The DNA Network |
| “You never know where the science will lead you…” [genomeboy.com] Posted: 06 Jun 2008 07:34 PM CDT |
| Now some comments from Raoul, the organic farmer [Tomorrow's Table] Posted: 06 Jun 2008 06:45 PM CDT Rather than another story about Me, the blogger here is a link to an interview conducted by The US News and World Report with my coauthor and husband, Raoul. In it, he discusses our book "Tomorrow's Table: Organic Farming and the Future of Food." Have you ever wanted to know what an organic farmer has to say about genetically engineered crops? Here is your chance. |
| What’s on the web (2008 June 6) [ScienceRoll] Posted: 06 Jun 2008 03:23 PM CDT
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| Epernicus: Where Science Meets [ScienceRoll] Posted: 06 Jun 2008 02:36 PM CDT There are more and more community sites dedicated to scientists, so they have to come up with at least one unique feature that may make them more useful than the other similar services. Here is a good example, Epernicus, that was created by researchers at Harvard and MIT:
The reason I really liked it was the BenchQ option where you can contact the whole community easily and fast:
Give it a try and let us know whether you like it. Further reading:
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| Scintilla’s Conversations has been nicely updated [Synthesis] Posted: 06 Jun 2008 02:16 PM CDT What Conversations does is to take an identifier, be it PMID, URL, or DOI, and pull in related information about the paper such as Postgenomic posts, Connotea bookmarks, citations, and related commentary around the web. Last time I looked, it was a bare-bones proof of principle, but I’m glad to see it’s looking like a proper webapp now. Great Job, Alf! .gif) This post is about scintilla, webappRelated posts |
| House, MD in different languages [ScienceRoll] Posted: 06 Jun 2008 02:12 PM CDT |
| Posted: 06 Jun 2008 02:03 PM CDT I mentioned this at lunch today, a drinking game called 'Wisest Wizard'. I'm pretty sure there are more complete rules somewhere else. But you get the idea. |
| Cancer Research Carnival #10 [Bayblab] Posted: 06 Jun 2008 01:27 PM CDT  Welcome to the latest edition of the Cancer Carnival: Your monthly carnival of news cancer care, treatment and latest research. Thanks to Ben for the logo design.Giovanna di Sauro gets us started off with a compound that's been in the news lately: Bisphenol A. She provides a nice literature review about the xenoestrogen and it's potential role as a carcinogen. She writes: Do you remember the recent studies published in the journal Cancer Research, which received strong media attention? One showed that BPA induces changes in gene expression in breast cancer cell lines coherent with those of high-grade lesions; the other suggested that BPA is also able to alter the epigenetic profile in the progeny of BPA-treated epithelial cells.Is BPA a cancer concern? Is it just the tip of the iceberg in a sea of xenoestrogens? Check out her post Who's afraid of Bisphenol A (part 2). (Check out part 1 as well). Giovanna follows that up with a review of a TED talk by Eva Vertes, a Princeton sophomore. 'Is cancer a cure?' explores the idea that cancer is part of a natural response to tissue damage. Wound repair gone awry. What follows is a discussion of that idea and why it may be overly simplistic. But if cancer is the result of over-active stem cells recruited to wound areas, how do they get there? Alexey at Hematopoeisis answers the question: What mediates stem cell tropism to tumors? CXCR4-SDF-1 interaction is also well known like an axis for tumor metastasis. Also some adult stem cells, neural and mesenchymal for instance, were shown to specifically migrate to tumor site. This ability has been exploited to selectively deliver a therapeutic gene to metastatic solid tumors.He also reports on two molecules recently shown to mediate stem cell migration to tumor sites: Urokinase Plasminogen Activator (uPA) and its receptor, uPAR. As the repertoire of molecules involved in pathotropism expands, specific targeting of cell-based therapies becomes more of a reality.  