RNA measurements may yield less insight than assumed

_{Denyse O'Leary

December 19, 2014

News, Origin Of Life}

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The majority of RNA expression differences between individuals have no connection to the abundance of a corresponding protein, report scientists from the University of Chicago and Stanford University in Science on Dec. 18. The findings point to a yet-unidentified cellular mechanism that regulates gene expression and suggest studies that rely only on RNA measurements to characterize gene function require further analysis.

“The chief assumption for studies of RNA differences is that they ultimately reflect differences in an end product, which is protein,” said senior study author Yoav Gilad, PhD, professor of human genetics at the University of Chicago. “But it turns out in most cases this may not be true.”

Interesting, when we consider the high hopes placed in RNA world.

See also: Welcome to “RNA world,” the five-star hotel of origin-of-life theories

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Comments

WD400 #118, Now this time it's you who misunderstands :) Drad is carrying multiple copies of its genome. 7 kGy of ionizing radiation shatters the genome and the copies - breakage is random (i.e., it doesn't occur on both copies at the same place). Now because there are multiple copies, repair by homologous recombination can occur between the copies. For this repair Drad needs overlapping genomic fragments. There are multiple homologous fragments - fragments stemming from the multiple copies. However Drad needs overlapping fragments (see fig.7). Because there are so many scattered fragments these are likely available. Hundreds of overlapping genomic fragments can be used as respective primers and templates for 3’ end elongations. The correctly sequenced hundreds of overlapping genomic fragments (see fig.7) function as a template for genome repair. Now, like I stated before, the mystery is how Drad lines them up in the correct sequence - 'whence the information?' I had an extensive email exchange with one of the researchers who explicitly confirmed the mystery.
Yes, that's exactly the biggest remaining mystery, how are the homologous fragments brought together. We know that there is no pre-alignment of the genomic copies, but perhaps alignment occurs before repair takes place. How this happens is a mystery. We wanted to test the possibility of 'post-alignment' (after IR) by tagging a certain locus with GFP and looking at whether we see two dots side by side or fart apart, but the resolution of light microscopy doesn't allow for the GFP foci to be visualized separately.
Box_{December 23, 2014
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#115 hrun0815
If you are a student (autodidactic or not) you should know how to quote things. The quotes should be clearly marked as such and they should not be altered — for example by leaving out stuff.
Thank you for the quoting tips.
And your point that as you student your opinion wouldn’t make a difference here is also disingenuous: You specifically asked for clarifications about a point before you voice your opinion. You were given the clarification, but still evade the point.
I still don't understand what was wrong about that text you were pointing to. Generally, I don't have opinion about things I don't understand well. The clarifications you provided were not enough for me to see your point. I don't think my opinion on that issue is important, but if you think it is, you would have to elaborate more on your argument. Again, I don't think that's necessary. It's not a big deal, is it?
In addition, remember that you were the one bemoaning the supposed inability or unwillingness of so-called Darwinists to have a serious discussion. But, clearly by your own admission, it is actually you who is unwilling (or maybe unable since you point to your status as a student).
