA sequences, a phenomenon known as epigenetics.,,, That genetics is complicated isn't news, but Parrington and Moore underline the limitations and the power of trying to understand its complexity by reducing it to simpler divisions. For example, the molecular and computing technologies spawned by such attempts are now giving researchers the potential to work out how to integrate it all to form a greater whole. Time, surely, to rip up the old metaphors and create some new ones. http://www.newscientist.com/article/mg22630251.000-dna-is-lifes-blueprint-no-master-controller-of-the-cell.html#.VXySfUbcBCB
bornagain77
August 24, 2015
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I have no problem admitting "we simply don't know," when necessary. But in this case there is simply too much working against your hunt for unknown regulatory mechanisms that would involve thousands of bases of a transcript that is rapidly cleaved and then degraded. Sorry.Alicia Cartelli
August 24, 2015
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Dr JDD
I remember questioning, how do they know it is junk? Just because they don’t know of a function NOW with our current understanding and technology doesn’t mean one day we won’t find function – surely that is what science is about! I was OK with not knowing what that was – but I have always wanted to know what that function may be and definitely wanted people to study it.
Interesting point. In order to declare that 99% of it is junk, they would have to know, for certain, its origin and its relationship to everything within the cell. But the fact is, this is unknown. The resistance to stating "we don't know" is telling, since it is a resistance to the truth of things. As the 99% junk number changed, it revealed the error of those who made the claim. But they were willing to risk being exposed like that, rather than simply admit "we don't know, but it could be 99% junk". It remains the same. AC is willing to bet her soul on it, rather than just admit that she doesn't know the origin and doesn't have a full understanding of how it works.Silver Asiatic
August 24, 2015
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Right, so we need to invent some new regulatory mechanism to support your argument. Got it. Degradation of the strands of thousands of extra bases is not linked directly to their cleavage from the pri-miRNA, so unlikley. Free nucleases still need to find these strands to liberate the individual nucleotides. And it definitely would not be of any energetic benefit, so don't try that road. I must admit, though, it would be pretty cool if the pri-miRNA could fold into some sort of ribozyme or something. Who knows. Highly unlikely though.Alicia Cartelli
August 24, 2015
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Thanks for your sober and insightful input Dr JDD. Of related interest to the bogus 99% junk figure is the bogus 98% similarity figure. Here are a few relevant notes in that regards:
The Myth of 98% Genetic Similarity (and Chromosome Fusion) between Humans and Chimps - Jeffrey Tomkins PhD. – video https://www.youtube.com/watch?v=EKO5mtdA0o4 Geneticist Jeff Tomkins vs. Evolutionary Biologist who got laughed off stage - August 12, 2013 Excerpt: Tomkins described the origin of the fallacious comparison as a myth that got started in reassociation kinetic methods of comparison in the mid-1970's prior to the advent of modern sequencing techniques (like Illumina and Solexa). Reassociation kinetics was a technique where fragments of chimp and human DNA were mixed in the same chemical soup, and the DNAs that were reasonably similar would pair up, hence we got a biased sampling! If we take genes that are found in both humans and chimps and disregard the indels, we get the 98% figure. When indels are considered, the similarity drops to 80-85%! When including other sequences, the similarity drops even further, down to 70%. But that 70% figure itself, imho, is too generous. I don’t think Tomkins used ORFans or pseudo genes or many other intergenic sequences, and he explicitly avoided the complication of Synteny.... Tomkins pointed also to reports where lab workers may have contaminated the sequencing labs for Chimps with their own human DNA and thus biasing the figures! Hence re-sequencing has been done, and there is more sequencing pending to clean up these errors. He joked about the coughing and sneezing that may have gone on to cause contamination. https://uncommondescent.com/genetics/icc-2013-geneticist-jeff-tomkins-vs-evolutionary-biologist-who-got-laughed-off-stage/ Human and Chimp DNA--Nearly Identical? by Jeffrey Tomkins, Ph.D. - 2014 Excerpt: Major research published over the past decade comparing human and chimpanzee DNA was recently reviewed and critiqued.1 In every single publication, researchers only reported on the highly similar DNA sequence data and discarded the rest—apparently because it was too dissimilar. In fact, when the DNA similarities from these studies were recalculated using the omitted data, markedly lower levels—between 81 and 86 percent similarity—were found. Even the well-known chimpanzee genome paper published by evolutionists in 2005 provides a genomic similarity of only about 80 percent when the discarded nonsimilar data are included and only 70 percent when the estimated size of the chimpanzee genome is incorporated.2,3,,, Not counting the Y-chromosome, the results of my comparison showed variability between 66 and 76 percent similarity for the different