Imagine you are a eukaryotic cell. You have many genes and make many mRNAs. One problems is mutated genes, pseudogenes and mistakes by RNAPII all make mRNAs which contain Premature Stop Codons (PTC). These then make truncated proteins which could be toxic to the cell. Eukaryotes have evolved a mechanism to recognise these and degrade them. I guess prokaryotes do not have an analogous system (that I know of) because the half-life of these mRNAs are minutes long not hours long like most eukaryotic mRNAs. Eg the average mRNA half-life in Arabidopsis is between 4-6 hours and is very variable between mRNAs. Personally I am not convinced this is an important enough reason to have a quality control check mechanism. The system I am referring to is called Nonsense-Mediated mRNA Decay (NMD). Mediators of it have been found in the early branching Giardia and is conserved between fungi/animals to plants. A PTC is recognised as wrong rather than a correct stop codon at the end of a ORF during the first round of translation by the ribosome. When the ribosome reaches a stop codon it has two choices, terminate correctly or stall and cell effectors of NMD to take it away for degradation by whatever nucleases that cell uses. It was first found in yeast and the mutants were called upf1-3 (for up-frame shift 1-3) and these yeast grow fairly normally but have increased levels of transcripts with stop codons. Raises the question why did it evolve if not very important when you KO it. In C. elegance SMG1-7 were identified having genital defects. Strangely, these were involved NMD with SMG2-4 corresponding to UPF1-3. Homologues of most of these proteins are found in many other eukaryotes. UPF1 is generally phosphorylated when ribosome stalling takes place and condemns it to degradation. Interestingly, it is a DEAD box RNA helicase (SF2 I believe).
The two questions I find interesting is 1) how do organisms tell the difference between a PTC and normal stop codon and 2) how this can be used to regulated gene expression in cell signalling. You may ask ‘James, you charismatic stallion, how can something degrading useless mRNAs be useful or regulated for controlling gene expression’ and I would reply ‘wait and read the rest of this post you $#£!&%’. The first question is rather interesting as different organisms do different things. Yeast and invertebrates such as C. elegance and the fly pushers Drosphilia use something called the 3’ faux model. Something in the 3’ end allows normal termination when the stop codon is here but NMD starts when the stop codon (PTC) is distant from the 3’ end. It has been found the distance from the poly-A tail and therefore the Poly-A Binding Protein (PABP) determines this. When a long 3’ UTR is present the mRNA is degraded. When PABP is tethered close to the stop codon termination occurs normally. This also works in plants and mammals. However, another mechanism also works in both of them. When an introns is spliced out an Exon-Junction Complex (EJC) is left behind and if a EJC is found near a stop codon by the ribosome NMD starts. Why this operates in both plants and mammals but not yeast and invertebrates is curious. Did both mechanisms operate in the last common ancestor of plants and animals and has been lost a few times in the fungi and animal kingdoms or is it convergent evolution? I hope to better understand that.
Another and perhaps more important question is what is NMD role in plants and animals. Does it provide another function other than keeping toxic protein levels low? Short answers, yes. It affect development in C. elegance and embryo lethality in mice. Clearly it plays a role in animal development. In yeast the cells senesce sooner in upf1-3 mutants because telomeres shorten. In mammals, amino acid deletion causes problems for the ribosome and NMD is down regulated and genes for amino acids biosynthesis are up-regulated so more amino acids will be made. In Arabidopsis, when upf-1 is completely KO we see embryo lethality but Knock-down alleles see some developmental phenotypes (such as in the flowers) and altered stress responses.
I will finished up now but feel free to ask questions. I have just finished writing a 4-page grant proposal on this. Just to piss Mel off, I will say this. I didn’t do any reading for this. This was all from memory when I got home. No PDF files were opened – not one!
