John Smith’s genome sequenced

Springville University’s Genome Center in collaboration with Prof. I. M. A. Bigschotte from IvyLeague University have announced that the genome of Mr. John Smith from Centertown, USA has been sequenced and is now available online.

Dr. James Williams, director of the Center said: “We were running out of things to sequence, but I still had a budget to justify before the end of the fiscal year”.

“This project will give us insights into the 99% of the population we care nothing about, and frankly, I would not want to meet” says Prof. Bigschotte. “I don’t even know where Centertown is”.

“Johnny graduated from the local high school, and now working at the KFC”. Said Mr. Smith’s mother,  Mary, in whose basement Mr. Smith lives. “He cuts the grass and takes out the trash sometimes, but I really have to nag him to get to do something”.  “I wish he will just move out” added Mrs. Smith.

Mr. Smith, who may or may not start classes at the local community college this fall, was unfazed by his recently found fame. “Like, I guess it’s nice to have all this stuff online, but, like, I couldn’t get it to fit on my Facebook wall”, said Mr. Smith, while digging into a party-size bag of Cheetos.

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Guest Post: Thoughts on the Superjournal

Guest post by Leighton Pritchard

The new top-tier competitor to Science and Nature proposed by three leading funders of scientific research last week is a great idea, but I think runs a risk of opening the scientific process to a potentially damaging slander by opponents of science.

As practising academic scientists we’re all concerned, and intimately entangled, with the scientific publication process. We are authors, reviewers, editors, sometimes journal chiefs and, in a very real sense, our entire careers may hang upon whether and where our work is published. Impact factors, journal reputations, author counts and ordering, and other actuarial metrics are foremost in our minds every time a promotion case or job application is submitted. The cost of publishing work raises its head every time we have to dip into consumables to fund a colour figure. Each time we submit to peer review we set sail anew, all paranoid, on the Sea of Judgement by Anonymous Colleagues and Competitors. We are, as a group, highly sensitive to changes in the scientific publishing ecosystem. So it’s no surprise that the scientific world and its experimental dog have opinions on this potential competitor to Science, Nature and Cell.

And, at first glance, the new journal could be a beautiful thing.

The journal is planned to be fully Open Access, underwritten at least initially by the funding bodies, so there will be no, or reduced, author charges. Author charges can be a problem where projects lack money allocated to publication costs. I’ve usually been lucky enough to obtain support for Open Access publication, but this still adds a level of political and financial consideration when deciding where to submit work. Where funding bodies require OA publication (and this is increasingly a condition of funding) I think it is only right that they support this route financially, and the Howard Hughes Medical Institute, Wellcome Trust, and the Max Planck Society are to be congratulated for taking this stand.

Michael Eisen points out that the new journal is a triumph for Open Access, and I think he’s right, there. Even in the short 15 or so years that I’ve been an active researcher, the internet has transformed me from a troll at the library copy machine into a blasé, and heavy, consumer of online PDFs. As befits one of the driving personalities behind PLoS, he says a great many sensible and worthwhile things about the new journal in his blog article. But I do think he overstates the potential impact on peer review. In his article, Eisen identifies three key areas of peer review that this new journal wants to shake up:

1) Rapid review and turnover: I think there’s a realistic chance, particularly with a financial incentive, of encouraging scientists to prioritise reviews for this journal, reducing turnaround time. And if there’s a flat payment to the reviewer per manuscript reviewed, then there’s no perverse incentive to cycle through rounds of revision. I think this will work, but I do share Eisen’s worry that uncompensated review requests from other bodies could come somewhat down the list of Things To Do Today, as a result.

2) Fewer demands for changes and additional experiments: The press release from the funding bodies states their desire to limit reviewers’ calls for more work. But really, if a piece of work is unconvincing because it lacks a key experiment, then that’s the fault of the work and not the fault of the review process. A competent peer review process would bounce the manuscript until the supporting evidence is provided. All that an editorial policy of fewer requests for changes and experiments can do is either accept a manuscript with insufficient support and so dilute journal quality, or reject at an earlier stage in the process.