Sticking with a stem cell theme, Alexey tells of new research that shows the potential for targeting quiescence of cancer stem cells. Why is this important?Because the majority of anti-cancer drugs target actively-dividing (cycling) cells, quiescent CSC stayed alive and caused relapses and progression of disease. It would be cool to target CSC precisely based on their unique qualities and eradicate cancer. Quiescence could be the new potential target for anticancer therapy.The paper, published in Nature, targets PML to impair quiescence and make leukemia cells more sensitive to standard treatment. Read more about it at Hematopoeisis. On the cancer detection side of things, Walter at Highlight Health, reminds us of the importance of regular check-ups. Consider these statistics: when CRC [colorectal cancer] is detected early, the 5-year survival rate is 90%. If the cancer has spread locally, the 5-year survival rate decreases to 68%. For patients with advanced CRC that has metastasized, the 5-year survival rate is 10%To this end, he describes a new blood test for colorectal cancer based on 6 biomarkers that is being developed for laboratory use. From a dietary perspective, flavonoids are the molecule-du-jour. Research out of UCLA published in a recent issue of Cancer suggests that certain flavonoids found in fruits, vegetables and tea may be protective against smoking-induced lung cancer. ThinkGene has more: Researchers found that study participants who ate foods containing certain flavonoids seemed to be protected from developing lung cancer. Zhang said the flavonoids that appeared to be the most protective included catechin, found in strawberries and green and black teas, kaempferol, found in Brussels sprouts and apples, and quercetin, found in beans, onions and apples.Of course, the article also reminds us that for smokers the best course of action is quitting. Finally, Rob reports from the recent Canadian Gene Therapy and Vaccines Symposium about using IL-24 as a cancer therapeutic. Rob writes: IL-24 is a potentially useful agent for differentiation therapy for cancer treatment. Dr. Fisher reported, both at the conference and in publications, that ectopic expression of IL-24 has antiproliferative and proapoptotic effects in cancer cell lines but not in normal cells.No 'magic bullet' is without controversy though, and Rob discusses some of the issues surrounding IL-24 even as it heads to Phase III clinical trials. That concludes the 10th edition of the Cancer Research Blog Carnival. If you'd like to host in the future, send an email to bayblab[at]gmail.com and submit posts to future editions here. |
| Ice on Mars [Mailund on the Internet] Posted: 06 Jun 2008 09:36 AM CDT Phoenix’s found ice on Mars. Will we find life? Will life on Mars be different from life on Earth? There’s a chance that the planets can contaminate each other with life, but it would be really exciting if we some day discover life completely different from life on Earth. I’m not really sure what to think of astrobiology, but I find it very exciting… |
| You know the conference you are at is too big when .... [The Tree of Life] Posted: 06 Jun 2008 09:32 AM CDT    Now - I confess I was really impressed with how ASM handled this enormous meeting I was just at. If you are going to have a big meeting, ASM does a smashing job. And I can see how such big meetings can have their appeal - the diversity of work and activities relating to Microbiology are amazing. However, big meetings are still not my cup of tea. So here is my top 10 list of "You know the conference you are is too big when ...". All are based on experiences from this meeting.
