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Short peptides from junk RNA regulate fruitfly development

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‘Non-coding’ pieces of RNA can encode short proteins that regulate genes, researchers have found.

Various non-coding RNA molecules do not produce protein but either regulate gene expression or carry out other functions in the cell. Many researchers question whether the rest of the apparently non-coding RNA made in cells has any function.

Some believe many RNA molecules in the cell are merely junk — the accidental by-products of the process that transcribes RNA from a DNA template.

“We missed microRNA for decades — maybe we missed ‘micropeptides’ for even longer.”

Researchers in Japan have found a ‘non-coding’ RNA that directly codes for four peptides, short chains of amino acids from 11 to 32 amino acids long, that act to regulate fruitfly development. It is likely that many more of these mysterious RNA molecules could produce peptides too small to be considered true proteins but which have important functions within cells.

This potentially paradigm-changing discovery “might be something very big,” says Claude Desplan, a developmental biologist at New York University. “We missed microRNA for decades — maybe we missed ‘micropeptides’ for even longer.”

“Short peptides could be lurking virtually anywhere in the genome” says Desplan.

These findings could also have implications for how we view so called psueodgenes, which have long been thought to be defunct relics of protein-coding genes. “Maybe this would provide a new way for pseudogenes to have some sort of function,” he says.

Comments
In regards to Al Kafir’s comment, I think you actually made it more difficult to make sense of what he suggest.
I think he might have been referring to the fact that some of the patentable electronic circuits created using evolutionary algorithms have more parts that commercially available designs. the article I linked discusses the problem that evolved designs -- at the time the paper was written -- were not economically competitive. Still, I find the commercial applications of evolutionary algorithms more interesting than academic discussions of why they don't work or can't produce novel designs.Petrushka
July 23, 2010
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Petrushka, This is very interesting, but evolutionary design methods are unfortunately all about specification and very little about the complexity generated by evolutionary algorithms. There is hardly any relationship between this modern design method and any unguided evolutionary proposal. Maybe it would do you good to read some of the EVOLUTIONARY INFORMATICS articles. But in the end, if you want to take this work as some sort of analogy of evolutionary processes, then you have to admit that initial and continued specification of biological systems would be at least as well designed as these design methods. In regards to Al Kafir's comment, I think you actually made it more difficult to make sense of what he suggest.mullerpr
July 23, 2010
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I am also very interested in any form of logical outline you can give for coming to this suggestion. (You will find that you can expect a very high level of insight into complex-system theory.
This is not exactly the answer to your question, but it addresses some issues in the complexity of evolved systems. Abstract: http://www.demo.cs.brandeis.edu/papers/long.html#rieffel-dissertation Paper: http://www.demo.cs.brandeis.edu/papers/rieffel-dissertation.pdfPetrushka
July 23, 2010
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Also, remember that the systems in question need to have many interacting components towards a common end. In the case of a 747, we are told there are six million parts, half of them being fasteners [which shows the importance of interactions and coupling to get a complex whole to work]. 747's are known artifacts, and have been plying our skies for what, forty years? There are also now a lot of computer programs that use millions of lines of code and megabytes of associated data.kairosfocus
July 20, 2010
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Al Kafir, This is a gem!
Probably too complex to have been designed, since complex-system theory shows that evolved systems tend to be more complicated than designed systems for a given function.