chimp chromosomes, with an overall genome average of only 70 percent similarity to human chromosomes. In reality, many chromosomal regions are vastly different between chimps and humans, and several areas of the genome that are present in chimps are completely absent in humans—and vice versa. While it is true that there are sections of the chimp genome that are very similar to humans, this is not the complete picture. DNA sequence comparisons that include all the relevant data plainly show that the human and chimp genomes are not nearly identical at all. Instead, they are as distinct as one might expect based on the obvious differences in the resulting anatomies and behavioral capacities. Hypothetical evolutionary processes cannot explain the extremely broad differences between chimp and human DNA when the whole genomes are considered. The similar regions between genomes are easily interpreted as the basic reuse of effective code—a concept very familiar to software engineers.,,, http://www.icr.org/article/7892/ Chimp DNA Mutation Study—Selective Yet Surprising - Jeffrey Tomkins - August 16, 2014 Excerpt: It was initially noted by another group of evolutionary scientists that when comparing random chimp genomic sequence only "about two thirds could be unambiguously aligned to DNA sequences in humans”(2). In confirmation of this widely known, but seldom discussed, inconvenient fact among those evolutionists working in the field was a comprehensive study published in 2013 by this author (3). In that research, I compared each individual chimpanzee chromosome to human (piece-by-piece) and it was shown that the chimpanzee genome was only 70% similar on average to human, with only short regions being highly similar. ,,, 30% difference in their genomes—some 900,000,000 DNA letter differences.,,, When the entire genomes are compared between humans and chimps, it becomes clear that they were each engineered uniquely and separately by an Omnipotent Creator. http://www.designed-dna.org/blog/files/baf81fbc404eb8e24c9b6bd7953817c5-110.php
The same lack of integrity is found in the way Darwinists handled the supposed Chromosomal fusion evidence:
More DNA Evidence Against Human Chromosome Fusion - Jul 31, 2015 Excerpt: First, the sequence was only about 800 bases long—not the 10,000 bases or more you would expect if two 5,000-base (or larger) telomeres fused together. Second, the fusion-like sequence was very degenerate and only 70% similar to what one would expect of a pristine fusion sequence of the same size. Even if you assume an evolutionary timeline of up to six million years since the fusion event occurred, the data do not match up with known mutation rates or the variability found in human DNA. A third major problem is the fusion site contains no type of sequence called satellite DNA (satDNA). In chromosome fusion events that occur in nature in living mammals—a very rare event—the DNA signature always involves satDNA producing a DNA signature that occurs as either satDNA-satDNA or satDNA-teloDNA sequence.4,5,6 Thus, the alleged fusion event should contain satDNA—a problem the fusion site discoverers openly acknowledged in their initial 1991 paper. When teloDNA-teloDNA fusions do occur in humans, they involve tissues and cell lines associated with cancerous tumors.7,8,9 A fourth major problem for the alleged fusion signature on chromosome 2 is that it occurs in a region of the genome that is full of genes. Telomeres do not contain genes, yet the fusion site is in the midst of a hotbed of genetic activity. The gene neighborhood surrounding the alleged fusion lacks overall synteny (similar gene order) to the chimp genome and does not support a fusion scenario in any way. This was first noticed in 2002 by secular researchers, although the chimp genome had not been well sequenced at that time.10,11 This author has recently verified that an overall lack of synteny supporting fusion still holds true for over 2.7 million bases surrounding the fusion site based on the most recent version of the chimpanzee genome compared to human (Tomkins, unpublished data). Despite all of these serious difficulties, the greatest problem that evolutionists now have is the fact that the alleged fusion sequence is located in the middle of a functional gene.12 It is not a fossil remnant of a chromosomal accident at all but an important DNA regulatory feature called a promoter (genetic switch) inside a highly expressed gene. More specifically, the purported fusion site is located inside a crucial RNA helicase gene called DDX11L2 that produces long non-coding RNAs. This gene is expressed in at least 255 different tissue and cell types in humans and is highly coregulated with many other important genes in the cell.12 So not only is the gene highly active throughout the human body, it is tightly networked with many other genes, including those that are involved in the development of blood cells. But the evolutionary fusion story gets worse. The fusion-like sequence itself has an important functional purpose based on recent data available at the UCSC Genome Browser (genome.ucsc.edu) genomic database. Specifically, the fusion site sequence binds to at least 11 different transcription factors, including RNA polymerase II, the key enzyme that transcribes genes. Transcription factors are specialized proteins that turn genes off and on. The fact that these proteins specifically bind to the alleged fusion site sequence indicates that it is a promoter located inside the gene (Figure 2). It is common for human genes to have these promoter regions located both in front of the main body of the gene and inside them. http://www.icr.org/article/8830