3) Arbitrary editorial decisions on the grounds of sexiness: The new journal will have an editorial team of experienced, active scientists, rather than “junior scientists who are no longer active researchers”. This is quite obviously a pointed comment about the editorial composition of publications such as Science and Nature, rather than fair comment about scientific publication on the whole. Most journals I deal with have editorial and review boards comprising active researchers, and I believe that outside the usual extremely high-impact suspects, it is the norm to have an editorial panel of experienced, active scientists. I don’t see this policy being particularly ground-shaking.

Where I think that the new journal will shake up peer review is in its intent to publish reviewers’ comments publicly, but anonymously. This cuts both ways: authors will no longer be able to “get away with” ignoring potentially serious criticisms from a minority reviewer, unnoticed, after publication; But nor will poor or unreasonable reviewers be able to hide behind the opaqueness of the current review process. If readers can comment on or rate the quality of reviews, as well as papers, honest and insightful reviewers could be rewarded at the expense of the half-hearted and overly pedantic.

But I do have one serious criticism, which comes not from being a scientist, but instead thinking about how the public sees science.

In recent times, public trust, or rather the lack of it, in science as a human endeavour has been exemplified by the events of ClimateGate, and European attitudes towards genetic modification. Popular media presentation of difficult ethical issues in science is, well, difficult, and it’s useful in the face of criticism to be able to fall back on demonstrable claims of the independence of results from financial inducements, and the anonymity and stringency of peer review in journals that are disinterested in the outcome of our work. And that is where I think the new journal risks offering an easy target to those who would seek to undermine public confidence in science.

In 2009, it was revealed that the publisher Elsevier had been paid by the pharmaceutical company Merck, Sharp and Dohme to “produce several volumes of a publication that had the look of a peer-reviewed medical journal, but contained only reprinted or summarized articles–most of which presented data favourable to Merck products” : The Australasian Journal of Bone and Joint Medicine. Intuitively, suspicions of vested interests can be expected to arise where there is no obvious and transparent independence in the chain that links the funder of research to the lab that carries out that research, and to the journal that publishes it. Even PLoS Medicine‘s policy on research funded by tobacco companies perpetuates this common perception that, unless the source of funding can be decoupled in some way from the outcome of research, and ‘review’ for publication, then publication amounts to little more than advertising.

When a piece of work is carried out by scientists funded by body X, reviewed by scientists funded by body X (who are even paid to review the paper by body X), and published in a journal bankrolled by body X, this intuitively looks like self-publication or advertising by body X. Where ‘body X’ is “Big Tobacco”, or “Big Pharma”, the conflict of interest is so self-evident that it has become a cliché. When ‘body X’ is “HHMI/Wellcome/MPS”, as a scientist I recoil at the potential association of such respected investors in science with cheap and shady practices. I don’t have any doubt that, as the journal’s press release states, the “editorial team will be editorially independent of the funders”, and that all published manuscripts will be competently assessed and of the highest quality. But from the point of view of those outside the circle of science, there is always an option to suggest sleight of hand, however ethically clean the journal is. Without independence and transparency in the cycle of funding and publication, we risk delivering an opportunity for slander into the hands of those who would undermine science for political goals.

DISCLAIMER: L.P. adds that the views represented here are his own, and do not reflect those of his employer, or those of any other of his professional affiliations.

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Music Monday Double Feature: They are Climate Scientists

Australian climate scientists lip-syncing “I’m a Climate Scientist” from Hungry Beast. (Warning: profane language.)

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Music Monday: 4th of July Special

The obligatory Hendrix.


Watch Jimi Hendrix – Star Spangled Banner in Music  |  View More Free Videos Online at Veoh.com

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Google+ at first blush: too complex and too simple

 

I have recently been invited to Google+, (thanks Ruchira!)  and as social timesucks go, it is quite enjoyable.  Here are my first impressions about g+. In a nutshell: g+’s attempt at compartmentalized communication is laudable, but falls short of the mark. Mainly because, no social network can emulate the real-life way we communicate (or not) with the people we know. Not that g+ ‘s goal  emulating real-life social interactions (for those of us who still have them), but let me explain myself.

Compartmentalized communication is what we do every day: my wife reminds me about my medical appointment, but not in front of the kids, because the little one still freaks out over doctors. At work I tell someone I need to cover for me teaching (because I need to take a day off) but not my other colleagues (none of their damn business). While waiting at the Doctor’s office I receive an email that my paper is finally published. I email the info to all the co-authors, and I may also just put it up on Facebook, because I am kinda proud. But of my 100 or so FB “friends” maybe 30 will understand why this is important to me.