I am also very interested in any form of logical outline you can give for coming to this suggestion. (You will find that you can expect a very high level of insight into complex-system theory. Someone in this discussion will understand you or have a very informed follow-up question.) Personally I would like to see why this would be a parsimonious conclusion.mullerpr
July 20, 2010
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Al Kafir: You are probably new here, so let's make some order: gpuccio ORFans are not a type of gene, such as a pseudogene. A gene can be an ORFan today, and not an ORFan next month. I know very well what ORFans are, but in my post I was referring to a very specific subset of them, those 1000+ human orphans which were recently "eliminated" from the list of human protein coding genes by a paper which was the object of a long methodological discussion in a previous thread here. Sorry if you did not catch the reference. As to regulatory functions, one of the significant findings of evolutionary development (Evo Devo) is that most evolutionary changes since the Cambrian have been primarily regulatory. Very few “new” genes have appeared in the past few hundred million years. Although I agree with the general concept that recent information growth has been primarily regulatory, I disagree that "very few “new” genes have appeared in the past few hundred million years". Indeed, even if we look simply at protein domains appearance, it can be seen that about a quarter of all known protein domains originated in metazoa. That's certainly not "very few". You might want to read up on this subject, because it’s complex. (And, I think, very interesting.) In this moment I am discussing with you, and i will take into consideration the arguments you explicitly make. Anyway, thank you for the reading advice. For example, temperature or stress causes cells to producer “heat shock” proteins to limit damage to other proteins. Once cells have differentiated, their switches for other functions get turned off—by methylation of their DNA, e.g. And so? Now, please, don't come with all the evo-devo stuff as though it were astonishing news. Evo-devo is certainly interesting, and certainly over-inflated, and certainly badly interpreted in many contexts. Now, let's go directly to the core of the question. The genome is one (I mean, in a single multicellular being). It differentiates into different cell types, organs, tissues, systems, according to a specific body plan. The question is: where is the information which controls all that? Beware, I am not askin which are the mechanisms regulating all that. I know that many mechanisms are know (at least, a few of them). I am not denying the importance of hox genes, or of DNA methylation, or of epigenetic factors. I am asking what controls the regulation, and guides it. For instance, every single cell type in multicellular beings is characterized and determined by a specific transcriptome. A transcriptome is in turn controlled by transcription factors (and other factors), which are transcribed proteins. We can imagine a specific transcriptome as a specific subset of genes which is activated from the general pool in a specific cell. But, obviously, the information which guides the activation of those genes (and not others) must also specify: a) the sequence of activation b) the life span of each activation c) the relative quantitative regulation of each gene, so that each protein is producted in the right quantity d) the detailed transciptional and post-transcriptional regulations which can modify the mRNA and the protein e) the post-translational modifications of the protein itself and probably many other things. Now, would you please explain how do you think all that is regulated in each cell type, starting form the same genomic information? Hox genes do not contain all the info to produce a leg. They start the process, then the cascade of regulation (that I mentioned before) takes over automatically to produce the necessary detailed structures. They obviously don't. They are just switches. For example, the same hox gene that produces a bvutterfly’s wing structure in its first 2 iterations has a third iteration that produces the colored spots, an entirely different structure. And so? Hox genes are regulatory proteins, they can regulate different functions, without having the information for those functions. PS: The set of regulation components in a cell is called its “regulome.” Those components can be genes, mRNAs, proteins, and metabolites that interact with each other and with subcellular localization, tissue, developmental stage, and pathological state. So, now that we have a new "ome" word, would ypou explain what controls the regulome? Why has each dofferent cell type a different regulome? How do cells "know" which specific set of "genes, mRNAs, proteins, and metabolites" are to be included in its regulome, or how those components should "interact with each other and with subcellular localization, tissue, developmental stage, and pathological state". Details or explicit models, please. Regulomes are quite complex. You bet! Probably too complex to have been designed, since complex-system theory shows that evolved systems tend to be more complicated than designed systems for a given function. I can only repeat BA's statement: it's "the most ludicrous statement I have ever heard". Granted that complex-system theory is very new, and not well known, even among scientists. Again, please, not just reading advices. Could you please give us some concepts which justify your statements, since you certainly understand this fundamental theory so well? Be kind. For example, Meyer never quantifies “information,” so it is impossible to argue how whatever it is might be generated. We have quantified functional information a lot of times here, and in great detail. If you are interested, I can give you the links to some pertinent posts. And finally, as you have named BA "an intron" (which, IMO, was not kind: I have the highest opinion of introns, but you probably don't), and as you probably consider yourself an exon, can I be a transposon? That would make my day.gpuccio
July 18, 2010
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one of the significant findings of evolutionary development (Evo Devo) is that most evolutionary changes since the Cambrian have been primarily regulatory.