You seem confused again. Are you referring to my comments addressed to Box? Are you sure you're not misquoting my comments? Apparently, Box was trying to engage in a serious discussion with some folks in this blog, but things didn't seem to go quite right, so I expressed my opinion about discussion requirements. I don't recall saying I was able, capable or willing to engage in serious discussions. Can you show me that text where I said so? If I did, I will correct it. But first, show it to me. It was Box who seemed trying to engage in a deep discussion that was getting nowhere. I know it won't work, so I don't even try. However, if I see signs that it could happen, then I give it a try. But the sign must be very clear. I usually ask a few questions to help my interlocutors to reveal their true motives. If their motives seem sincere and serious, I go ahead with the discussion, assuming I'm interested in the discussed subject. Otherwise, I just skip it or withdraw and move on to something else. My comments were about the need for both parties to be interested in a serious discussion. Both parties mean that both Box and his interlocutors must be willing to mutually benefit from the discussion. That did not seem to be the case. Do you understand this now? I can try to explain it another way, but first let me know if you get it. Thanks.Dionisio_{December 23, 2014
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This reminds me of our short discussion, a little over a year ago, on Deinococcus radiodurans. I still hold that this is an extremely claer example of the need for a top-down explanation.
Re-reading this thread, I think I see what you were missing. DNA-repair in in D. radiodurans takes advantage of homologous sequences. There's no need for master plan of the "correct" sequence to aim for, the bits that get joined up are the bits that match each other and so an bind to complimentary sequence. One those overlapping sections are joined up the polymerases can make new double stranded copies. Fig 7 here (pdf) might give you a clearer picture of what's going onwd400_{December 23, 2014
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#116 hrun0815
Oh, and re your post 57: it is an iPhone.
Thank you for this information. I forgot to check the post #s on my wife's iPhone and iPad yesterday. Does this mean that MSFT devices work better than Apple gadgets? Well, at least in relation to this particular issue? Hmmm... that's interesting.Dionisio_{December 23, 2014
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Oh, and re your post 57: it is an iPhone.hrun0815_{December 23, 2014
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Dionisio, I'm neither upset nor confused. If you are a student (autodidactic or not) you should know how to quote things. The quotes should be clearly marked as such and they should not be altered -- for example by leaving out stuff. And your point that as you student your opinion wouldn't make a difference here is also disingenuous: You specifically asked for clarifications about a point before you voice your opinion. You were given the clarification, but still evade the point. In addition, remember that you were the one bemoaning the supposed inability or unwillingness of so-called Darwinists to have a serious discussion. But, clearly by your own admission, it is actually you who is unwilling (or maybe unable since you point to your status as a student). And with that, happy holidays to you, too.hrun0815_{December 23, 2014
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To Whom This May Concern Please, don't be upset at my posts. Remember that the OP author, the thread moderator, has the right and the tools to screen out my posts anytime. I will not complain if that happens to my posts. The OP author/ thread moderator also has the right to ask me publicly here or privately by email that I change my posting style or refrain from posting completely. I will quietly obey if that happens to me. But so far, that hasn't occurred, hence I keep posting at my convenience. If someone doesn't like a particular post, write what exactly is wrong with the post or just skip it. Merry Christmas! :)Dionisio_{December 23, 2014
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hrun0815 @109
If you mainly hold yourself to fake-quoting work by real scientist, but evade efforts to any clear statements about your opinions then it is no wonder you don’t have to backtrack: just like BA77 you don’t actually say anything of substance to begin with.
You seem a little confused. Let me try to clarify a few things for you. Currently, I'm a student (autodidact), hence my opinion here, where so many folks know much more than I do, would not make any difference. Perhaps one thing I can do is to read what others write and ask questions in order to learn more. Also I like to post here some of the materials I'm reviewing lately, in order to share them with other people who might be interested in the given subjects. These days I'm collecting and organizing research papers with the help of tools like Zotero and Mind Meister, along with WordPress web logs, which I share only with folks that are helping me with my studies or are interested in the stuff I have gathered in there. BTW, I don't recall seeing your answer to my post #57:

