High-Performance Transistors Produced from Carbon 60




Description

Using room-temperature processing, Georgia Tech researchers have fabricated high-performance field effect transistors with thin films of Carbon 60, also known as fullerene. The work represents another milestone toward practical applications for large area, low-cost electronic circuits on flexible organic substrates.


Using room-temperature processing, researchers at the Georgia Institute of Technology have fabricated high-performance field effect transistors with thin films of Carbon 60, also known as fullerene. The ability to produce devices with such performance with an organic semiconductor represents another milestone toward practical applications for large area, low-cost electronic circuits on flexible organic substrates.

The new devices – which have electron-mobility values higher than amorphous silicon, low threshold voltages, large on-off ratios and high operational stability – could encourage more designers to begin working on such circuitry for displays, active electronic billboards, RFID tags and other applications that use flexible substrates.

“If you open a textbook and look at what a thin-film transistor should do, we are pretty close now,” said Bernard Kippelen, a professor in Georgia Tech’s School of Electrical and Computer Engineering and the Center for Organic Photonics and Electronics. “Now that we have shown very nice single transistors, we want to demonstrate functional devices that are combinations of multiple components. We have everything ready to do that.”

Fabrication of the C60 transistors was reported in the journal Applied Physics Letters on August 27th. The research was supported by the U.S. National Science Foundation through the STC program MDITR, and the U.S. Office of Naval Research.

Researchers have been interested in making field-effect transistors and other devices from organic semiconductors that can be processed onto various substrates, including flexible plastic materials. As an organic semiconductor material, C60 is attractive because it can provide high electron mobility – a measure of how fast current can flow. Previous reports have shown that C60 can yield mobility values as high as six square centimeters per volt-second (6 cm2/V/s). However, that record was achieved using a hot-wall epitaxy process requiring processing temperatures of 250 degrees Celsius – too hot for most flexible plastic substrates.

Though the transistors produced by Kippelen’s research team display slightly lower electron mobility – 2.7 to 5 cm2/V/s – they can be produced at room temperature.

“If you want to deposit transistors on a plastic substrate, you really can’t have any process at a temperature of more than 150 degrees Celsius,” Kippelen said. “With room temperature deposition, you can be compatible with many different substrates. For low-cost, large area electronics, that is an essential component.”

Because they are sensitive to contact with oxygen, the C60 transistors must operate under a nitrogen atmosphere. Kippelen expects to address that limitation by using other fullerene molecules – and properly packaging the devices.

The new transistors were fabricated on silicon for convenience. While Kippelen isn’t underestimating the potential difficulty of moving to an organic substrate, he says that challenge can be overcome.

Though their performance is impressive, the C60 transistors won’t threaten conventional CMOS chips based on silicon. That’s because the applications Kippelen has in mind don’t require high performance.

“There are a lot of applications where you don’t necessarily need millions of fast transistors,” he said. “The performance we need is by far much lower than what you can get in a CMOS chip. But whereas CMOS is extremely powerful and can be relatively low in cost because you can make a lot of circuits on a wafer, for large area applications CMOS is not economical.”

A different set of goals drives electronic components for use with low-cost organic displays, active billboards and similar applications.

“If you look at a video display, which has a refresh rate of 60 Hz, than means you have to refresh the screen every 16 milliseconds,” he noted. “That is a fairly low speed compared to a Pentium processor in your computer. There is no point in trying to use organic materials for high-speed processing because silicon is already very advanced and has much higher carrier mobility.”

Now that they have demonstrated attractive field-effect C60 transistors, Kippelen and collaborators Xiao-Hong Zhang and Benoit Domercq plan to produce other electronic components such as inverters, ring oscillators, logic gates, and drivers for active matrix displays and imaging devices. Assembling these more complex systems will showcase the advantages of the C60 devices.

“The goal is to increase the complexity of the circuits to see how that high mobility can be used to make more complex structures with unprecedented performance,” Kippelen said.

The researchers fabricated the transistors by depositing C60 molecules from the vapor phase into a thin film atop a silicon substrate onto which a gate electrode and gate dielectric had already been fabricated. The source and drain electrodes were then deposited on top of the C60 films through a shadow mask.