The average Facebook user just likes to post stuff on his wall, assuming interested friends will be reading and posting back. Most FB friends are not real friends, in the social sense, but many are acquaintances, professional colleagues, and people you just do not want to turn away when you get a FB Friend Request.  G+ breaks those myriad people into circles: family, friends, acquaintances, followers. I also added “bioinformatics” and “science”.  This compartmentalization by circles initially makes sense because it is more in harmony with what our social life is supposedly like. We have our family, out really good friends, our drinking buddies, our professional colleagues, people we play sports with on weekends, etc. This is where the “too complex” part comes in: in FB, the network rigidly bins my connections into family, friends, friends of friends and everybody else. These are essentially fixed sets, concentric, that are more driven by privacy than anything else. In g+, the circles are supposed to be driven by interest rather than privacy. Stuff I’d like to share with my professional colleagues goes to the “bioinformatics” circle and/or the “science” circle. Personal stuff goes to “friends” or “family”. Like I said, this makes sense initially, because it follows our ideas of social interactions. But keeping people binned in your head, deciding who belongs where and who is privy to what information form which aspect of your life is something really fuzzy and complex. We do it every day, hopefully well, because we have been developing the social skills needed for compartmentalized communications since we were born. Just think back to the “paper published” situation. You want to inform your professional colleagues, family, maybe some closer friends, but your weekend running mates couldn’t care less. Except those two that you run with and are also scientists. Using FB you would just broadcast this information to all FB friends, and let those who care write comments on your post or wall. Supposedly g+ gives you a better option: post only to scientists, to friends, and family. But what about those two runners/scientists? OK, they may be also in your scientists circle but if they are not, that misses out. Compartmentalizing acquaintances in real life for information is complex enough, and I think that the g+ attempt to emulate this will not work well. This is where the “too simple” part comes in: to emulate your real-life compartmentlization, you need to perform dynamically complex intersections and deletions between those circles. Of course, doing this in real life is complex enough, and few, if any, would care to be bothered tweaking this on a social network for each and every post. Google+ circles is somewhat like the compartmentalization solution offered by FriendFeed rooms, but with a better interface.

What I foresee is a kind of facebook/friendfeed mashup. At most the average user will have handful of circles, with many messages going out to all where precision in targeting messages is sacrificed to ensure that all will get the message.

Oh, and nobody will give up Facebook quite yet, as inadequate as it is. So g+ should implement it’s FB and Twitter import/export plugins to draw in the crowds.

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CAFA Update

Nearly a year ago, I posted about the Critical Assessment of Function prediction with which I am involved. The original post from July 22, 2010 is in the block quote. After that, an update about the meeting which will be held in exactly 2 weeks.

The trouble with genomic sequencing, is that it is too cheap. Anyone that has a bit of extra cash laying around, you can scrape the bugs off your windshield, sequence them, and write a paper. Seriously?

Yes, seriously now: as we sequence more and more genomes, our annotation tools cannot keep up with them. It’s like unearthing thousands of books at some vast archaeological dig of an ancient library, but being able to read only a few pages here and there. Simply put: what do all these genes do? The gap between what we do know and what we do not know is constantly growing. We are unearthing more and more books (genomes) at an ever-increasing pace, but we cannot keep up with the influx of new and strange words (genes) of this ancient language. Many genes are being tested for their function experimentally in laboratories. But the number of genes whose function we are determining using experiments is but a drop in the ocean compared to the number of genes we have sequenced and whose whose function is not known We may be sitting on the next drug target for cancer or Alzheimer’s disease, but those proteins are labeled as “unknown function” in the databases.

The red line is the growth of protein sequences deposited in TrEMBL, a comprehensive protein sequence database. The blue line illustrates the growth proteins in TrEMBL whose function is know, or at least can be predicted with some reasonable accuracy. The green line is the growth in the proteins whose 3D structure has been solved. Note the logarithmically increasing gap between what we know (blue) and what we do not know (red). Image courtesy of Predrag Radivojac.