#48 hrun0815 Since I don’t have numbered posts on my phone…
Interesting. What kind of phone is that?
I'm just curious. Thanks. Merry Christmas! :)Dionisio_{December 23, 2014
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#109 hrun0815 Hey buddy, are you upset at my posts? Calm down, take it easy. It's Christmas season, rejoice! :)Dionisio_{December 23, 2014
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Post-translational Regulation of Mitogen-activated Protein Kinase Phosphatase (MKP)-1 and MKP-2 9, 2014, doi: 10.1074/jbc.M114.591925 MAPK phosphatases (MKPs) are critical modulators of the innate immune response, and yet the mechanisms regulating their accumulation remain poorly understood. Interestingly, p38 inhibition prior to LPS stimulation had little effect on MKP-1 and MKP-2 protein levels, but hindered their detection by an M-18 MKP-1 antibody. Remarkably, the stability of both MKP-1 and MKP-2 was markedly decreased in macrophages in the presence of an ERK pathway inhibitor. Surprisingly, enhanced stabilities of the MKP-1 and MKP-2 mutants were not associated with decreased ubiquitination. Our studies suggest that MKP-1 and MKP-2 stability is regulated by ERK-mediated phosphorylation through a degradation pathway independent of polyubiquitination. http://www.jbc.org/content/289/42/28753.shortDionisio_{December 23, 2014
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The regulation of BK channel activity by pre- and post-translational modifications doi: 10.3389/fphys.2014.00316 The diversity of BK channel activity results from the considerable alternative mRNA splicing and post-translational modification (e.g., phosphorylation) of key domains within the pore-forming ? subunit of the channel complex. Most of these modifications are regulated by distinct upstream cell signaling pathways that influence the structure and/or gating properties of the holo-channel and ultimately, cellular function. The channel complex may also contain auxiliary subunits that further affect channel gating and behavior, often in a tissue-specific manner. BK channels derive functional diversity through the alternative post-transcriptional splicing of mRNA... The impressive range of phenotypic products that can result from differential splicing of the KCNMA1 gene product contributes to diversity of BK channel function between tissues, cells and intracellular compartments. The molecular mechanisms by which ?-subunits interact with and influence BK channel gating and kinetics are currently an area of active investigation. The dynamic post-translational “tuning” of BK channels permits considerable diversity in the biophysical properties of the current. Their function, however, varies between cell types and layers, and generally is dependent on the associated macromolecular signaling complex. Dynamic regulation of BK channel subunit co-assembly and interaction at the plasma membrane may thus represent a novel paradigm for the modulation of ion channel activity. these studies indicate that the expression and function of BK channels in the vasculature involves complex expression and signaling pathways, and may vary between cells, tissues, vascular beds and pathophysiological profiles. Heteromeric BK channel complexes are the subject of extensive post-translational modifications, which can significantly alter channel behavior. Some modifications are highly-complex and require prior upstream modification(s) to the channel subunits. observations suggest that constitutive phosphorylation may help stabilize BK channel tertiary structure and/or create binding sites for interacting proteins. The various protein kinases responsible for these in vivo modifications are presently unknown, as is the extent to which channels from other tissues or expressed heterologously exhibit constitutive phosphorylation. Future studies examining the direct phosphorylation of native BK channels by tyrosine kinases in situ are needed to clarify the physiologic importance of this regulatory event. Protein ubiquitination has emerged as a ubiquitous quality control mechanism for the regulation of protein trafficking and turnover and has been implicated in the dynamic control of diverse cellular processes (e.g., gene transcription, synaptic development and plasticity, oncogenesis, etc.) Recent evidence indicates that BK channels also undergo ubiquitination, which appears to have important functional implications. BK channel activity is regulated both directly and indirectly through a diverse range of modulatory pathways involving covalent modifications, metabolic factors, trafficking events and transcriptional processes... BK channels represent powerful effectors in tissue health and dysfunction and that understanding their modes of regulation may lead to novel therapeutic strategies in disease treatment. http://journal.frontiersin.org/Journal/10.3389/fphys.2014.00316/fullDionisio_{December 23, 2014
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And even more links with quotes (that by the way are somewhat modified yet taken more or less verbatim without being marked as such) from Dionisio. Again a good indicator who is interested in serious discussion. And another thing is pretty funny, too. It's no wonder that you can brag to Box about how you supposedly never had to backtrack.
I don’t recall any instance where I had to backtrack when discussing anything with our ‘n-D e’ interlocutors.
If you mainly hold yourself to fake-quoting work by real scientist, but evade efforts to any clear statements about your opinions then it is no wonder you don't have to backtrack: just like BA77 you don't actually say anything of substance to begin with.hrun0815_{December 23, 2014
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So Joe, I take it you are unable to find a scientific source that only claims ATP synthase evolved and does not provide evidence for this claim? Got it. Here's some things you can look at that talk about the evolution of ATP synthase: Rotary DNA motors Doering C, Ermentrout B, Oster G Ectopic bold beta-chain of ATP synthase is an apolipoprotein A-I receptor in hepatic HDL endocytosis Martinez LO ATP synthases: structure, function and evolution of unique energy converters. Müller V, Grüber G Evolution of the F0F1 ATP synthase complex in light of the patchy distribution of different bioenergetic pathways across prokaryotes. Koumandou VL, Kossida S Bioenergetics: the evolution of molecular mechanisms and the development of bioenergetic concepts. Skulachev VP1 DNA sequence of a gene cluster coding for subunits of the F0 membrane sector of ATP synthase in Rhodospirillum rubrum. Support for modular evolution of the F1 and F0 sectors. Falk G, Walker JE. I suggest that you and your friends stop falling back on the argument that "evolution hasn't explained this, so evolution must be wrong." It just makes you look like a bunch of idiots to those who actually know what they're talking about. Also, it's not that evolution can't be modeled, the problem is it is too complex a process for us to successfully model right now.AVS_{December 22, 2014