Kippelen’s team has been working with C60 for nearly ten years, and is also using the material in photovoltaic cells. Beyond the technical advance, Kippelen believes this new work demonstrates the growing maturity of organic electronics.

“This progress may trigger interest among more conventional electronic engineers,” he said. “Most engineers would like to work with the latest technology platform, but they would like to see a level of performance showing they could actually implement these circuits. If you can demonstrate – as we have – that you can get transistors with good reproducibility, good stability, near-zero threshold voltages, large on-off current ratios and performance levels higher than amorphous silicon, that may convince designers to consider this technology.”
(Newswise)

NEUROSCIENCE : Optimistic neurons

In rats given a choice between two rewards, neurons that predict the value of expected rewards responded as though the animal had chosen the best available reward, no matter what the rat actually did. These results suggest that the opportunity to make a choice may be as valuable as the best available option on the menu.

The authors trained rats to learn to associate each of three odours with an action. Two of the odours signalled that the rat was required to move either left or right to receive a reward, with one location containing a better reward than the other. The third odour indicated that the animal could choose to go to either location. Dopaminergic neurons in the ventral tegmental area, part of the brain’s “reward processing system,” responded more for the odour that cued the rat to move to the location associated with the better reward, as expected from previous studies.

The rewards varied either in the amount of juice or in how long the rat had to wait for its delivery, and responses to the odour cues were correlated with both reward size and delay. The dopaminergic neurons responded just as strongly to the odour indicating that the rat could choose which reward to collect as to the better reward, even though the rat eventually chose the worse reward nearly 30% of the time on the free choice trials.



Author Contact:

Matthew Roesch (University of Maryland School of Medicine, Baltimore, MD, USA)

Tel: +1 410 706 8910; E-mail: mroes001@umaryland.edu

GENETICS : Gene prevents sudden death in mice after infection


Mice that lack a particular gene die suddenly and without overt signs of illness in response to an infection that is usually harmless, according to a study. This work may lead to new insights into the origins of sudden death in humans, although such a link has not yet been made.

Bruce Beutler and colleagues treated mice with a chemical mutagen – an agent that changes genetic information; and examined the third-generation offspring of the mutant mice for susceptibility to cytomegalovirus (CMV). This virus, at the dose delivered, is normally harmless. The progeny of four of the original mutants, however, died suddenly between 36 hours and 3 days after inoculation. One of these lines has a large deletion in Kcnj8, a gene encoding a component of a potassium channel expressed in smooth muscle and endothelial cells of the coronary artery (two of the other lines carry different mutations in Kcnj8).

The protein that interacts with Kcnj8 has a counterpart in the fruit fly, and the authors show that it similarly protects flies against sudden death after challenge with flock house virus (FHV). The authors propose that this potassium channel is required for the coronary arteries to survive the systemic metabolic stress and arterial constriction that accompanies the innate immune response to viruses such as CMV and FHV.



Author contact:

Bruce Beutler (Scripps Research Institute, La Jolla, CA, USA)

Tel: +1 858 784 8610; E-mail: bruce@scripps.edu

PHYSICS : Neural networks organise themselves



Neural networks dynamically organize themselves to operate in a range that is optimal for information processing, according to a theoretical model. The results provide an understanding of how neurons interact with each other and how they can build efficient networks.

Neurons signal to each other through junctions known as synapses. Using these connections they can build extended networks. Computer simulations of neural networks indicate that for specific connection patterns, properties such as computational power or memory capacity are maximized. This picture is supported by experimental findings in cell cultures. However, how neural networks can be tuned to the optimal setting is still an open question.

Michael Herrmann and colleagues argue that there is no need for fine-tuning. They factor in that synapses are not static — that is, the efficiency of transmission through synapses depends on the frequency of their use — and show in their model that neural networks dynamically organize themselves to operate in a favourable range.



Author contact:

Michael Herrmann (Universität Göttingen, Germany)

Tel: +49 551 517 6424; E-mail: michael@nld.ds.mpg.de

Immunity: Holding dormant cancers in check


Dormant cancer cells are actively kept in check by the host’s immune system — those that escape go on to develop into clinically detectable tumours. A paper identifies a crucial stage in the battle, at which point defences stall the expansion of cancer cells that may have managed to dodge past early immunosurveillance.