Don't you mean "speculations" instead of "significant findings". And even granting that most of the change is regulatory, it hardly means Evo Devo solve the mechanism of evolution of regulation since Evo Devo itself assumes regulation is already in place to spawn more regulation! Evo Devo strikes me like the geek observing the regulatory mechanims on his computer known as the "on off switch". He notices that when he presses the on switch it regulates all the power in the computer and hence all the marvelous function comes to life. He then concludes this regulatory mechanism is the explanation for all the other regulatory functions in the computer (like the logic gates and memory managment and disk drives). What passes off as "significant scientific finding" in evoltionary biology is almost beyond belief!scordova
July 18, 2010
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Kafir at 21: Functional information and the emergence of bio-complexity: Robert M. Hazen, Patrick L. Griffin, James M. Carothers, and Jack W. Szostak: Abstract: Complex emergent systems of many interacting components, including complex biological systems, have the potential to perform quantifiable functions. Accordingly, we define 'functional information,' I(Ex), as a measure of system complexity. For a given system and function, x (e.g., a folded RNA sequence that binds to GTP), and degree of function, Ex (e.g., the RNA-GTP binding energy), I(Ex)= -log2 [F(Ex)], where F(Ex) is the fraction of all possible configurations of the system that possess a degree of function > Ex. Functional information, which we illustrate with letter sequences, artificial life, and biopolymers, thus represents the probability that an arbitrary configuration of a system will achieve a specific function to a specified degree. In each case we observe evidence for several distinct solutions with different maximum degrees of function, features that lead to steps in plots of information versus degree of functions. http://genetics.mgh.harvard.edu/szostakweb/publications/Szostak_pdfs/Hazen_etal_PNAS_2007.pdf Mathematically Defining Functional Information In Molecular Biology - Kirk Durston - short video http://www.metacafe.com/watch/3995236 further note: "There are no detailed Darwinian accounts for the evolution of any fundamental biochemical or cellular system only a variety of wishful speculations. It is remarkable that Darwinism is accepted as a satisfactory explanation of such a vast subject." James Shapiro - Molecular Biologist Michael Behe on Falsifying Intelligent Design - video http://www.youtube.com/watch?v=N8jXXJN4o_Abornagain77
July 17, 2010
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bornagain77, as to your comment of 07/17/2010 8:54 pm, i do not grant many of your assumptions, so cannot answer your questions. For example, Meyer never quantifies "information," so it is impossible to argue how whatever it is might be generated.Al Kafir
July 17, 2010
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Al Kafir, If you don't mind let's cut to the chase and please just so me what you consider is your best example of actually demonstrated evolution.bornagain77
July 17, 2010
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bornagain77: "Al Kafir, this has absolutely got to be the most ludicrous statement I have ever heard:" Granted that complex-system theory is very new, and not well known, even among scientists. You might try S.Y. Auyang's 1999 book, "Foundations of Complex System Theories in Economics, Evolutionary Biology, and Statistical Physics." Melanie Mitchell's newer book "Complexity" shows some examples of how complex systems evolve.Al Kafir
July 17, 2010
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Al Kafir, this has absolutely got to be the most ludicrous statement I have ever heard: "Regulomes are quite complex. Probably too complex to have been designed, since complex-system theory shows that evolved systems tend to be more complicated than designed systems for a given function." So that is why nobody can create life nor observe evolution happening in the lab because it is just to complex for us to understand. ROTFLOL,, I'm crying!!!bornagain77
July 17, 2010
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Sorry to intron on your Hox gene discussion, but please Al Kafir, just how do you explain the generation of novel functional information for novel body plans with a genetic code that is severely polyconstrained to any random mutations in the first place,, polyconstrained because it is intertwined in a multi-tiered overlapping way with the higher levels of information found in other parts of the cell??? "operational information belongs as much to the cell body and to its cytoplasmic regulatory protein components and other endogenous or exogenous ligands as it does to the DNA database." Stephen Meyer - DNA - Complexity Of The Cell - Layered Information - video http://www.metacafe.com/watch/4798685 ,,,, functional information that is indeed intertwined in a polyfunctional way that steadfastly