bornagain77
August 24, 2015
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Alicia - I don't know. Perhaps the sequences themselves offer a regulation event of some description. Perhaps there is a necessity to rapidly liberate a vast number of nucleotides in the vicinity of the finalised miRNA for some sort of event requiring large numbers of free nucleotides (hence rapid degradation in proximity to the miRNA for some purpose). Probably not though, I'm just making that up. However, it is OK to say that "I don't know why this happens" as long as it is followed by "we should try to understand why that happens as there may be a good purpose for it." I think nature even if you are a materialist has earnt that assumption - we see purpose in virtually everything else that functions in the cell to such level of complexity and efficiency yet we aren't willing to give the same grace to this process and say, hey, you know what, maybe there is a good reason the cell does that as generally it does things for a good reason! However it then removes the low-hanging fruit that evo's like to grasp at to mock and chastise any supposed creator or designer as a poor one at best. I remember as an undergraduate studying biochemistry being told 99% of the genome was junk, at 18 years old. I remember saying I didn't believe that and there must be some function we just don't know about it. I remember questioning, how do they know it is junk? Just because they don't know of a function NOW with our current understanding and technology doesn't mean one day we won't find function - surely that is what science is about! I was OK with not knowing what that was - but I have always wanted to know what that function may be and definitely wanted people to study it. And over time more and more that 99% figure has come down and down and in one of my most naive states as a scientist I made an accurate prediction - not through any special intelligence or that I had some insight but rather through what I believe is the best science. Things happen for a reason. However that approach leads to the rational and logical conclusion that there is a reasoner behind the reason. That is what people don't like, probably yourself too.Dr JDD
August 24, 2015
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JDD, if not regulation based on binding sites, what other forms are we talking about?Alicia Cartelli
August 24, 2015
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Alicia @ 96: You are presuming what PaV or others are referring to by equating regulatory function with regulatory binding sites alone. I don't think PaV or anyone here is being that simplistic. Far from it, we are being quite the opposite and expect great complexity. Let us put this into context. Back a number of years ago in the early 00's we "had the technology" to be able to sequence the human genome and annotate it with genes and other genetic elements. These were well defined and we were confident and proud of our acheivement. Yet the technology used was flawed and simplistic - it relied on methods that are now out of date and superceded. For example, it could not cope with areas of large repetition. Things had to be assigned based on other sequenced genomes (like a chimps genome, for example). It was litered with inaccuracies and a serious point - it assumed that one human's genome would look the same as another right down to a "consensus" sequence that was the norm. Roll forward into the age where NGS (next generation sequencing) is becoming more standard in gene analysis and sequencing, a real buzz word in the biotech and pharma industry, and you will find talking with genetics that they are already stating the limitations of NGS, and newer technologies or complementary technologies need to be used to be more precise and accurate. Talk further with proper geneticists and they will tell you that if you sequence a common tumour suppressor gene of one human and compare it to the next - in healthy individuals - they won't be the same. What is "wild-type" even then? It does not really exist and the variation is much greater than most think. Now go a step further and think how we define genes and how confident we have been about that for years. Then realise that there are "genes" that are non-coding and have completely different promoter, initiation, transcription sites etc that are non-canonical. The look at draft copies of the human proteome which used sensitive mass spectrometry to identify proteins in various tissues by their fragments (which are probably outdated already in terms of sensitivity and accuracy as MS seems to move quite fast in that regard) and see that only 50% of the identified peptides could be attributed to the current ProtRefSeq data out there. So yes we have technology that allows us to study things - just like they had technology to sequence the human genome 10-15 years ago. But that does not mean it provides the most accurate picture, the actual full picture, and is not limited in detection of something that is really going on but the techniques and methodologies currently around cannot begin to tease apart.Dr JDD
August 24, 2015
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Alicia Cartelli sums up evolutionism:
Where we talk about things we know nothing about, everything’s made-up, and the points don’t matter.