Robert Schreiber and co-workers use a mouse model to show that the animal’s immune system can keep tumour growth in check over an extended period. Clinicians have suspected the existence of such an ‘equilibrium’ state, because dormant cancers sometimes take off when inadvertently transferred from a donor to an immunosuppressed recipient during organ transplantation.

This newly discovered staging post could also explain the presence of occult tumour cells — in the prostate, for example — in individuals with no symptoms of disease. Eventually it could be used to devise immunotherapies for tightening control of tumour growth, suggest the authors.

In an accompanying News & Views article, Cornelis Melief comments on the ‘startling results’ and says: ‘they demonstrate that considering cancer as a fatal disease is not always appropriate’.



Author contact:

Robert Schreiber (Washington University School of Medicine, St Louis, MO, USA)

Tel: +1 314 362 8747; E-mail: schreiber@immunology.wustl.edu



Cornelis Melief (Leiden University Medical Center, Netherlands) N&V author

Tel: +31 71 526 3800; E-mail: C.Melief@lumc.nl

STRUCTURAL AND MOLECULAR BIOLOGY : Stalling chemotherapy damage

The understanding of how healthy cells cope with damages caused by anti-cancer drugs is furthered by new findings.

Transcription is the process whereby genetic information is transferred from DNA to RNA, in most cases leading to production of a particular protein. DNA damage, such as that caused by some anticancer drugs, can lead to errors in the RNA produced during transcription, resulting in incorrect protein production that may be harmful to the cell.

Patrick Cramer and colleagues have investigated how transcription machinery avoids DNA lesions caused by cisplatin, a widely used chemotherapy drug. They found that the cisplatin lesion forces the transcription machinery to stop before it reaches the lesion. This transcriptional “stalling” triggers a DNA-repair pathway that can remove the toxic lesion.


Author contact:

Patrick Cramer (Gene Center Munich, Germany)

Tel: +49 89 2180 76965; e-mail: cramer@LMB.uni-muenchen.de

METHODS : Controlling protein stability in parasites



Methods to regulate protein expression in two hazardous parasites. This research will provide valuable tools for understanding disease development.

Toxoplasma gondii, a parasite that can cause encephalitis and neurological diseases, and Plasmodium falciparum, a malaria parasite, have both had their genome sequenced. Still lacking are methods to control protein expression on a large scale, so the effects of proteins on parasite biology and pathogenesis can be studied.

The research groups of Daniel Goldberg and Markus Meissner adapted a system, originally developed in mammalian cells, that allows them to trigger the degradation of any protein at will. The only pre-requisite is that the protein is coupled to a short peptide that makes protein stability dependent on the presence of another component, appropriately named Shield. If Shield is added to the parasites the targeted protein is stable, but if Shield is withdrawn, the protein is degraded and the effect of its loss on the parasite can be studied.

This fast and efficient method for regulating protein levels will allow a genome wide analysis of their roles in the parasite life cycle and the interaction with its host.



Author contacts:

Markus Meissner (University Hospital Heidelberg, Heidelberg, Germany)

Tel: +49 6221 566518; E-mail: markus.meissner@med.uni-heidelberg.de



Daniel Goldberg (Washington University School of Medicine, St. Louis, MO, USA)

Tel: +1 314 362 1514; E-mail: goldberg@borcim.wustl.edu

Getting to the root of a developmental mystery


Researchers have revealed how two closely related proteins trigger opposing effects in developing roots


The formation of root epidermis in Arabidopsis thaliana, a popular plant research model, offers a valuable means for studying cell differentiation in developing tissues. During root development, progenitor cells yield two classes of epidermal cells, hair cells and hairless cells, which form in a fixed pattern along the root.

Previous research has identified factors that determine whether hair cells or hairless cells form. Two of the genes involved, CAPRICE (CPC) and WEREWOLF (WER), encode closely related transcription factors that exhibit notable functional differences, which piqued the interest of Takuji Wada, a researcher at the RIKEN Plant Sciences Center in Yokohama. “CPC activates root-hair cell differentiation whereas WER represses it, even though both belong to the same family of transcription factors,” explains Wada, “so I wondered why these two factors have opposite effects.”