prevents any imagined "beneficial point mutations" from occurring in the DNA because it is severely polyconstrained to any "random mutations", of any type, happening in the first place,,, See here for a clear example: Poly-Functional Complexity equals Poly-Constrained Complexity - Dr. John Sanford - Genetic Entropy http://docs.google.com/Doc?docid=0AYmaSrBPNEmGZGM4ejY3d3pfMjdoZmd2emZncQ On top of that Al Kafir, I could just as well have used the polyfunctional nature of the DNA code by itself, without even invoking the higher levels of layered regulatory information found within the cell body and environment (epigenetic/ontogentic information),, thus preventing your Hox gene conjecture from being true even if the DNA reductionism scenario were true for the evolutionists,, which it IS NOT!!!, Splicing Together the Case for Design, Part 2 (of 2) - Fazale Rana - June 2010 Excerpt: Remarkably, the genetic code appears to be highly optimized, further indicating design. Equally astounding is the fact that other codes, such as the histone binding code, transcription factor binding code, the splicing code, and the RNA secondary structure code, overlap the genetic code. Each of these codes plays a special role in gene expression, but they also must work together in a coherent integrated fashion. The existence of multiple overlapping codes also implies the work of a Creator. It would take superior reasoning power to structure the system in such a way that it can simultaneously harbor codes working in conjunction instead of interfering with each other. As I have written elsewhere, the genetic code is in fact optimized to harbor overlapping codes, further evincing the work of a Mind. http://www.reasons.org/splicing-together-case-design-part-2-2 DNA - The Genetic Code - Optimal Error Minimization & Parallel Codes - Dr. Fazale Rana - video http://www.metacafe.com/watch/4491422 Al Kafir,, though you may find my objections to be "introns" into your Hox gene discussion, and not worthy of your consideration, I find the principle of the DNA being polyconstrained by polyfunctional information to be a extremely valid point of concern that should in all honesty be dealt with with the utmost seriousness by anyone who truly believes material processes can "randomly" generate these staggering levels of unmatched complex information we find in life. And concisely demonstrate how such random processes can overcome this sheer level of complexity necessary to be dealt with to explain novel body-plan morphogenesis. Hopefully you can see the clear reasonableness of my disbelief of you, or anyone else, being able to do so. further note: "There is abundant evidence that most DNA sequences are poly-functional, and therefore are poly-constrained. This fact has been extensively demonstrated by Trifonov (1989). For example, most human coding sequences encode for two different RNAs, read in opposite directions i.e. Both DNA strands are transcribed ( Yelin et al., 2003). Some sequences encode for different proteins depending on where translation is initiated and where the reading frame begins (i.e. read-through proteins). Some sequences encode for different proteins based upon alternate mRNA splicing. Some sequences serve simultaneously for protein-encoding and also serve as internal transcriptional promoters. Some sequences encode for both a protein coding, and a protein-binding region. Alu elements and origins-of-replication can be found within functional promoters and within exons. Basically all DNA sequences are constrained by isochore requirements (regional GC content), “word” content (species-specific profiles of di-, tri-, and tetra-nucleotide frequencies), and nucleosome binding sites (i.e. All DNA must condense). Selective condensation is clearly implicated in gene regulation, and selective nucleosome binding is controlled by specific DNA sequence patterns - which must permeate the entire genome. Lastly, probably all sequences do what they do, even as they also affect general spacing and DNA-folding/architecture - which is clearly sequence dependent. To explain the incredible amount of information which must somehow be packed into the genome (given that extreme complexity of life), we really have to assume that there are even higher levels of organization and information encrypted within the genome. For example, there is another whole level of organization at the epigenetic level (Gibbs 2003). There also appears to be extensive sequence dependent three-dimensional organization within chromosomes and the whole nucleus (Manuelides, 1990; Gardiner, 1995; Flam, 1994). Trifonov (1989), has shown that probably all DNA sequences in the genome encrypt multiple “codes” (up to 12 codes). (Dr. John Sanford; Genetic Entropy 2005)bornagain77
July 17, 2010
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PS: The set of regulation components in a cell is called its "regulome." Those components can be genes, mRNAs, proteins, and metabolites that interact with each other and with subcellular localization, tissue, developmental stage, and pathological state. Regulomes are quite complex. Probably too complex to have been designed, since complex-system theory shows that evolved systems tend to be more complicated than designed systems for a given function.Al Kafir