Thursday, 22 January 2009
Thursday, 1 January 2009
Arch nemesis
Evidence is the cornerstone of science. It is what allows scientists to reject or accept hypotheses, and a robust piece of evidence can force the staunchest defender of a theory to completely reject it. People tend to like evidence when it supports their "beliefs", and dislike it when it refutes them, but scientists have no choice, they need to be apathetic and disinterested towards any results, so as to avoid introducing bias. However, scientists are also (rumoured to be) people, and the tendency to like or dislike a piece of evidence can be quite hard to resist.
How could a scientist maintain an interest in their research while avoiding interest in the data generated from it? It seems almost self-contradictory. What goals do scientists usually have when carrying out research? For a scientist working at a pharmaceutical company (assuming they wanted to keep their job), this goal would be to get a drug on the market. For a graduate student, the goal could be to find something surprising or revolutionary in order to jump-start their career. For a hardened senior professor, it could be to prove their own hypotheses right and boost their reputation (and maybe get in line for a Nobel prize?). All these goals are fundamentally selfish, and you would be hard pressed to find pure altruism in even the "most moral" scientist (whatever that means...). Perhaps that's because scientists tend to be ambitious, competitive animals, and that's a selfish motivator in itself, but I would say it's because people's goals tend to be selfish in nature.
These selfish goals scientists have certainly pose the most danger in making them introduce bias into their data. However, the drive that these goals give to scientists is what has led to so many historical discoveries. I'm sure some discoveries had altruistic motives but let's just say Watson and Crick weren't really thinking about saving humanity from terrible doom. Not to paint a sad picture of scientists, but sometimes the only thing that scientists get up for in the morning is the tiny chance that today's experiment will get them even slightly closer to achieving their goal.
I think that scientists manage to minimize the danger of introducing bias by finding the one person on Earth they most disagree with and establishing an intimate, life-long professional relationship with them, manifested mostly through heckling at conferences and angry e-mail exchanges. This works much more efficiently in academia than in industry, because industry scientists are usually either unwilling or not allowed to talk to outsiders about anything they do. Academics are also secretive to a certain extent in order to avoid being scooped, but the spirit of collaboration and criticism is much stronger. This kind of mutually abusive relationship is what every scientist needs, and I personally can't wait to meet my arch nemesis!
P.S. Happy 2009!
How could a scientist maintain an interest in their research while avoiding interest in the data generated from it? It seems almost self-contradictory. What goals do scientists usually have when carrying out research? For a scientist working at a pharmaceutical company (assuming they wanted to keep their job), this goal would be to get a drug on the market. For a graduate student, the goal could be to find something surprising or revolutionary in order to jump-start their career. For a hardened senior professor, it could be to prove their own hypotheses right and boost their reputation (and maybe get in line for a Nobel prize?). All these goals are fundamentally selfish, and you would be hard pressed to find pure altruism in even the "most moral" scientist (whatever that means...). Perhaps that's because scientists tend to be ambitious, competitive animals, and that's a selfish motivator in itself, but I would say it's because people's goals tend to be selfish in nature.
These selfish goals scientists have certainly pose the most danger in making them introduce bias into their data. However, the drive that these goals give to scientists is what has led to so many historical discoveries. I'm sure some discoveries had altruistic motives but let's just say Watson and Crick weren't really thinking about saving humanity from terrible doom. Not to paint a sad picture of scientists, but sometimes the only thing that scientists get up for in the morning is the tiny chance that today's experiment will get them even slightly closer to achieving their goal.
I think that scientists manage to minimize the danger of introducing bias by finding the one person on Earth they most disagree with and establishing an intimate, life-long professional relationship with them, manifested mostly through heckling at conferences and angry e-mail exchanges. This works much more efficiently in academia than in industry, because industry scientists are usually either unwilling or not allowed to talk to outsiders about anything they do. Academics are also secretive to a certain extent in order to avoid being scooped, but the spirit of collaboration and criticism is much stronger. This kind of mutually abusive relationship is what every scientist needs, and I personally can't wait to meet my arch nemesis!
P.S. Happy 2009!