CPC and WER belong to the MYB family of transcription factors, whose distinguishing characteristics include several domains with repeated amino acid sequences. Wada and his colleagues generated several CPC and WER variants, swapping different portions of one of these repeat domains (Myb R3) between the two proteins. These were expressed in plant strains that lack functional CPC or WER in order to understand the relevant regions that determine each protein’s function1.

Wada’s team found that WER only inhibited hair cell formation when its entire R3 domain was intact. On the other hand, most of CPC’s R3 domain could be replaced without impeding its activity (Fig. 1). Subsequent experiments showed that both proteins bind common targets—GL3 and EGL3, two proteins that induce hairless cell formation. Myb R3 substitutions had no effect on this activity, but did affect the ability of WER to bind DNA—a property absent in CPC. “The sequence of the WER MYB R3 domain is restricted—the equivalent domain of CPC cannot be substituted for it,” says Wada. “Therefore, these restricted sequences are necessary for binding to DNA.”

Wada’s group believes that both WER and CPC compete for binding GL3 and EGL3. When WER binds, its unique DNA-binding sequences allow it to recruit these proteins in order to regulate genes responsible for hairless cell formation. However, when CPC is present as a competitor, no DNA binding takes place and hair cells develop instead. Based on the findings from this study, Wada suggests that CPC probably originated from a duplicate copy of the WER gene, a truncated younger sibling that nevertheless evolved into an effective rival.
Reference

1. Tominaga, R., Iwata, M., Okada, K. & Wada, T. Functional analysis of the epidermal-specific MYB genes CAPRICE and WEREWOLF in Arabidopsis. Plant Cell 19, 2264–2277 (2007).

Cell fusion may create niche for immune cell education

Japanese researchers have identified a subset of cells they believe may induce the formation of a network of follicular dendritic cells (FDC) in the spleen and lymph nodes.


Researchers identify possible precursors of lymphoid tissue cellular network

Japanese researchers have identified a subset of cells they believe may induce the formation of a network of follicular dendritic cells (FDC) in the spleen and lymph nodes.

A recent paper by Hiroshi Ohno and colleagues at the RIKEN Research Center for Allergy and Immunology, Yokohama, suggests that in the mouse, spleen cells expressing the cell surface marker proteins CD35, involved in processing and clearance of immune complexes, and B220, found on almost all immune system cells, can induce the formation of these networks and ultimately lymphoid follicles1 (Fig. 1).

These so-called FDC form a reticular network of cells in the spleen and lymph nodes that trap immune complexes of antibodies, antigens and associated molecules. The network plays a critical role in the development and maturation of the antibody-producing B lymphocytes (B cells). If a B cell binds weakly to an antigen trapped on the surface of an FDC, it undergoes programmed cell death (apoptosis). On the other hand, a B cell that has a high affinity for the trapped antigen survives to become an antibody-producing plasmablast, and ultimately a memory B cell. This is the fundamental process that underpins the ability of the immune system to respond quickly to attack by pathogenic infection.

But it is not simply a matter of recognition; it appears that a complex interaction of cells and molecules and cellular architecture within the dynamic microenvironment of the lymphoid follicle is required for B cell maturation. The players include connective tissue cells called stromal cells.

“The intrigue of the lymphoid follicle stems from the complexity of its microarchitecture, comprising immune cells and stromal cells, adhesion molecules, cytokines and antigen-antibody complexes, and the relationships between these components, in the formation of B cell-follicular dendritic cell aggregates and the regulation of B cell differentiation,” says Takaya Murakami, the first author of the paper.

Results from a series of experiments both in vitro and in vivo suggest that the splenic cells with the CD35 and B220 proteins on their surface (CD35+B220+ cells) interact with stromal cells to create a niche for migrating B cells, forming cell clusters. The researchers believe that this may play a critical role in FDC network development and the subsequent formation of lymphoid follicles. There is also some evidence that the stromal cells may fuse with the CD35+B220+ cells during this process.

Further investigation of the role of stromal cells in the development of the lymphoid follicles and B cell maturation is planned, says Murakami.

Reference

1. Murakami, T., Chen, X., Hase, K., Sakamoto, A., Nishigaki, C. & Ohno, H. Splenic CD19-CD35+B220+ cells function as an inducer of follicular dendritic cell network formation. Blood 110, 1215–1224 (2007).