July 17, 2010
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Sorry, Phaedros, we were interrupted by an intron. Hox genes do not contain all the info to produce a leg. They start the process, then the cascade of regulation (that I mentioned before) takes over automatically to produce the necessary detailed structures. For example, the same hox gene that produces a bvutterfly's wing structure in its first 2 iterations has a third iteration that produces the colored spots, an entirely different structure. The transition from fish fins to tetrapod limbss occurred when a hox gene became active 3 times during limb development, instead of the 2 times needed to produce a fin. You really should read Carroll's book, or something else on evo-devo. This area has opened up a whole new world for evolution. We used to think that you needed a new set of genes for every new structure. Now it appears that hox and other regulatory genes can do the job with previous genes and their modifications, merely by changes in the activation of switches on other genes.Al Kafir
July 17, 2010
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Cool ID related song: Creation Calls (Brian Doerksen) http://jojoagot.com/2010/07/15/creation-calls/ Do Hox genes help the neo-Darwinists in his illusions of generating functional information from material processes? I don't think so! In the following comment, from a 2005 Nature review article, evolutionary geneticist Jerry Coyne (not particularly a friend of ID) expressed skepticism at the proposed mechanism of "gene switches" for evo devo (short hand for 'evolutionary developmental biology'): "The evidence for the adaptive divergence of gene switches is still thin. The best case involves the loss of protective armor and spines in sticklebacks, both due to changes in regulatory elements. But these elements represent the loss of traits, rather than the origin of evolutionary novelties...We now know that Hox genes and other transcription factors have many roles besides inducing body pattern, and their overall function in development - let alone in evolution - remains murky." http://www.evolutionnews.org/2010/06/scott_f_gilbert_developmental035931.html The inability of body plans to be reduced directly to the DNA code is clearly shown by Cortical Inheritance. Cortical Inheritance: The Crushing Critique Against Genetic Reductionism - Arthur Jones - video http://www.metacafe.com/watch/4187488 “Live memory” of the cell, the other hereditary memory of living systems - 2005 Excerpt: To understand this notion of “live memory”, its role and interactions with DNA must be resituated; indeed, operational information belongs as much to the cell body and to its cytoplasmic regulatory protein components and other endogenous or exogenous ligands as it does to the DNA database. We will see in Section 2, using examples from recent experiments in biology, the principal roles of “live memory” in relation to the four aspects of cellular identity, memory of form, hereditary transmission and also working memory. http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T2K-4FJXNG6-1&_user=10&_coverDate=06%2F30%2F2005&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1273117547&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=0bfa74d6bb0937402472343daa6bdef8 The Case Against Molecular Reductionism - Rupert Sheldrake and Bruce Lipton - video http://www.metacafe.com/watch/4899469 This inability for the DNA code to account for body plans is also clearly shown by extensive mutation studies to the DNA of different organisms which show "exceedingly rare" major morphological effects from mutations to the DNA code. Stephen Meyer - Functional Proteins And Information For Body Plans - video http://www.metacafe.com/watch/4050681 The Origin of Biological Information and the Higher Taxonomic Categories - Stephen Meyer"Neo-Darwinism seeks to explain the origin of new information, form, and structure as a result of selection acting on randomly arising variation at a very low level within the biological hierarchy, mainly, within the genetic text. Yet the major morphological innovations depend on a specificity of arrangement at a much higher level of the organizational hierarchy, a level that DNA alone does not determine. Yet if DNA is not wholly responsible for body plan morphogenesis, then DNA sequences can mutate indefinitely, without regard to realistic probabilistic limits, and still not produce a new body plan. Thus, the mechanism of natural selection acting on random mutations in DNA cannot in principle generate novel body plans, including those that first arose in the Cambrian explosion." http://eyedesignbook.com/ch6/eyech6-append-d.html Hopeful monsters,' transposons, and the Metazoan radiation: Excerpt: Viable mutations with major morphological or physiological