Enter bioinformatics. CPU hours are cheaper than high throughput screening assays. And if the algorithms are good, software can do the work of determining function much cheaper than experiments. But therein lies the rub: how do we know how well function prediction algorithms perform? How do we compare their accuracy? Which method performs best, and are different methods better for different types of function predictions? This is important because most of the functional annotations in the databases come from bioinformatic prediction tools, not from experimental evidence. We need to know how accurate these tools are. Think about it this way: even an increase of 1% in accuracy  would means that hundreds of thousands of sequence database entries are better annotated, which in turn means a lot less time in the lab or in high throughput screening labs going after false drug leads.

So a few of us got together and decided to run an experiment to compare the performance of different function prediction software tools.  We call our initiative the CAFA challenge: Critical Assessment of Function Annotation. There are many research groups that are developing algorithms for gene and protein function prediction, but those have not been compared on a large scale, yet. OK then: let’s have some fun. We, the CAFA challenge organizers, will release the sequences of some 50,000 proteins whose functions are unknown. The various research groups will predict their functions using their own software. By January 2011 all the predictions should be submitted to the CAFA experiment website. Over the net few months, some of these proteins will get annotated experimentally. Not many, probably no more than a few hundred judging by the slow growth of the experimental annotations in the databases. But we don’t need that many to score the predictions. A few dozen will do.

On July 15, 2011 we will all meet in Vienna, and hold the first-ever CAFA meeting as a satellite meeting of ISMB 2011. This will be the fifth Automated Function Prediction meeting we have been holding since 2005. Only this time, there won’t just be the usual talks and posters, there will be the results of a very interesting experiment. The International Society for Computational Biology is generously hosting our meeting, and judging by the response we are getting so far, we will need one of the larger halls.

Learn more at http://biofunctionprediction.org If computational protein function prediction is your thing, join the CAFA challenge. If you are just an interested observer, keep an eye on the site. In any case, please spread the word.  Finally, if your company wants some publicity, get in touch! We could use the sponsorship ^_^

Acknowledgements: I would like to thank the CAFA co-organizers, Michal Linial and Predrag Radivojac. The CAFA steeering committee: Burkhard Rost, Steven Brenner, Patsy Babbitt and Christine Orengo for supporting us, keeping us on the straight and narrow and for incredibly useful and insightful suggestions.  Sean Mooney and Amos Bairoch for hashing out the assessment.  Tal Ronnen-Oron and the rest of Sean Mooney’s group for setting up the CAFA website. The International Society for Computational Biology for sponsoring us. The community of computational function predictors that have participated in and supported past meetings on computational function prediction, the research groups that have registered to CAFA so far, and those that will register soon 🙂  Finally, Inbal Halperin-Landsberg for coining the name CAFA. I apologize in advance if I left someone out.

GO CAFA!

Fast forward to July 1, 2011: the meeting is so on. We have 38 teams participating in the challenge, with over 50 algorithms. We have about 600 proteins whose functions have been predicted. We have a great line up of speakers including Janet Thornton the Director of the European Bioinformatics Institute and Amos Bairoch, the founder of SwissProt. The full program is available. The Radivojac, Mooney and Friedberg labs have been working very hard, and we do have some really great results to report, and some surprising activities. We are also grateful to the NIH and the US Department of Energy for their support.

So if you are planning on being at ISMB this year, drop by  the AFP/CAFA SIG. We are messing with something brand-new, which is what science is all about.

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That being said, I still want a Google+ invite…

… because, um, I dunno. Just too nerdy I guess. Click here to send me one, if you are so inclined: http://is.gd/Ag43 Thanks!

.

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Suggest a name for the next BIG journal

The Max Planck society, Howard Hughes Medical Institute and Wellcome Trust have announced their plans for a new journal for biomedical and life science research to be launched summer 2012. From the joint press release:

The journal will employ an open and transparent peer review process in which papers will be accepted or rejected as rapidly as possible, generally with only one round of revisions, and with limited need for modifications or additional experiments. For transparency, reviewers’ comments will be published anonymously.

Nice. The journal will be online-only and open access too, and they promise  “an opportunity to create a journal and article format that will exploit the potential of new technologies to allow for improved data presentation.” I especially like the “limited need for modifications or additional experiments”, especially since even Nature has recently published a scathing opinion piece about reviewers’ almost reflexive demands for additional experiments.

With these three giants behind the journal, it’s a safe bet this journal will be up there with PLoS Biology, Nature and Science.

For now, Byte Size Biology readers are welcome to suggest a name for this new journal. Maybe you can strike a deal with the yet-to-be-named editor-in-chief: a lifetime  publication fee waiver if your name gets chosen.