Friday, 17 October 2008
Kinetoplastid DNA
It seems to be that time of the year in which we post about something to do with our posts, as these are the topics we are supposed to be reading about now. Therefore, a post on parasites. That’s where the connection with my project finishes, but anyway.As you might know, tryponosomatids are organisms from the family Troponosomatidae, which include some pretty nasty unicellular parasites such as Trypanosoma brucei, causer for African sleeping disease, and Leishmania, causer of leishmaniasis. As other higher eukaryotes, these parasites are characterised by two genomes: a nuclear genome and a mitochondrion genome, 10-30% of all the cell DNA, situated in the kinetoplast (the name given to the mitochondrion in these organisms).
Fig.1 A- Schematic minicircle organization. B- in vivo network organization, seen sideways.
(Adapted from reference 1)
So far nothing extraordinary. Things get interesting, when one looks at the structure of the kinetoplast DNA (kDNA) in these species. The kDNA is constituted by thousands of small DNA circles, the minicircles, and a few dozen of large DNA circles, the maxicircles. These are interlocked, as in a chain mail of medieval armour. Each circle is interlocked with 3 other neighbouring circles. The minicircles and maxicircles are stretched into a disk-shaped structure, situated near to the flagellar basal body (Fig.1). The maxicircles are those more similar to normal mitochondrion genome. They include rRNAs and genes encoding proteins associated with the respiratory processes that takes place in this organelle. However, the maxicircles mRNA requires extensive editing, namely the introduction or deletion of uridylate. The minicircles encode the guide RNAs used as templates for this editing. Since there are many types of editing required, as well as maxicircles with different sequences, there is the need for the thousand minicircles with different sequences. Seems a bit of a wasteful system, but what do I know!
More interesting is to think of the replication process. The minicircles must stop being interlocked, replicated, interlocked again, and in the end originate two new networks of thousands of minicircles that separate into the two new daughter cells. Let us look at the different steps, following an individual minicircle (Fig.2):
Fig.2 kDNA replication model. (From reference 2)
1- A minicircle must first be released from the network into the so-called kinetoflagellar zone (KTZ), where several proteins involved in the process exist. Here the unidirectional replication of the circle occurs, although the details of this process are not well known.
2- The two daughter minicircles move to opposite antipodal sites of the circle, where there are two protein assemblies. Here a variety of reactions occur: the RNA primers are removed, the gaps between
3- Minicircles are attached by topoisomerase II to the network periphery adjacent to the antipodal sites.
The way the minicircles are attached to the disk varies with the species of trypanosomatid. In T.brucei, for example, the minicircles accumulate at the network poles. In T.cruzi, and C.fasciculata, the minicircles seem to be uniformly attached around the periphery of the disk, creating a ring of new minicircles, of increased thickness. How this uniform attachment is done is not certain, but it is though that either the antipodal protein complexes or the disk itself must rotate! (Fig.3)
Fig.3 Replication in C.fasciculata. New minicircles have been labelled with fluorescent nucleotides. The arrangement of the new minicircles around the periphery of the disk is obvious (from reference 2).
4- Regardless of the method, new minicircles are attached to the disk, and the valence must increase to 4 to 6 attachments per minicircle, in order to ensure twice as many minicircles in the same space (the mitochondrion membrane has not doubled at this point). When the space increases, topoisomerase II ensures that valence returns to 3.
5- Finally, the nicks are repaired and the network splits into 2, although how exactly this division occurs is not well known. Most importantly, it is not known for sure how to guarantee that the two daughter networks have the exactly same minicircles. Considering their importance in maxicircle mRNA editing, the loss of one minicircle could have dramatic consequences.
There is much to be explained in this process, namely identify exactly how the minicircles are moved to the different antipodal sites, or the details of individual minicircle replication, but such understanding will require the identification of the proteins involved. Considering the complexity of the process, many must be involved, but only a few have been identified so far.