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AVS, there isn't any evidence that natural selection can produce any ATP synthase. There isn't any evidence that unguided evolution can produce anything beyond disease and deformities.Joe_{December 22, 2014
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Unguided evolution can't even be modeled. It is unscientific.Joe_{December 22, 2014
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With or without natural selection. Doesn't matter mungy. Just want to see the claim made without any evidence provided. I doubt you'll be able to find it seeing as science (including evolution =) ) is based on claims that are supported by evidence. Unlike ID.AVS_{December 22, 2014
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AVS must agree that there isn't any evidence for natural selection producing any ATP synthase. And seeing tat unguided evolution doesn't have any other creative mechanism AVS must also agree that unguided evolution is unscientific. This is a good dayJoe_{December 22, 2014
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Post-translational mechanisms related to PAR-4 regulation doi: 10.1158/1538-7445.AM2014-3386 Further analyses of the post-translational mechanisms involved in cl.PAR-4 activity still need to be investigated to better understand the regulation of this potential tumor suppressor. http://cancerres.aacrjournals.org/content/74/19_Supplement/3386.shortDionisio_{December 22, 2014
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Translational and Post-Translational Regulation of XIAP by eIF2? and ATF4 promotes ER stress-induced Cell Death during the Unfolded Protein Response doi: 10.1091/mbc.E13-11-0664 ER protein misfolding activates the Unfolded Protein Response (UPR) to help cells cope with ER stress. If ER homeostasis is not restored, UPR promotes cell death. The mechanisms of UPR-mediated cell death are poorly understood. http://www.molbiolcell.org/content/early/2014/03/10/mbc.E13-11-0664.abstractDionisio_{December 22, 2014
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Well Joe, AVS got you there. If no scientist ever claimed that ATP synthase evolved it follows that no scientist ever claimed that ATP synthase evolved by the process of natural selection.Mung_{December 22, 2014
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Joe according to you, scientists have made the claim that ATP synthase evolved by the process of natural selection, yet these scientists failed to provide evidence of this claim. I am simply asking for one example of this. If you can't provide a single example to back up what you said, then feel free to retract your statement.AVS_{December 22, 2014
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AVS:
Can you point me to a piece of scientific literature that says “natural selection can produce protein complexes like ATP synthase” without providing any evidence?
Can you show me ONE in which they do? What other creative mechanism do you have? Natural selection is the only one I am aware of.Joe_{December 22, 2014
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Post-translational Regulation of the Gamete Fusogen GCS1 doi: 10.1128/EC.00330-13 Recent studies of the gamete fusogen GCS1/HAP2 indicate that this protein is deeply conserved across eukaryotes, and its exclusive and/or functional expression generally resides in males or in male homologues. However, little is known regarding the conserved or primitive molecular traits of males and females within eukaryotes. http://ec.asm.org/content/early/2014/03/10/EC.00330-13.abstractDionisio_{December 22, 2014
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Ok, let's start with the first one. Can you point me to a piece of scientific literature that says "natural selection can produce protein complexes like ATP synthase" but does not provide any evidence for this claim?AVS_{December 22, 2014
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AVS:
Can you give me an example of “what they say without evidence?”
That natural selection can produce protein complexes like ATP synthase. That universal common descent is a fact when they don't even know A) what makes an organism what it is and B) can't get beyond populations of prokaryotes given starting populations of prokaryotes without making magical claims. That is a startJoe_{December 22, 2014
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Post-translational regulation of COX2 activity by FYN While increased COX2 expression and prostaglandin levels are elevated in human cancers, the mechanisms of COX2 regulation at the post-translational level are unknown. http://www.impactjournals.com/oncotarget/index.php?journal=oncotarget&page=article&op=view&path%5B%5D=1983Dionisio_{December 22, 2014
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Wow, you should make a list of those 400 PTMs and post them. That would be very useful.AVS_{December 22, 2014
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Post-translational modifications, or PTMs, create the enormous structural and functional diversity required to integrate information regarding the nutrient/stress status of the cell and regulate essential cellular functions. There are more than 400 known PTMs, and, almost without exception, virtually all polypeptides are post-translationally modified. https://www.asbmb.org/asbmbtoday/201402/ SpecialSymposiaSeries/PostTranslation/Dionisio_{December 22, 2014
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Can you give me an example of "what they say without evidence?"AVS_{December 22, 2014
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AVS:
I think it’s funny how certain people here rely almost entirely on scientists to “prove their point” via direct copy/paste, and yet these certain people are also so comfortable disagreeing with these scientists on evolution.
Yes we agree with what they can demonstrate and are skeptical of their claims that they cannot even model. What they say without evidence can be dismissed without evidence.Joe_{December 22, 2014
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