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| Lead Astray [Sciencebase Science Blog] Posted: 06 Jun 2008 08:40 AM CDT
Anyway, the article in question (Instruments and Applications - Lead astray, from the now defunct Today’s Chemist at Work, can be downloaded here as a PDF) discussed TIMS’ analytical prowess and the serendipitous discovery by Australian researchers that it is not only those looking down the barrel of a gun who can end up with a nasty dose of lead, but perhaps even those holding the shooters themselves. With that article, it seems I hit a rather raw nerve in ending my feature with a rather glib question asking whether this might be a “healthy argument against bearing arms.” In finishing with this throwaway query I was apparently jeopardising the very US Constitution. At least that’s the impression I got when my Editor began to forward the deluge of letters of complaint. I was accused of ignorance (not the first time), of having a political agenda (never), and even of being a “liberal” (perish the thought). One shooting chemist emailed in all uppercase letters to show his indignation: “THE LAST SENTANCE SHOW YOU TO BE A LIBERAL WHO THINKS THAT GUNS ARE AN EVIL.” Iron-ically, or should I say lead-ingly, another correspondent critical of the inaccurate portrayal of guns in fiction came to my rescue: “Keep up the good work, and kudos to David Bradley for a well-written article!” he proclaimed. So everything I wrote wasn’t all bad, after all. Spelling, grammar, capital errors, and green spidery ink aside, the comments received highlighted an issue about which many readers of the magazine were, and probably still are obviously very passionate. I must confess, nothing I have written before has generated quite so many letters, perhaps with my repeating the misconception that a poison frog = a poison dart frog (not always, the case apparently). Was I naïve to throw scorn, albeit flippantly, on the idea of bearing arms? My Editor and her colleagues were as stunned as I at how many letters the article generated, especially given that the magazine was targeted at industrial chemists and not the general public. However, the 99,967 or so subscribers who didn’t write in obviously didn’t feel that the attitude gap between opposite sides of the Atlantic was quite as wide as the few who did. A post from David Bradley Science Writer |
| Genomics by Press Release in Science. [T Ryan Gregory's column] Posted: 06 Jun 2008 08:09 AM CDT Jonathan Eisen, who blogs at The Tree of Life, has coined the phrase "Genomics by Press Release", and has even given out two ignominious awards for particularly egregious examples. |
| Map that Campus XLVI [The Daily Transcript] Posted: 06 Jun 2008 07:32 AM CDT The first one since April. Here it is:
hint: Blogs are hot. So if you know the identity of the mystery campus please leave a comment. If you're at this campus, maybe I'll see you next week! Read the comments on this post... |
| 23andMe, deCODEme and Navigenics at Cold Spring Harbor [Genetic Future] Posted: 06 Jun 2008 03:17 AM CDT Just in case anyone has been wondering why I've been so quiet, I'm in beautiful Cold Spring Harbor this week for the Biology of Genomes meeting. Be warned that I'll have a lot more to say about this meeting once I've recovered from the combined effects of jet-lag and the punishing schedule (last night's evening session finished at 11:30pm!), most of which will include the words "next", "generation", "sequencing" and "wow".
I also chatted with both Stephan and Avey after the session - for what it's worth, they're both extremely personable, and there was no overt animosity between any of the three competitors (somewhat to the disappointment of the audience, I suspect).  Subscribe to Genetic Future. |
| Free personal genomics! [Genetic Future] Posted: 06 Jun 2008 03:17 AM CDT Over at Eye on DNA, Hsien wonders about the effects of a slowing economy on the personal genomics market. Well, no matter how hard it's getting to make your mortgage repayments, you can probably still afford personal genomics if it doesn't cost you anything:
(From a recent piece in Wired). You can sign up here; there is a pretty extensive FAQ here. Note that you will need to physically attend an enrollment session at the Coriell Institute in New Jersey. Also, I see that Coriell is adopting the paternalistic "need to know" approach pioneered by Navigenics, and won't provide participants with any information about genetic variants that aren't "medically actionable" (e.g. incurable disease risk variants), although they will hand out information on non-disease traits like eye colour. Still, if I lived anywhere near New Jersey I'd be signing up right now rather than wasting time writing this post. (As an aside, I wonder why Coriell is using a saliva-based method when it could be using its considerable expertise to create and store cell lines from blood - essentially generating an endless source of DNA for researchers to analyse. That seems like a missed opportunity that someone will be seriously regretting in a few years when there's no DNA left for whole-genome sequencing, or epigenome analysis, or whatever.) If you're more ambitious, you could also sign up for (eventual) free genome sequencing via the Personal Genome Project. Subscribe to Genetic Future. |