:cool:Virgil Cain
August 24, 2015
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"This is over-simplification" Welcome to UD. Where we talk about things we know nothing about, everything's made-up, and the points don't matter.Alicia Cartelli
August 24, 2015
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Carpathian, Please produce the evidence that supports your claim. Or keep your unscientific opinions to yourself.Virgil Cain
August 24, 2015
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Virgil Cain:
Does Alicia know how emails get transmitted? How much of what is transmitted is the actual message, Alicia? Would you say that all of the other stuff is junk?
You're not just comparing apples and oranges here, you're not even in the same food group. Computer communications and life cannot be compared at this level. This is over-simplification.Carpathian
August 24, 2015
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Does Alicia know how emails get transmitted? How much of what is transmitted is the actual message, Alicia? Would you say that all of the other stuff is junk?Virgil Cain
August 24, 2015
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"Darwinism" cannot account for any miRNAs. It can't account for the system that breaks down the miRNAs. If that system broke, well "Darwinism" could explain that.Virgil Cain
August 24, 2015
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No, we can study the pri-miRNA sequences now, that's what the point of the original article was. We now have the ability to study potential early regulatory mechanisms of miRNA production. What my issue has been from the start is that the production of miRNAs is tightly regulated pre-transcriptionally, just as genes are, but the transcript itself is 10,000s-100,000s of bases long while the final product merely ends up being a few fragments of this. You're talking about finding regulatory function in thousands of bases of the transcript, when binding sites for regulatory proteins are typically on the order of only 5-20 bases. The speed with which Drosha functions also means that any post-transcriptional regulatory processes would have to be incredibly fast to have an effect on miRNA production. Like I said, I won't hold my breath.Alicia Cartelli
August 24, 2015
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AC: Dr JDD has stated it well: what prevents us from finding function in these areas is the lack of proper technology, right now, at least. The fear is this: as more function is found in the 1000's of nucleotides you feel are "wasted," the response will be: "Oh, but of course it has function. We knew all along that it would have function. How can you have that many nucleotides involved and not think there's function." And off the EVO's go. We can almost even now that this will become the standard answer. Science cannot advance with this disregard for failed predictions. Time will tell. Maybe six years from now, we'll have the right answer. Just don't forget this discussion. That's all I'm asking. (And, of course, this bit of advice cuts both ways!);)PaV
August 24, 2015
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All I'm saying is that if function(s) can be determined for just half of any pri-miRNA sequence, then I will denounce "darwinism" and pray to the god of your choice. It ain't gonna happen =)Alicia Cartelli
August 24, 2015
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AC
If they find a function for let’s say half of the pri-miRNA sequence, of just one specific miRNA, then I will denounce “Darwinism” and begin praying to the god of your choice. =)
It sounds like you're establishing the existence of God on the percentage (50% in this case) of function found in those sequences. Do you think that evolution sufficiently explains the percentage of function already observed, but it could not explain it if it was 50% or more? If so, that would be something to add to Edge of Evolution arguments, although you should be more precise. For example, "Evolution can explain up to 49.99% function but at 50% it's definitely evidence of ID".Silver Asiatic
August 24, 2015
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Yes, Pav, it’s unexpected because huge nucleotide strands are being generated and then immediately degraded. Hence why I called it a massive waste of energy. They have found a potential regulatory mechanism in a subset of pri-miRNAs, but still this doesn’t account for the vast majority of the transcribed bases and the majority of miRNAs. If they find a function for let’s say half of the pri-miRNA sequence, of just one specific miRNA, then I will denounce “Darwinism” and begin praying to the god of your choice. =) Be sure to let me know when that happens. That’s how confident I am that most of the transcribed bases are what I, at least, would call “waste.”Alicia Cartelli