 

 

Of course, I have no affiliation with this new journal, so don’t bet on it happening.

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Music Monday: Playing for Change

The Playing for Change Foundation is dedicated to musical education worldwide. From their mission statement:

A decade ago a small group of documentary filmmakers set out with a dream to create a film rooted in the music of the streets. Not only has that dream been realized, it has blossomed into a global sensation called Playing For Change, a project including musicians of every level of renown, that has touched the lives of millions of people around the world.

While traveling the world filming and recording musicians, the crew became intimately involved with the music and people of each community they visited. Although many of these communities had limited resources and a modest standard of living, the people in them were full of generosity, warmth, and above all they were connected to each other by a common thread: music.

Out of these discoveries, the Playing For Change Foundation was born and made its mission to ensure that anyone with the desire to receive a music education would have the opportunity to do so. The Playing For Change Foundation is dedicated to the fundamental idea that peace and change are possible through the universal language of music.

Playing for Change’s hallmark is a series of videos of street musicians as well as better-known names from around the world, all performing the same song. Here is their take on the Stones’ Gimme Shelter:

 

Gimme Shelter | Playing For Change from Playing For Change on Vimeo.

 

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Alan Turing’s 99th Birthday

I can’t bring myself to say Happy Birthday Alan Turing, for Turing was definitely not a happy man towards the end of  his life. All his contributions science and society amounted to naught when he was persecuted for his homosexuality, eventually driving him to suicide. What that brilliant mind could have contributed to society beyond his 42nd year, when he was driven to take his own life. During the 42 years of his life, he gave us the the Turing machine, formalized the concept of algorithms, helped crack the German Enigma cipher — saving countless lives on the allied side and by all accounts helping win the war in the Atlantic. He also designed the earliest stored program computer, and even wrote a seminal paper on morphogenesis — he became interested in biology in his latter days.

And those are just the highlights. A bleak example of how bigotry which demeans and devastates a person, demeans and devastates society. We are all the poorer for having lost Turing at such a young  age.

Hyperboloids of wondrous Light
Rolling for aye through Space and Time
Harbour those Waves which somehow Might
Play out God’s holy pantomime

Alan Turing c. 1954

 

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Zombie science roundup

 

I am fascinated with zombies. Always have been, but even more so since I took an interest in microbiology. The zombie apocalypse is the best known and best chronicled viral infection which hasn’t happened. But it could happen any day, so stock up on non-perishable food, medical supplies, water purification tablets, chainsaws, machetes, baseball bats, crossbows, semi-automatic firearms, and as many disposable acquaintances as you can get hold of. Signs of the zombie apocalypse may include your significant other turning a putrid-greenish shade of rotten and trying to chew your neck off. Beware of the differential diagnosis that they might just be using a bit too much makeup, are not wearing deodorant and feeling flirtatious. Remember to eliminate that possibility before cracking your beloved’s head open with a crowbar.

 

Here are three interesting studies all having to do with zombies.

The Zombie Roach

One problem that has to do with zombification is the loss free will. Do zombies have free will? More to the point, do humans have free will? 28 Days Later and both versions of Dawn of the Dead have survivors finding refuge from the zombie apocalypse at shopping centers. While at the shopping center, the survivors copiously consume the goods in the stores, making you think who really is the mindlessly-obsessed drone lacking free will. In two papers entitled A Wasp Manipulates Neuronal Activity in the Sub-Esophageal Ganglion to Decrease the Drive for Walking in Its Cockroach Prey and  On predatory wasps and zombie cockroaches — Investigations of “free will” and spontaneous behavior in insects, Ram Gal and Frederic Libersat from Ben Gurion University explore free will in cockroaches. Do cockroaches have free will, or are they just sophisticated automatons? And where do we draw the line between the two? Gal and Libersat  use the following definition for free will: the expression of patterns of “endogenously-generated spontaneous behavior”. That is, a  behavior which has a pattern (i.e. not just random fluctuations) and must come from within (i.e. not entirely in response to external stimuli). They cite studies where such behavior — which they define as a “precursor of free will in insects” — is observed. They then show how this behavior is removed from cockroaches when the roaches are attacked by a wasp. Their description of the process is so colorful, I shall simply reproduce it here. This is some of the most delightful and engaging prose I have ever read in a scientific paper.