| Brain scanning vs personal genomics [Genetic Future] Posted: 06 Jun 2008 03:16 AM CDT  Personal genomics companies like 23andMe, deCODEme and Navigenics have taken substantial media flak recently over their limited ability to make useful disease risk predictions based on genome scan data. Subscribe to Genetic Future. |
| DNA Excerpt: Fermat’s Last Theorem [Eye on DNA] Posted: 06 Jun 2008 03:05 AM CDT
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| Around the Blogs [Bitesize Bio] Posted: 06 Jun 2008 02:47 AM CDT In this week’s around the blogs: How to talk to your professor, fragrant E.coli and chromatography-inspired poetry. Short and Schweeeeet. The Female Science Professor gives some hilarious advice to students on the etiquette of talking to their professors. Flash DNA sequencing. This post at Discovering Biology In a Digital World flags up some neat flash animations of Sanger DNA sequencing that are worth taking a look at. …and even more movies. Andre at Biocurious highlights some amazing movies and illustrations of RNA and fatty acid dynamics on the website of Janet Iwasa, scientist-turned-graphic designer and animator. Janet publishes her work under a Creative Commons license that allows the movies to be used for non-commercial purposes, like teaching. What we don’t know, Part I and Part 2. Alex at The Daily Transcript weighs in with two excellent posts that he promises the first in a series concentrating on topics where our understanding is less than complete. Part I is on organellar shape and part 2 on glycosylation. Minty fresh E. coli. Aminopop picked up on a story about a group of MIT students who engineered an E. coli strain that smells like mint. This strain is a must for fermentation scientists everywhere! Philosophies on Open Access. Cortunix draws out an expert from an article written by Peter Suber on the benefits of Open Journal Access. Poetry in Motion. David at The World’s Fair tells us about the world’s largest [or only??] collection of chromatography-inspired poems. |
| Researchers observe spontaneous ‘ratcheting’ of single ribosome molecules [Think Gene] Posted: 06 Jun 2008 01:46 AM CDT Researchers report this week that they are the first to observe the dynamic, ratchet-like movements of single ribosomal molecules in the act of building proteins from genetic blueprints. Their study, published in the journal Molecular Cell, reveals a key mechanism in the interplay of molecules that allows cells to build the proteins needed to sustain life. Cells use a variety of tools to build proteins, beginning with messenger RNA, a ribbon-like molecule that codes for the sequence of amino acids in the protein. Another molecule, transfer RNA (tRNA) is uniquely qualified to read this code, but can do so only within the confines of the ribosome. Transfer RNAs bring individual amino acids into the ribosome where they are assembled into proteins. Various other proteins also participate in the process. When protein translation occurs, single tRNAs enter specific sites in the ribosome, read the code and deliver their amino acids – one by one – to a growing protein chain. The ribsome transits along the messenger RNA as the protein is built, releasing the “deacylated” tRNA through an exit site. A ribosome is made up of two subunits composed of ribonucleic acids (RNAs) and about 50 individual proteins. The ribosome was once considered a static “workbench” for the assembly of new proteins. A recent study by researchers at the Wadsworth Center in Albany, N.Y., using cryo-electron microscopy, showed the ribosomal subunits in two distinct positions relative to one another, however. They proposed that the motion of the subunits depended on a protein catalyst, elongation factor G (EF-G). In the new study, a team led by University of Illinois physics professor Taekjip Ha used fluorescence resonance energy transfer (FRET) to observe in real time the movement of the ribosomal subunits that is essential for protein synthesis. The team collaborated with Harry Noller, of the University of California at Santa Cruz, who provided expertise on the ribosome. FRET makes use of fluorescent molecules whose signals vary in intensity depending on their proximity to one another. By labeling each of the two subunits of a single ribosomal molecule with these fluorescent markers, the researchers were able to watch the subunits move in relation to one another. When Ha and postdoctoral fellow Peter Cornish observed the signal from the labeled ribosomes, they saw a spontaneous back-and-forth rotation between the subunits – even in the absence of the elongation factor, EF-G. “Other researchers proposed that this rotation is induced by EF-G – that you have to have EF-G to cause this rotation,” Ha said. “But we showed that no, that’s not the case. Actually the ribosome can rock back and forth spontaneously, and can do it quite rapidly.” The researchers were able to view this motion even in the absence of tRNA. The ribosomal subunits were spontaneously switching back and forth between the classical (that is, non-rotated) state and a hybrid (rotated) state. When they added a single tRNA