August 24, 2015
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eigenstate, scientists not in the thrall of scientism because wilfully blinkered by atheism, would be absolutely fascinated to discover something that suggested that there is no divine, intelligent designer. It is simply that your sneered at 'God of the Gaps', as someone mentioned, is in fact, the God of everything, so that sneer, God of the Gaps' does nothing but highlight the gross inadequacy of that expression as a slur. It is simply too inane to make sense, never mind, serve to disparage and mock. You are throwing Brer Rabbit into the most luxuriant briar patch imaginable. But then you couldn't see it, never mind, imagine it. What people 'with eyes to see' (and understand QM even in layman's terms) cannot avoid seeing, no matter how hard they try, you can't begin to see. "The eye is the lamp of the body; so then if your eye is clear, your whole body will be full of light. 23 But if your eye is bad, your whole body will be full of darkness. If then the light that is in you is darkness, how great is the darkness!"Axel
August 24, 2015
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Dr JDD: The walls are cracking and crumbling, and the foundation will soon be found to be absent and it will come crashing down.
Great post Dr JDD!Box
August 24, 2015
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This is just the tip of the iceberg. Every time this is brought up the staunch evolutionists decry that these novel RNA’s and novel functions are a mere drop in the ocean, and that the majority of the genome is still junk. That is always the answer I hear. Yet for years, many including myself have stated that a genome vastly full of junk goes against the prediction of design therefore as a design advocate our model predicts functionality to these apparent “junk” regions and that we will soon find function, it is just we are limited by our technology and what we currently know.   This is something we actually agree on with our materialist friends – that a genome vastly full of junk provides more credence towards a materialistic accidental sloppy mechanism than it does a designer. Yet, what we predict is that if we find function for the majority of the genome, this is very good evidence for design and also given the amount of information contained in genomes around us including our own, if this is not vastly junk the complexity itself becomes too large (although it can be argued it already is too large) for accidental evolution to account for, in the time frames considered to be relevant for divergence and OOL.   It is clear that the driving force behind labelling much of the genome as junk is a mixture of arrogance (seeming to believe our technology is at its peak for detecting function at the molecular level) and a need for the materialistic paradigm. As stated above, it relied on most of the huge genome being junk, and if that is not true, materialistic evolution is found to be the emperor without clothes.   So what are the most recent publications on this matter pointing towards?  
SINEUPs: A new class of natural and synthetic antisense long non-coding RNAs that activate translation Abstract Over the past 10 years, it has emerged that pervasive transcription in mammalian genomes has a tremendous impact on several biological functions. Most of transcribed RNAs are lncRNAs and repetitive elements. In this review, we will detail the discovery of a new functional class of natural and synthetic antisense lncRNAs that stimulate translation of sense mRNAs. These molecules have been named SINEUPs since their function requires the activity of an embedded inverted SINEB2 sequence to UP-regulate translation. Natural SINEUPs suggest that embedded Transposable Elements may represent functional domains in long non-coding RNAs. Synthetic SINEUPs may be designed by targeting the antisense sequence to the mRNA of choice representing the first scalable tool to increase protein synthesis of potentially any gene of interest. We will discuss potential applications of SINEUP technology in the field of molecular biology experiments, in protein manufacturing as well as in therapy of haploinsufficiencies.