This is probably not life-changing research, but it is surely interesting. It is important to remind ourselves once in a while that though we learn the textbook pathways and processes, Nature seems to like using hundreds of alternatives. Just to make scientists lives harder, I assume!
Liu, B., Liu, Y., Motyka, S., Agbo, E., & Englund, P. (2005). Fellowship of the rings: the replication of kinetoplast DNA Trends in Parasitology, 21 (8), 363-369 DOI: 10.1016/j.pt.2005.06.008
(2) Smith D. and Parsons M. (1996). Molecular Biology of Parasitic Protozoa, Kinetoplast DNA: Structure and Replication, Oxford University Press, USA
Sunday, 12 October 2008
Apical dominance, MAX and my project
One of the most important things the plant hormone auxin does is play an important role in is apical dominance. This is where the Shoot Apical Meristem (SAM), the growing part of the above ground half of the plant, produces a signal that inhibits growth from other auxiliary meristems. The SAM and auxiliary meristems contain the plant’s ‘stem cells’ and generate new leaves, stems and flowers. They both have the same ability to generate new organs. When the plant grows and leaves emerge from the meristem, an auxiliary meristem is left behind with the leaf, which may or may not grow out, just above where the leaf meets the stem. For years it was known auxin from the SAM inhibited their outgrowth. Auxin is produced in the SAM and moved down the plant and when it is stopped, the auxiliary meristem can grow out. The best person to tell you this is a gardener. When pruning, they remove the SAM on a plant, like a rose bush, to allow dormant growing parts of the plant grow out and make it bushier. It is also a pain for, let’s say for example, tobacco farmers. They ‘top’ tobacco plants so it does not grow up and make the leaves fatter. However, this stops auxin travelling down the stem and auxiliary meristems grow out. The addition of unpleasant chemicals is used to solve this problem.
Auxin does not travel up into the auxiliary meristem, so how does auxin inhibit bud outgrowth? A second signal must be involved. This ‘second messenger’ is not an easy thing to understand. It turns out to be a complex interplay of plant hormones that I will try to explain now control bud outgrowth. I will start by explaining the players involved. The hormone cytokinin (Ck) often plays the opposite role to auxin in plant grow. When it is applied to an auxiliary meristem it will grow out. Ck is generated both in the roots and locally in the stem but it is unclear which is more relevant to shoot branching (I think it varies from species to species). The auxin signalling pathway does regulate Ck synthesis but this is not the whole story. Auxin signalling pathway mutants do show some increase in shoot branching but it is lower than those affected by mutations in MAX genes (see below) and the effects of these are additive to auxin signalling.
Mutant screens reviled the MAX genes. max mutants have increased shoot branching. To cut a long story short, the MAX pathway does not produce the inhibitory signal but helps auxin regulate shoot-branching. MAX3 and 4 produce enzymes that alter a caratinoid. MAX1 is a P450 that acts downstream of MAX3 and 4 and alters the chemical further, producing the MAX-dependent hormone (more on the identity below). MAX2 does not produce the graft-transmissible signal but helps perceives the MAX-dependent hormone. In fact, it is an F-box protein like TIR1 from my post on auxin signalling. However, I think it is unlikely to bind the MAX-dependent hormone directly as TIR1 does auxin. I suppose this cannot be looked at until the hormone has been characterised better. MAX2 is also involved with leaf senescence and some features of light perception but its roles in these are not very well understood either.
The Leyser lab has been working on finding the identity of the MAX-dependent hormone but two papers published in the same September issue of Nature (just after my subscription ended!) suggest the identity in pea and rice. Ottoline has just written a short review on them (below). They found a chemical, called strigolactones, was involved. Previously shown to be involved with germination, formation of mycorrhiza with fungi and growth of parasitic plants, now it appears they are a key regulator of shoot branching. The exact identity of the biological active strigolactone is still yet to be found.