Unlike most other parasitoids, this tropical Ampulicine wasp does not simply paralyze its prey to immobilize it. Instead, it stings a cockroach in the head (Fig. 1A) and injects a neurotoxic venom cocktail directly inside the cerebral ganglia (Fig. 1B). This turns the cockroach, metaphorically, into a submissive ‘zombie’: it gradually enters a long-lasting hypokinetic state, during which it becomes unresponsive to aversive stimuli and fails to self-initiate walking or escape behaviors. Although the stung cockroach is not paralyzed, it allows the wasp to cut both its antennae and drink hemolymph from the cut ends. The wasp then grabs one of the antennal stumps and pulls backwards, leading its prey into a pre-selected nest. The intoxicated cockroach, rather than fighting or fleeing its predator, actually follows the wasp submissively. In doing so it demonstrates a completely normal walking pattern, as if it was a dog led by his Master’s leash. The wasp then lays one egg on the cockroach’s leg, seals the nest and leaves the lethargic prey inside, still alive but powerless to escape under the influence of the venom. As the wasp larva hatches from the egg, it penetrates through the cockroach’s cuticle and feeds on its internal organs for several more days. Only then, roughly five days after the sting, does the cockroach finally die and the larva pupates inside its abdomen, safe from predators outside the nest.

A. The parasitoid Jewel Wasp A. compressa stings its cockroach prey inside the head. B. Schematic drawing of the cerebral nervous system (yellow) inside the cockroach's head capsule. the wasp's stinger (st., scanning electron micrograph drawn to scale) reaches to inject venom into both cerebral ganglia, namely the supra-esophageal ganglion (SupEG) and sub-esophageal ganglion (SEG). Scale bar: 0.5 mm. Source: Commun Integr Biol. 2010 Sep-Oct; 3(5): 458–461.

What they also found was that the venom injection does not affect the roach’s muscle, motor neurons or sensory neurons. Those are all intact. Stung cockroaches will walk slower and submissively follow their wasp mistress, but if placed in water they will start paddling frantically like unzombified cockroaches trying to save themselves from drowning. Indeed, the zombies paddle as frantically as non-zombies, but for a much shorter time, as if they despair quicker.

But ah, you say —  these cockroaches are not “real” zombies are they? Or rather, not the type of zombies from which the zombie apocalypse would be created. After all, a zombified roach is not infectious, and thus the disease would not spread from roach-to-roach in exponentially rising numbers by having mad roaches bite each other. In fact, the roach becomes catatonic and subservient to its mistress, more like the original Voodoo zombie, a reanimated corpse under the control of a shaman.

So how about molecular zombies?

Consider plants. Not zombie plants, but zombie genes in plants. Actually, transposable elements or TEs. TEs are DNA elements that self-replicate, in their own genomes or may be transferred into other genomes. Most eukaryotes have them. Indeed, 17% of the human genome is composed of Long Interspersed Integrated Elements or LINES. LINES simply replicate through the genome, and their contribution, if any, to the fitness of the organism is not known. some TEs are like internal viruses: replicating, adding their sequence, but little else, to their “host” genome. Only by increasing their numbers, they may at some point change their host genome. They may write themselves into some vital piece of DNA, and cause genetic damage that, if it does not kill the carrier while still an embryo, may cause long-term debilitating damage to the species by fixing itself in the population and moving down the generations. The genetic load of TEs in plants is huge: in Maize they make up the majority of the genome, with 85% of the genome coding for TE genes.

ResearchBlogging.org

But the self-selection of TEs to spread in the genome is also their undoing. Small pieces of RNA derived from TEs are used by the host to target full TEs and degrade them through a group of processes known collectively as RNA silencing. Some TEs do generate an RNA or a protein end product. Those smaller, derived aberrant TEs were nicknamed ‘zombies’ in a paper by Damon Lish from University of California, Berkeley and Jeffrey Bennetzen from the University of Georgia, Athens. There is an ongoing battle between the TEs and the zombie TEs, with the latter silencing the former, yet metaphorically feeding off the original TEs existence. If the ‘live’ TEs did not exist, the ‘zombie’ version of them would not either. The more copies of TEs a genome has, the more zombie TEs it will have. TEs inserting themselves near active genes may subject these genes to silencing by zombie TEs. This ability of plants to silence their own genes by shuffling TEs around generates new patterns of gene expression. Also, the same genes that may be inhibited due to their proximity to TEs may, at some point, re-express themselves if the TE is removed from that position in the chromosomse. So zombie TEs, which are a form of defense against viral TEs that cause chromosome damage, are also a mechanism for generating new genes and expression patterns: an evolutionary tool.