effects are exceedingly rare and usually infertile; the chance of two identical rare mutant individuals arising in sufficient propinquity to produce offspring seems too small to consider as a significant evolutionary event. These problems of viable "hopeful monsters" render these explanations untenable. Paleobiologists Douglas Erwin and James Valentine “Yet by the late 1980s it was becoming obvious to most genetic researchers, including myself, since my own main research interest in the ‘80s and ‘90s was human genetics, that the heroic effort to find the information specifying life’s order in the genes had failed. There was no longer the slightest justification for believing that there exists anything in the genome remotely resembling a program capable of specifying in detail all the complex order of the phenotype (Body Plan)." Michael John Denton page 172 of Uncommon Dissent This includes the highly touted four-winged fruit fly mutations: ...Advantageous anatomical mutations are never observed. The four-winged fruit fly is a case in point: The second set of wings lacks flight muscles, so the useless appendages interfere with flying and mating, and the mutant fly cannot survive long outside the laboratory. Similar mutations in other genes also produce various anatomical deformations, but they are harmful, too. In 1963, Harvard evolutionary biologist Ernst Mayr wrote that the resulting mutants “are such evident freaks that these monsters can be designated only as ‘hopeless.’ They are so utterly unbalanced that they would not have the slightest chance of escaping elimination through natural selection." - Jonathan Wells http://www.evolutionnews.org/2008/08/inherit_the_spin_the_ncse_answ.html#footnote19 Darwin's Theory - Fruit Flies and Morphology - video http://www.youtube.com/watch?v=hZJTIwRY0bs As well as "cloning" studies: "There is now considerable evidence that genes alone do not control development. For example when an egg's genes (DNA) are removed and replaced with genes (DNA) from another type of animal, development follows the pattern of the original egg until the embryo dies from lack of the right proteins. (The rare exceptions to this rule involve animals that could normally mate to produce hybrids.) The Jurassic Park approach of putting dinosaur DNA into ostrich eggs to produce a Tyrannosaurus rex makes exciting fiction but ignores scientific fact." The Design of Life - William Dembski, Jonathan Wells Pg. 50bornagain77
July 17, 2010
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Phaedros I agree with you that the HOX gene story is over inflated. It seems that they often function as a "repeat previous operation" command. The determination of the body plan of even the simplest of multicellular organisms is poorly understood. Even the amoeba's body plan can not yet be derived from the genome. There are a lot of people talking with great confidence about HOX genes and body plans but in my experience it is mostly noise to cover gross ignorance.idnet.com.au
July 17, 2010
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That wasn't my question. My question was if it is true that hox genes do contain all of the information necessary for the development of a leg, for example , (which I highly doubt) how is that infornation regulated, i.e. expressed at the right time and place, etc. Yes, I would love to read up on this subject but i'm not sure that mainstream evolutionary biology is even asking the questions i am interested in. Essentially the question is where are the higher level instructions for body plan.Phaedros
July 17, 2010
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You might want to read up on this subject, because it's complex. (And, I think, very interesting.) For example, temperature or stress causes cells to producer "heat shock" proteins to limit damage to other proteins. Once cells have differentiated, their switches for other functions get turned off---by methylation of their DNA, e.g. As to the insect-leg example, modifying a single hox gene at a particular time and place will produce all of the structures of a leg---exoskeleton, muscles, nerves, everything---in a regulatory cascade. That's why hox genes are often called "master genes."Al Kafir
July 17, 2010
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Also, it's my understanding that hox genes only turn on and off the development of legs for example. However, my question is do they also provide the information for the development of the various cell types, for how those cell types are organized into the necessary shapes for bones, as only one part of all that is necessary for a leg to work, do thy also provide the ne essary information for the shape of the leg, i.e. the shape abd structure of the leg so that it can be functional at all? In other words how is this one or few segments of DNA to account for all of that? Is it read in multiple ways, if so what provides tye necessary regulation that determines how and when it is read, is it also spliced in multiple ways and read forwards and backwards?Phaedros