with an amino acid permanently attached to it, the ribosome became “essentially stuck in the classical, non-rotated state,” Cornish said. “And as soon as we removed that, it started to move spontaneously.” To better understand the role of EF-G, the researchers added a modified EF-G molecule that could not deliver its normal energy payload to the ribosome. The modified EF-G bound to the ribosome only in the rotated, hybrid state. These findings led the researchers to propose that EF-G has a critical role in the process of protein translation: It stabilizes the rotated position of the ribosomal subunits relative to one another. This allows the tRNA molecules to add amino acids to the growing protein and to exit, making room for the next tRNA specified in the messenger RNA code. The researchers believe that EF-G acts as a linchpin, temporarily holding the ribosome in its rotated position until the deacylated tRNAs reposition themselves in the molecule as they move toward the exit. Once the tRNAs have accomplished this, the EF-G goes away, the ribosome ratchets back into its non-rotated position and the process begins again. The researchers propose that this ratcheting motion allows the ribosome to advance along the messenger RNA as protein translation progresses. Without EF-G, the ribosomal subunits move in relation to one another, but are unable to progress along the messenger RNA as a protein is built. “Many people would argue that the ribosome is one of the most important machines in our cells,” Ha said. “What’s really amazing is that it is such a massive complex that is still able to move spontaneously, to rock back and forth at a fairly rapid rate. And that movement is not just some random movement, but it’s the most important movement of the ribosome for its locomotion.” Future studies will use FRET by labeling both the ribosomal subunits and the messenger RNA to see if the movement of the subunits and the ribosome’s transit along the messenger RNA are synchronized, Ha said. Source: University of Illinois at Urbana-Champaign Josh says: Below is a video of an “interpretive dance” preformed at Stanford in 1971 showing the synthesis of a protein/polypeptide from mRNA by a ribosome. If any biology students or professors have never seen this, it’s definitely worth watching (and is also pretty funny). You can probably skip past the introduction in the beginning. |
| Off to give (yet another) talk [Mailund on the Internet] Posted: 06 Jun 2008 01:05 AM CDT In a few minutes I’m off to give a talk at CLC Bio.
It is essentially the same talk as I gave at the Department of Biology a few weeks ago. These days I feel like I am talking more about association mapping than I manage to work on it. At least the talk I’m giving in Copenhagen next week is on a different topic… |
| Programming for (non-computer) scientists [Mailund on the Internet] Posted: 06 Jun 2008 12:56 AM CDT A few days ago, bbgm wrote about Programming and Science Education and how people advocating that students use Excel (or similar) instead of “real” programming languages. I quote:
I guess I agree, but I haven’t made up my mind to which degree I agree. How much programming do you really need?You can do a lot with spreadsheets and they are a really powerful tool once you get used to them. I have never bothered myself, but I have seen what my colleagues manage to do with them. So they may be sufficient for what you need and then it makes sense to learn how to get the most of them. That being said, it is not a substitute for a programming language, and when you need a proper programming language you need a lot of hacking to do the same tasks in a spreadsheet. If you need a complex statistical analysis of your data, you are better off using a language/environment such as R than trying to do the analysis in Excel. Sure, Excel can do a lot of statistics, but only the most common types of analysis. If you need more, you need something like R. Depending on how much manipulation of your data — and how much mathematical modelling you need to implement yourself — R might not be enough. If you need to combine a lot of output of various programs, do a few manipulations on the output, and analyse that, you probably want to consider a scripting language like Python or Perl. For heavy duty scientific programming, you want MATLAB or Octave or such. When you need the extra speed, and your language does not already have an optimised solution, C or C++ is useful (either for a full application or for a module in your scripting or statistical language — they usually will allow you to make extensions in C/C++ that you can then use as any other module). How much programming you need to do in scientific work varies a lot and there is not really any reason to spend time learning something that you will never use. Maybe a spreadsheet is all you will ever need. Just make sure that you are doing the analysis you want to do, not the one your tools limits you to, and if you need more, then spend the time learning how to program! Learning how to programRemember, though, that learning to program a computer takes time. It can take a lot of time before you do it well. There is a lot more to it than learning the syntax of a