Transposable elements ("jumping genes") are responsible for the different colors in Indian corn. TEs are controlled by their "zombie offspring": short interfereing RNAs whose sequences comlement those of the TEs, silencing TE expression.

Finally, there are the zombie ants

I have written about zombie ants before:

Here is a parasitic fungus that infects ants. The infected ant wanders away from its nest; the ant then reaches a leaf or another plant part. The fungus makes the ant to bite the leaf so powerfully, it hangs from the leaf until it eventually dies; and then (excited-by-gross-stuff six-year old emerging): the fungus grows an upside down stalk out of the dead ant’s head, releasing spores that fall to the ground. The spores are then picked up by ants that walk over them, causing them to wander away from the nest, bite other leaves…  Ad nauseam. Wow.

Briefly, once infected, the ant’s behavior is hijacked to  act as a delivery system for the fungus, which is finding a  good location to die and infect more ants.

 

Ophiocordyceps unilateralis is the fungus that wreaks this havoc on the ants. Indeed, an O. unilateralis infection in ants is the closest parallel we can find to the human zombie apocalypse. The infection changes the ant’s behavior to infect more ants, and can decimate whole colonies.

But is there only one species of fungus? Harry Evans, Simon Elliot and David Hughes were inrigued by the original description of Torrubia unilateralis, as it was called at the time. In 1865, Louis René Tulasne a French mycologist, described a leaf-cutting and as the host for the fungus. His brother, Charles Tulasne, worked with him and illustrated their findings. Charles’s drawing of an infected ant does not depict the leaf-cutter: rather, it appears to be a carpenter ant, with its characteristic spines. The fungus has only ever been found infecting carpenter ants. Could Louis have made a mistake? Maybe there other species of ant-zombifying fungi out there?

 

a. Original plate from the 1865 Selecta Fungorum Carpologia of the Tulasne brothers, illustrating the holotype of Ophiocordyceps (Torrubia) unilateralis and said to be on the leaf-cutting ant, Atta cephalotes; b. Detail from plate showing the distinctive pronotal plate of Camponotus sericeiventris, as well as a side view of the host which is clearly a carpenter ant and not a leaf-cutter; compare with c. Live worker of C. sericeiventris showing the spines on the pronotal plate (arrow). Source: doi:10.1371/journal.pone.0017024.g001

Indeed there are, and the authors of this study found four new species in the Brazilian rain forest, all distinct by shape and development. All infecting carpenter ants, (no leaf cutter ants found to be infected yet!)  but four different species of carpenter ants: Camponotus rufipes, C. balzani, C. melanoticus and C. novogranadensis — are each attacked by a distinct species of Ophiocordyceps. Plenty of great pictures in the paper describing the differences between the ant-zombifying fungi.

Happy zombie-bashing! (Warning: Pop-up link to an external flash game).

 

 


 

Gal, R., & Libersat, F. (2010). A Wasp Manipulates Neuronal Activity in the Sub-Esophageal Ganglion to Decrease the Drive for Walking in Its Cockroach Prey PLoS ONE, 5 (4) DOI: 10.1371/journal.pone.0010019

Gal, R., & Libersat, F. (2010). On predatory wasps and zombie cockroaches: Investigations of free will and spontaneous behavior in insects Communicative & Integrative Biology, 3 (5), 458-461 DOI: 10.4161/cib.3.5.12472

Lisch, D., & Bennetzen, J. (2011). Transposable element origins of epigenetic gene regulation Current Opinion in Plant Biology, 14 (2), 156-161 DOI: 10.1016/j.pbi.2011.01.003

Evans, H., Elliot, S., & Hughes, D. (2011). Hidden Diversity Behind the Zombie-Ant Fungus Ophiocordyceps unilateralis: Four New Species Described from Carpenter Ants in Minas Gerais, Brazil PLoS ONE, 6 (3) DOI: 10.1371/journal.pone.0017024

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Music Monday (late): Hey Jude Flowchart

Wow, I’ve been busier than a one-legged man in an ass-kicking contest. So busy I forgot Music Monday.