July 17, 2010
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Ok, now which parts of the DNA regulate gene and gene expression throughout the life of the organism?Phaedros
July 17, 2010
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Many genes serve regulatory functions. Probably the most interesting class are the homeobox ("hox") genes, which produce proteins that bind to DNA directly, thus controlling when and in what part of the embryo the genes that match the hox protein template will be expressed. Since these proteins usually bind to switches for the gene, rather than to the coding region, multiple hox proteins can control a single gene, and a single hox protein can control many genes. (Hox genes are the ones that scientists modify to produce legs where antennae should be on fruit flies, for example.) A good explanation of hox genes and their origin is in Sean B. Carroll's book, Endless Forms Most Beautiful.Al Kafir
July 17, 2010
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Al Kafir- What, specifically, are those regulatory functions and which genes, or otherwise, serve them?Phaedros
July 17, 2010
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gpuccio ORFans are not a type of gene, such as a pseudogene. A gene can be an ORFan today, and not an ORFan next month. As to regulatory functions, one of the significant findings of evolutionary development (Evo Devo) is that most evolutionary changes since the Cambrian have been primarily regulatory. Very few "new" genes have appeared in the past few hundred million years.Al Kafir
July 17, 2010
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gpuccio- " It could be intriguing to view them as regulatory, which would again confirm that in higher beings the main expansion ofn information is at the regulatory level, rather than at the basic terminal effector level." It seems to me that this would be a reasonable speculation/educated guess even without knowing anything about coding and non-coding DNA.Phaedros
July 17, 2010
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Very interesting indeed. A whole new class of regulators could be revealed, based "as usual" ( :) ) on non coding DNA information. I believe that this paper could be relevant not only to our recent discussion about pseudogenes, but also to our recent discussion about human ORFans: it is interesting to remember that ORFans are usually shorter than classical genes. It could be intriguing to view them as regulatory, which would again confirm that in higher beings the main expansion ofn information is at the regulatory level, rather than at the basic terminal effector level.gpuccio
July 17, 2010
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In a related article in Nature, we find this:
In the latest study, researchers led by Harm van Bakel of the University of Toronto in Ontario confronted the discrepancy directly by analysing samples from the same tissues, using both tiling microarrays and RNA-Seq. The team found that whereas the microarrays reported many mysterious transcripts, the RNA-Seq technology found few transcripts other than those linked to genes coding for proteins. The team's work is published in PLoS Biology5.
This makes perfectly good sense. It would be highly inefficient to transcribe the entire length of DNA; further, if one wanted to regulate the activities of gene products, it would make sense to have those regulatory elements coded along with the gene products. This is what now appears to be happening. Again, this has implications for the role of pseudogenes.PaV
July 17, 2010
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Sal: speaking of psuedogenes, did you see this part of the blurb:
Meanwhile, Gerstein notes that the polished rice peptides could also have implications for how we view psueodgenes, which have long been thought to be defunct relics of protein-coding genes. Pseudogenes often contain many signals that would stop protein synthesis and, as a result, could only encode short amino-acid chains. "Maybe this would provide a new way for pseudogenes to have some sort of function," he says.
We just had discussion here a few weeks ago about pseudogenes with some poster saying he was a major in religious studies and that he sent this researcher the information that was out that psuedogenes were involved with microRNAs in regulation, and his friend just laughed. I wonder if his friend is laughing now.PaV
July 17, 2010
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Just as a reminder what Darwinists like Ken Miller have stated (and testimony which Judge Jones accepted from Miller under oath) in Kitzmiller vs Dover:
the designer made serious errors, wasting millions of bases of DNA on a blueprint full of junk and scribbles. Evolution, however, can explain them easily. Pseudogenes are nothing more than chance experiments in gene duplication that have failed, and they persist in the genome as evolutionary remnants Ken Miller
scordova
July 17, 2010
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