The MAX pathway’s mode of action is through limiting auxin transport. This work was published with a PhD student at York as the lead author in the Leyser lab (he was a very well known blue coat). Auxin is transported from the SAM to the roots. To move in and out of cells, auxin needs proteins to transport it. One important class are the PIN proteins. They can become localised to a particular part in a plant cell, such as the basal side, to ensure auxin only moves in one direction. This is very important in creating a vascular system in the plant. First of all, auxin is made by the auxiliary meristems but it is their ability to transport auxin out that allows them to grow out. It is best to imagine the auxin transport network as roads. Auxin (the cars) leaves the SAM and moves down the stem via PIN proteins (lanes on a motor way). In a normal plant, not all lanes are open. So auxin from the SAM fills most of the PIN proteins and only a little auxin from the buds can enter, letting some grow out. max mutants have an increase transport capacity because more PIN proteins are present. This is like opening extra lanes on a motor way so auxin from all the buds can enter and move freely, letting them grow out! Integrating the actions of all hormones leads to something like this: auxin moves down the plant and its movement down is limited by the MAX-dependent hormone from the roots. This limits the amount of auxin auxiliary merisetems can transport out, so large amounts of auxin accumulate in these buds. This (somehow) inhibits Ck production to limit growth of the bud. The integration of multiple hormones has been described as the brain of plants.
The reason max mutants and auxin signalling double mutants have an additive effect is because auxin works both through its classical signalling pathway but also through auxin transport. This is where, for me, things get confusing. How does auxin in the bud know not to be exported and form vascular tissue to connect to the main flow in the stem? This has been a long standing question, not for shoot branching but for the formation of a vascular network, yet there is no answer (or good one at least).
My final year project is in the Leyser lab, for what I hope are obvious reasons now. They have done lots of great work. A modifier of the max1 phenotype was found in a mutants screen and mapped to a location on chromosome 1. My job is to widdle the candidate genes down from around 20 to one! I don’t want to give too much away about the project on here but the mutation alters the max1 phenotype and has its own slight developmental phenotype. Hopefully understanding it will help in the long term goal of understanding plant development. I doubt it will have a direct role synthesis or degradation of the MAX-dependent hormone but I believe it will affect downstream events. I hope this has been enlighting.
Here is a very good review and explains these things better than I can do by someone in the Leyser lab:
http://www.ncbi.nlm.nih.gov/pubmed/17728300?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
Here is an ahead of print short review on the identity of the MAX-dependent hormone by Ottoline:
http://www.ncbi.nlm.nih.gov/pubmed/18804430?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
Auxin does not travel up into the auxiliary meristem, so how does auxin inhibit bud outgrowth? A second signal must be involved. This ‘second messenger’ is not an easy thing to understand. It turns out to be a complex interplay of plant hormones that I will try to explain now control bud outgrowth. I will start by explaining the players involved. The hormone cytokinin (Ck) often plays the opposite role to auxin in plant grow. When it is applied to an auxiliary meristem it will grow out. Ck is generated both in the roots and locally in the stem but it is unclear which is more relevant to shoot branching (I think it varies from species to species). The auxin signalling pathway does regulate Ck synthesis but this is not the whole story. Auxin signalling pathway mutants do show some increase in shoot branching but it is lower than those affected by mutations in MAX genes (see below) and the effects of these are additive to auxin signalling.
Mutant screens reviled the MAX genes. max mutants have increased shoot branching. To cut a long story short, the MAX pathway does not produce the inhibitory signal but helps auxin regulate shoot-branching. MAX3 and 4 produce enzymes that alter a caratinoid. MAX1 is a P450 that acts downstream of MAX3 and 4 and alters the chemical further, producing the MAX-dependent hormone (more on the identity below). MAX2 does not produce the graft-transmissible signal but helps perceives the MAX-dependent hormone. In fact, it is an F-box protein like TIR1 from my post on auxin signalling. However, I think it is unlikely to bind the MAX-dependent hormone directly as TIR1 does auxin. I suppose this cannot be looked at until the hormone has been characterised better. MAX2 is also involved with leaf senescence and some features of light perception but its roles in these are not very well understood either.