 

So here’s a flowchart of Hey Jude. Enjoy.

 

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Life is not a tree, it’s more of a…

 

OK, I think the tree of life is obsolete. I have been spending a lot of time looking at horizontal gene transfer, reading about it, looking at it in genomes until my eyes water and my brain dessicates, occasionally blogging about it and soon to be publishing about it. Life is not a tree. To what extent it is not a tree it is debatable, but horizontal gene transfer is pervasive, if not rampant, in all kingdoms.

Horizontal Gene Transfer. Credit: Wikimedia Commons

So we need another term to describe the interconnection of species and genes. In a tree structure, each node can have only one parent, whereas each parent can have many offspring. Sibling nodes always have the same parent. As far as genomes are concerned…. hoo boy. Too many HGT events to count. For any given gene or chromosome/plasmid segment, we cannot reliably assume that it was vertically transferred. So if a node in our tree represents a genome, it may have multiple parents. Hence, not a tree anymore. Rather, a Directed Acyclic Graph or DAG.

 

A Directed Acyclic Graph, (DAG). Credit: wikimedia commons

However, it may very well be that a genome which contributed genetic material may also be contributing genetic material to the genome that gave it material in the first place. That happens in endosymbiotic events, but not only. Can happen, for example, with many species of bacteria or archaea living in proximity. Contribution of genetic material may be reciprocal. So a more precise definition for life would be a directed reciprocal acyclic graph or a DRAG.

But then, you already know that, don’t you?

(Yeah, and I know that reciprocity technically voids the acyclic condition. Shaddup.)

 

 

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Music Monday: Start Wearing Purple

Because you can never have too much Gogol Bordello.

 

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Shavuot is a microbial holiday

 

Tonight is Shavuot. That wonderful holiday which includes midnight studies, water-bombing and dairy products. Mmmmm…. cheese. A food product heavily embedded in the science of microbiology. Cheese is the founding product of the biotech industry (along with beer and bread).

Boaz asking Ruth on a date to the cheese and wine festival.

So here’s to Lactobacilli and Lactococci which are at the center of the production of dairy products. Breaking down milk sugar (lactose) into lactic acid, which curdles the milk protein casein.   Left to its own devices, this process generally produces rotten milk, since other bacteria may join the fray. Cheesemaking starts the process by  adding some rennet first. Rennet was originally and still being produced from cows’ upper stomachs. The active ingredient in rennet is chymosin, used to curdle milk drunk by calfs.  But 90% of  cheeses produced in the US and the UK now are made using recombinant chymosin,  produced in the fungus Aspergillus niger.

Lactobacillus sp. Source: wikipedia

Cheese also needs to ripen. Propionibacterium freudenreichii ferments lactate in the cheese to produce, among other things, carbon dioxide. This produces the holes we see in Swiss cheese. But it’s a finicky bug, and needs its faithful symbiotic companion Lactobacillus helveticus (“Swiss Lactobacillus“) to provide it with essential amino acids necessary for its growth.  P. freudenreichii is named after Eduardo von Freudenreich, a 19th century microbiologist who, among other things, wrote a seminal book on dairy microbiology.

Some cheeses are somewhat riper than others, as Asterix, Obelix and Dogmatix discover.

By the way, Propionibacterium acne a relative of Propionibacterium freudenreichii is a bacteria found on our skin which at times causes… yes, acne. But don’t think about acne when you eat Swiss cheese. (Now I put some people off Swiss for quite a while).

"Acne" comes from "acme" which means point, edge or peak. Here is an acme, but not acne.

Finally, mold. Penicillinum roqufortii provides those beautiful blue streaks in the sheep-milk cheese Roquefort… and the taste. Only cheeses aged in the natural Combalou caves of Roquefort-sur-Soulzon may bear the name Roquefort. Which is why it is so damn expensive.

 

And I haven’t even started upon Camembert (the real one is made from unpasteurized milk) ripened by  Penicillium candidum and Penicillium camemberti. Or kefir, made from the eternal Kefir grains, a matrix of bacteria and polysaccharides  that can be reused forever…. but I’m too hungry for cheesecake to continue this.

 

EDIT: typos. Thanks Martin!

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