programming language. You need to know the right way to solve given problems in your language of choice — the optimal way in one programming language can be very different from the optimal way in another, depending on libraries, language features, underlying philosophy of the language, etc. — and in general you need to learn how to think like a programmer. It might be a different kind of problem solving skills than what you are used to. Most of all it takes practise. This can be frustrating if you pick up a language to solve a specific problem that you are more interested in than learning how to program. If you only very rarely need to program, don’t bother. Find someone to help you out. This is how we bioinformaticians get involved in various projects so although we complain about being over worked, we don’t really mind so much. It is not different from having to consult a statistician from time to time to make sure that you are analysing your data correctly. If you do not need it that often, your time might be better spend on other tasks. If you often need to solve programming problems, you should learn how to do it properly. You get a better feeling for the problems and for the data when you work with it, and you don’t want to out-source that to other people. If you decide you need programming in your research — and I think more and more sciences rely on IT so maybe you do before you know it — then practice practice practice. Experiment with your programming language. Read discussion fora and user groups. Read other peoples code and see how they solve similar problems. Just as it takes time to learn how to use a spreadsheet properly — and just learning all the features it offers — it takes time to learn how to program. Usually more so, as programming languages are much more powerful. Spend the time! There is no fast way around this, there really isn’t. |
| Another new wrinkle in treating skin aging [Think Gene] Posted: 06 Jun 2008 12:53 AM CDT Topical applications of a naturally occurring fat molecule have the potential to slow down skin aging, whether through natural causes or damage, researchers report. Through both the normal aging process and external factors like UV damage, smooth, young skin inevitably becomes coarse and wrinkled. The basis of this wrinkling is that time and damage both lower the production of new collagen while increasing the levels of enzymes called MMPs that chew up existing collagen. Covering up, slowing down, or even stopping the wrinkling process has become a big business, and as part of this research endeavor, Jin Ho Chung and colleagues tested seven naturally occurring lipids (greasy molecules that play many important biological roles) in their ability to reduce skin aging. In samples of skin cells, three of the lipids could prevent UV-radiation from both reducing collagen expression and increasing the levels of MMPs; they even increased collagen in undamaged skin cells. Of these three, the molecule phosphatidylserine (PS) seemed the most promising, so the researchers tested it on human skin. They applied a 2% PS solution to small areas of the buttock in both young and old volunteers; the young skin was subsequently given a dose of UV-radiation to simulate sun damage. In both natural and UV-induced aging, PS treatment prevented collagen reduction and an increase in MMPs when compared to no treatment. While larger and longer trials are needed to confirm any therapeutic benefits, these initial findings suggest topical PA application might be a simple and natural way to slow down the biological elements underlying wrinkling. Source: American Society for Biochemistry and Molecular Biology Josh says: I’m sure a lot of women will love to hear this. It would make a great alternative to using Preparation H to get rid of wrinkles (see page 2). |
| How cell’s master transcribing machine achieves near perfection [Think Gene] Posted: 06 Jun 2008 12:12 AM CDT One of the most critical processes in biology is the transcription of genetic information from DNA to messenger RNA (mRNA), which provides the blueprint for the proteins that form the machinery of life. Now, researchers have discovered new details of how the cell’s major transcriptional machinery, RNA polymerase II (Pol II), functions with such exquisite precision. With almost unerring accuracy, Pol II can select the correct molecular puzzle piece, called a nucleosidetriphosphate (NTP), to add to the growing mRNA chain, although these puzzle pieces can be highly similar molecules. Two papers in the June 6, 2008, issue of the journal Molecular Cell, published by Cell Press, describe advances in understanding Pol II copying fidelity. The papers are by Craig Kaplan of Stanford University and his colleagues; and Mikhail Kashlev of the National Cancer Institute Center for Cancer Research and his colleagues. The researchers said their findings not only offer unprecedented details about the fidelity mechanism of Pol II, but likely about fidelity in all cellular genetic copying machines. They said their discoveries also offer understanding of how defective Pol II can generate errors in transcribing mRNA—errors that can promote cancer formation. In their paper, Kaplan and colleagues