 
Widespread Inducible Transcription Downstream of Human Genes Summary Pervasive transcription of the human genome generates RNAs whose mode of formation and functions are largely uncharacterized. Here, we combine RNA-seq with detailed mechanistic studies to describe a transcript type derived from protein-coding genes. The resulting RNAs, which we call DoGs for downstream of gene containing transcripts, possess long non-coding regions (often >45 kb) and remain chromatin bound. DoGs are inducible by osmotic stress through an IP3 receptor signaling-dependent pathway, indicating active regulation. DoG levels are increased by decreased termination of the upstream transcript, a previously undescribed mechanism for rapid transcript induction. Relative depletion of polyA signals in DoG regions correlates with increased levels of DoGs after osmotic stress. We detect DoG transcription in several human cell lines and provide evidence for thousands of DoGs genome wide.
[Emphasis JDD]  
Nuclear Fractionation Reveals Thousands of Chromatin-Tethered Noncoding RNAs Adjacent to Active Genes. Abstract A number of long noncoding RNAs (lncRNAs) have been reported to regulate transcription via recruitment of chromatin modifiers or bridging distal enhancer elements to gene promoters. However, the generality of these modes of regulation and the mechanisms of chromatin attachment for thousands of unstudied human lncRNAs remain unclear. To address these questions, we performed stringent nuclear fractionation coupled to RNA sequencing. We provide genome-wide identification of human chromatin-associated lncRNAs and demonstrate tethering of RNA to chromatin by RNAPII is a pervasive mechanism of attachment. We also uncovered thousands of chromatin-enriched RNAs (cheRNAs) that share molecular properties with known lncRNAs. Although distinct from eRNAs derived from active prototypical enhancers, the production of cheRNAs is strongly correlated with the expression of neighboring protein-coding genes. This work provides an updated framework for nuclear RNA organization that includes a large chromatin-associated transcript population correlated with active genes and may prove useful in de novo enhancer annotation.
 
Role of chromatin, environmental changes and single cell heterogeneity in non-coding transcription and gene regulation Abstract The number and variety of factors underlying control of gene expression have been frequently underestimated. Non-coding RNAs generated through pervasive transcription have recently been implicated in shaping the transcriptional landscape in different organisms from bacteria to higher eukaryotes, adding a previously unexpected layer of complexity to the process of gene regulation. In this review, we highlight non-coding transcription-dependent regulatory mechanisms linked to chromatin organization and environmental changes, and particular emphasis is given to single-cell approaches, which have been crucial in dissecting cell-to-cell variability. These studies have revealed that non-coding transcription can underlie the extensive heterogeneity in patterns of gene expression within a cell population.
[Emphasis JDD]   These are a handful of peer-reviewed journal articles published in the last 3 months alone. This field is about to explode. The poor technology for sequencing of old and newer sequencing technologies and research (and taking these things seriously rather dismissing them as mere junk) mean that we must rethink the genome as a whole. In fact, protein translation is the overwhelmingly small role of the genome and genes. Only a fraction of the genome produces proteins yet this is entirely what the NS+RM paradigm has focused on! Despite this it appears that a whole host of other sequences and genetic material that is non-coding are highly important in the proper functioning of complex organisms and cellular mechanisms and regulation.   The irony of this all is that many molecular biologists are open to this complexity, and excitedly seeking it out. Those who oppose such novel work and adding importance to such sequences in the genome are the ones who truly understand the implications for materialistic evolution – namely those loudest proponents such as our friend Prof Moran and associates. They commonly play down (as we see on UD all the time) the importance of such findings and negate them to a fraction of the genome with little importance, with ad hominem attacks on those who cite these papers as not understanding this and how this in no way affects evolutionary thinking.   Further, one way they justify this approach (which is quite clever as it guarantees their theory stays intact) is to cite the best way to determine functionality of all these RNA transcripts is to demonstrate homology (to other organisms on the UCD tree). Prof Moran commonly will make that point and this therefore negates the possibility that some of these regulatory elements lack homology but still have important roles and function in the cell they are found, thus dealing a fatal blow to the materialistic view of evolution and common decent from accident.   “If it ain’t homologous, it ain’t important.”   The walls are cracking and crumbling, and the foundation will soon be found to be absent and it will come crashing down. (Yet I predict we will still hear some amongst the rubble crying out “evolution always predicted function for the majority of the genome – this is exactly what we expected!”)Dr JDD
August 24, 2015
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