The Leyser lab has been working on finding the identity of the MAX-dependent hormone but two papers published in the same September issue of Nature (just after my subscription ended!) suggest the identity in pea and rice. Ottoline has just written a short review on them (below). They found a chemical, called strigolactones, was involved. Previously shown to be involved with germination, formation of mycorrhiza with fungi and growth of parasitic plants, now it appears they are a key regulator of shoot branching. The exact identity of the biological active strigolactone is still yet to be found.
The MAX pathway’s mode of action is through limiting auxin transport. This work was published with a PhD student at York as the lead author in the Leyser lab (he was a very well known blue coat). Auxin is transported from the SAM to the roots. To move in and out of cells, auxin needs proteins to transport it. One important class are the PIN proteins. They can become localised to a particular part in a plant cell, such as the basal side, to ensure auxin only moves in one direction. This is very important in creating a vascular system in the plant. First of all, auxin is made by the auxiliary meristems but it is their ability to transport auxin out that allows them to grow out. It is best to imagine the auxin transport network as roads. Auxin (the cars) leaves the SAM and moves down the stem via PIN proteins (lanes on a motor way). In a normal plant, not all lanes are open. So auxin from the SAM fills most of the PIN proteins and only a little auxin from the buds can enter, letting some grow out. max mutants have an increase transport capacity because more PIN proteins are present. This is like opening extra lanes on a motor way so auxin from all the buds can enter and move freely, letting them grow out! Integrating the actions of all hormones leads to something like this: auxin moves down the plant and its movement down is limited by the MAX-dependent hormone from the roots. This limits the amount of auxin auxiliary merisetems can transport out, so large amounts of auxin accumulate in these buds. This (somehow) inhibits Ck production to limit growth of the bud. The integration of multiple hormones has been described as the brain of plants.
The reason max mutants and auxin signalling double mutants have an additive effect is because auxin works both through its classical signalling pathway but also through auxin transport. This is where, for me, things get confusing. How does auxin in the bud know not to be exported and form vascular tissue to connect to the main flow in the stem? This has been a long standing question, not for shoot branching but for the formation of a vascular network, yet there is no answer (or good one at least).
My final year project is in the Leyser lab, for what I hope are obvious reasons now. They have done lots of great work. A modifier of the max1 phenotype was found in a mutants screen and mapped to a location on chromosome 1. My job is to widdle the candidate genes down from around 20 to one! I don’t want to give too much away about the project on here but the mutation alters the max1 phenotype and has its own slight developmental phenotype. Hopefully understanding it will help in the long term goal of understanding plant development. I doubt it will have a direct role synthesis or degradation of the MAX-dependent hormone but I believe it will affect downstream events. I hope this has been enlighting.
Here is a very good review and explains these things better than I can do by someone in the Leyser lab:
http://www.ncbi.nlm.nih.gov/pubmed/17728300?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
Here is an ahead of print short review on the identity of the MAX-dependent hormone by Ottoline:
http://www.ncbi.nlm.nih.gov/pubmed/18804430?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
Friday, 3 October 2008
IgNobels 2008
'For achievements that first make people LAUGH and then make them THINK'
As I seem to be spending all my holidays memorizing hard words in english (Melly will know what I mean) I actually haven't had the time to read anything 'scientific' like you guys. I had, however, time to have a look to what Nature regards as, and I agree, 'the highlight of the scientific calendar'. Yes, my friends, the Ig Nobels are out again. As you will remember, I wrote a post last year when I realized that these amazing prizes existed, and have been eagerly waiting for this year's winners. So, below, enjoy the list of the IgNobel winners 2008!
NUTRITION
Massimiliano Zampini of the University of Trento, Italy and Charles Spence of OxfordUniversity ,UK
PEACE
The Swiss Federal Ethics Committee on Non-Human Biotechnology (ECNH) and the citizens of Switzerland for adopting the legal principle that plants have dignity.