explored a key component of the active site known as the “trigger loop.” This small bit of protein is highly mobile, and although researchers have believed that it plays a critical function in discriminating the correct NTP, that function was poorly understood. In studies with yeast, Kaplan and his colleagues produced a mutant form of Pol II with a subtly crippled trigger loop. This mutation substituted one amino acid with another in what was believed to be a key position in the trigger loop, His 1085, for interacting with incoming NTPs to discriminate the correct one. The researchers compared the detailed molecular function of normal and His 1085 mutant Pol II enzymes during the encounter with both correct and incorrect NTPs. They also compared the behavior of the mutant with the action of the mushroom toxin alpha-amanitin, which is theorized to block Pol II by interfering with the trigger loop. The researchers’ studies of the mutant and alpha-amanitin revealed crucial details showing how the trigger loop determines fidelity, said Kaplan. “We found that the amanitin-treated wild-type enzyme behaved very similar to our mutant enzyme,” said Kaplan. In fact, he said, the experiments, as well as structural information on the active site, indicated that alpha-amanitin targets the same His 1085 position in the trigger loop as does their mutation. Kaplan concluded that the findings reveal a specific and critical role for the trigger loop. “These findings reveal what is called a ‘kinetic selection’ mechanism for Pol II, which is like many polymerases,” he said. “That is, the active site in one condition has a similar affinity for both correct and incorrect NTPs. However, because of motion within the active site—in this case the action of the trigger loop—catalytic activity in the active site proceeds much faster with the correct NTP than with the incorrect NTP. The trigger loop is mobile, and only when it is positioned properly in response to a correct substrate can it really function. “We think this mode of substrate recognition is a general theme for systems that have to select the right molecule out of a giant pool of the wrong molecules,” said Kaplan. An example, he said, is when the protein-making ribosomal machinery must select the correct transfer RNA from among similar-but-incorrect transfer RNAs. Besides Kaplan, other co-authors on the paper were Karl-Magnus Larsson and Roger Kornberg. In the other Molecular Cell paper, Kashlev and colleagues used a different yeast mutant to explore the function of the Pol II active site. In their screen for Pol II mutants, they identified one, E1103G, that shows a several-fold increase in error rate over the normal, wild-type Pol II. Importantly, said Kashlev, the researchers could precisely measure the transcription error rate using a new assay, called a retrotransposition assay, developed by co-author Jeffrey Strathern. The researchers’ analysis of the effects of E1103G yielded significant insights into the function of the trigger loop, said Kashlev. “Normally, when an NTP diffuses into the active site of the polymerase, the trigger loop closes behind it like a door, long enough for the polymerase to perform the chemistry to add the NTP to the end of the RNA chain,” he said. “If the NTP is incorrect, there is a tendency for this door to stay open for a longer time, which means that the NTP has a chance to diffuse out of the active site before the polymerase can proceed to chemistry. “Our mutation occupies a strategic position important for keeping the loop open, like a latch,” said Kashlev. “So, in the mutant, the door wants to stay in the closed state for a longer time, which means if an incorrect NTP migrates into the active site, there is time for the polymerase to add this incorrect NTP to the RNA chain.” Kashlev said the motivation for their studies of Pol II transcription fidelity is to understand the effects of Pol II errors on genome stability. Specifically, error-prone Pol II could generate mRNA that produces aberrant versions of the critical enzyme DNA polymerase. As DNA polymerase is responsible for gene replication, the result of its malfunction could be a burst of gene mutation causing an “error catastrophe” that could lead to genome instability and cancer formation. Source: Cell Press Josh says: Perhaps it’s just because I had a class that focused primarily on DNA replication and RNA transcription, but I find this fascinating. I immediately recognized that the one paper came from Roger Kornberg’s lab. This also reminds me of a video from The Walter and Eliza Hall Institute of Medical Research (WEHI) of DNA transcription into RNA. More videos can be found at their site. Sorry for linking to a quicktime movie, but youtube (nor Linux) will play the Quicktime movie correctly, and wordpress won’t let me embed a quicktime movie Andrew says: Somebody from Reddit in the comments suggested we post this video: How Cell Achieves Perfection This posting includes an audio/video/photo media file: Download Now |
| Andrew’s 23andMe Kit [Think Gene] Posted: 05 Jun 2008 11:00 PM CDT I bought a 23andMe kit in March. Here’s what the kit looks like:
A close-up of the Oragene collector
The text of the Information card.
I filled the spit collector and returned the kit. Unfortunately, I happened to send my kit during the 23andMe CLIA-certified lab change, so my results took over a month to process. |
| american life [the skeptical alchemist] Posted: 05 Jun 2008 10:06 PM CDT How about some food for thought while you wonder what the heck happened at Hillary's house today? Only one thing: make sure to watch the video till the end, or you will miss the most important part. Cheers. In this video, the very last part has been censored. If you want to find out what really happens in the end, you should watch the last part of the video here. View blog reactions |
| Cuddle up to a phage! [Omics! Omics!] Posted: 05 Jun 2008 10:02 PM CDT While searching Amazon for a book, I came across a very funny (in a geeky way) line of plush toys: all sorts of microbes! GiantMicrobes.com has quite a taxonomy of them. I think my visual favorite is the T4 phage  , but there's lots of other fun stuff here. You can get a whole range of common (E.coli) and nasty (a whole line of venereal disease agents. Human pathogens are not monopolized: to terrorize Miss Amanda (or make voodoo chew toys) there's mange, rabies & heartworm. The E.coli are a flagellated strain. You can buy one or a trio (Petri dish)  . Surprisingly, there isn't a package deal on T4+E.coli, nor do they (yet?) have a pBR322 to accessorize your E.coli. Perhaps a future product line extension will include GFP-expressing glow-in-the-dark variants, or perhaps some scent-enhanced ones. |
| How to Date Your Fat Cells With Nuclear Bombs [adaptivecomplexity's column] Posted: 05 Jun 2008 09:26 PM CDT Scientists have been trying to understand how and when we gain or lose fat cells, and now a paper in this week's issue of Nature reports that nuclear bombs are the key to solving this problem. To understand how our bodies regulate our weight, researchers are interested in knowing how the number of fat cells changes over our lifetime - do we stop making more fat cells after adolescence? Do we keep the same fat cells all of our adult lives, or do some die off and get replaced by new ones? The typical way to study the birth and death of cells in live animals is to use radioactive tracers that label DNA, but these experiments are too toxic to try in humans. It turns out though, that the US and Soviet militaries did the experiment for us, with above-ground nuclear bomb tests in the late 1950's, tests which spewed large amounts of radioactive carbon in the atmosphere. That radioactive carbon is now in our DNA (at least for those of us alive during the cold war), and it provides a convenient "manufactured on" date for our long-lived fat cells. |
Reminiscences on a serious Stateside gun crime: You would think you wouldn’t find a less controversial topic to write about than the analysis of heavy metals using thermal ionisation mass spectrometry (TIMS). In some ways it must sound like the dullest topic in the world, beyond those who work with MS. However, when the metal in question is lead, and its source is ammunition then I should have been prepared for a flame-war from the US readership of one particular specialist publication for which I wrote on the subject a few years ago. The bottom line is don’t make flippant remarks connecting guns and ill health unless you want to be shot down in flames.
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