ARCHEOLOGY Astolfo G. Mello Araujo and José Carlos Marcelino of Universidade de São Paulo, Brazil, for measuring how the course of history, or at least the contents of an archaeological dig site, can be scrambled by the actions of a live armadillo. The Swiss Federal Ethics Committee on Non-Human Biotechnology (ECNH) and the citizens of Switzerland for adopting the legal principle that plants have dignity.
BIOLOGY Marie-Christine Cadiergues, Christel Joubert,, and Michel Franc of Ecole Nationale Veterinaire de Toulouse, France for discovering that the fleas that live on a dog can jump higher than the fleas that live on a cat.
MEDICINE
Dan Ariely ofDuke University , USA
COGNITIVE SCIENCE Toshiyuki Nakagaki of Hokkaido University, Japan, Hiroyasu Yamada of Nagoya, Japan, Ryo Kobayashi of Hiroshima University, Atsushi Tero of Presto JST, Akio Ishiguro of Tohoku University, and Ágotá Tóth of the University of Szeged, Hungary, for discovering that slime molds can solve puzzles.
ECONOMICS
Geoffrey Miller, Joshua Tybur and Brent Jordan of theUniversity of New Mexico , USA
PHYSICS Dorian Raymer of the Ocean Observatories Initiative at Scripps Institution of Oceanography,USA , and Douglas Smith of the University of California , San Diego , USA
CHEMISTRY Sharee A. Umpierre of the University of Puerto Rico, Joseph A. Hill of The Fertility Centers of New England (USA), Deborah J. Anderson of Boston University School of Medicine and Harvard Medical School (USA), for discovering that Coca-Cola is an effective spermicide, and to Chuang-Ye Hong of Taipei Medical University (Taiwan), C.C. Shieh, P. Wu, and B.N. Chiang (all of Taiwan) for discovering that it is not.
LITERATURE
David Sims ofCass Business School London , UK
Hehe, as usual, delicious to read... For more information on the Ig Nobels or this year's ceremony (I actually don't know yet what's this year's topic. Last year it was chicken and involved dressing proper Nobel laureates in egg outfits), see the link below
http://improbable.com/ig/winners/#ig2008
Dan Ariely of
COGNITIVE SCIENCE Toshiyuki Nakagaki of Hokkaido University, Japan, Hiroyasu Yamada of Nagoya, Japan, Ryo Kobayashi of Hiroshima University, Atsushi Tero of Presto JST, Akio Ishiguro of Tohoku University, and Ágotá Tóth of the University of Szeged, Hungary, for discovering that slime molds can solve puzzles.
ECONOMICS
Geoffrey Miller, Joshua Tybur and Brent Jordan of the
PHYSICS Dorian Raymer of the Ocean Observatories Initiative at Scripps Institution of Oceanography,
CHEMISTRY Sharee A. Umpierre of the University of Puerto Rico, Joseph A. Hill of The Fertility Centers of New England (USA), Deborah J. Anderson of Boston University School of Medicine and Harvard Medical School (USA), for discovering that Coca-Cola is an effective spermicide, and to Chuang-Ye Hong of Taipei Medical University (Taiwan), C.C. Shieh, P. Wu, and B.N. Chiang (all of Taiwan) for discovering that it is not.
LITERATURE
David Sims of
Hehe, as usual, delicious to read... For more information on the Ig Nobels or this year's ceremony (I actually don't know yet what's this year's topic. Last year it was chicken and involved dressing proper Nobel laureates in egg outfits), see the link below
http://improbable.com/ig/winners/#ig2008
One of last year's winners, Dan Meyer demonstrates his skills, after winning the 2007 IgNobel for medicine in collaboration with Brian Witcombe, for their study on sword swallowing and its side-effects
Subscribe to:
Posts (Atom)