Dependence on Illicit and Licit DrugsGenes Play Role in Risk for




Description
The genes that play a role in illegal drug abuse are not entirely the same as those involved in dependence on legal substances like alcohol and nicotine, and caffeine addiction appears to be genetically independent of all the others, according to a study led by Virginia Commonwealth University researchers.




Research Highlights:
• Genes that play a role in illegal drug abuse are not entirely the same as those involved in dependence on legal substances like alcohol and nicotine
• Caffeine addiction appears to be genetically independent of the others
• Findings could guide efforts to localize genes that influence risk for psychoactive drug abuse or dependence
• First study to examine across the sexes and the degree to which risk factors for dependence are shared between illicit and licit drugs

The genes that play a role in illegal drug abuse are not entirely the same as those involved in dependence on legal substances like alcohol and nicotine, and caffeine addiction appears to be genetically independent of all the others, according to a study led by Virginia Commonwealth University researchers.

The findings may guide efforts by researchers to use molecular genetic tools to localize genes that influence risk for psychoactive drug abuse or dependence, or A/D.

In the November issue of the Archives of General Psychiatry, a journal of the American Medical Association, researchers examined the degree to which genetic and environmental risk factors for dependence were shared between illicit and the more commonly used licit psychoactive drugs among men and women.

“We wanted to know whether there was a single set of genes that influence risk for A/D on all substances,” said Kenneth S. Kendler, M.D., a professor of psychiatry and human genetics in VCU’s School of Medicine and lead author on the study.

“Our findings suggested two genetic factors - one which strongly impacted on risk for A/D of illicit drugs, such as cannabis and cocaine, and one that impacted on risk for A/D of licit drugs, including caffeine, nicotine and alcohol. However, these two factors were rather strongly correlated,” he said. “It was also of interest to note that the genes for caffeine A/D were pretty independent of those found for all the other substances.”

Kendler and his colleagues examined lifetime symptoms of abuse of and dependence on marijuana, cocaine, alcohol, caffeine and nicotine among 4,865 male-male and female-female twin pairs through a series of personal interviews. The data collected from the interviews was analyzed using the methods of structural equation modeling.

The twin pairs that participated were from the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders. These twin pairs were ascertained from the Virginia Twin Registry. The Virginia Twin Registry, now part of the VCU Mid-Atlantic Twin Registry, contains a population-based record of twins from Virginia, North Carolina and South Carolina.

“This study also confirmed the strong role that genetic factors play in influencing our vulnerability to drug abuse and dependence,” Kendler said. Heritability – the proportion of individual differences in risk due to genetic differences – was estimated in this study to be more than 70 percent for cocaine, cannabis and nicotine A/D, nearly 60 percent for alcohol A/D, and, interestingly, quite a bit lower – around 35 percent – for caffeine A/D, he said.

In previous studies, researchers examined an array of illegal substances and did not include commonly used licit drugs, and included only male participates. This was the first study of its kind to examine across the sexes and degree to which risk factors for dependence were shared between illicit and licit drugs.

This work was supported by grants from the National Institutes of Health.

Kendler collaborated with John Meyer, M.S., from the Department of Psychiatry at VCU; and Carol A. Prescott, Ph.D., from the Department of Psychology, University of Southern California.


About VCU and the VCU Medical Center: Virginia Commonwealth University is the largest university in Virginia and ranks among the top 100 universities in the country in sponsored research. Located on two downtown campuses in Richmond, VCU enrolls more than 30,000 students in nearly 200 certificate and degree programs in the arts, sciences and humanities. Sixty-three of the programs are unique in Virginia, many of them crossing the disciplines of VCU’s 15 schools and one college. MCV Hospitals and the health sciences schools of Virginia Commonwealth University compose the VCU Medical Center, one of the nation’s leading academic medical centers. For more, see http://www.vcu.edu. (Newswise)

Caribbean reefs struggling to recover from ecological sucker punches

A new study highlights the series of setbacks that have beset Caribbean coral reefs over the past few decades. The study charts the combination of events that has left the coral reefs in danger of converting to a new ecosystem type — one dominated not by living coral but by blooms of algae.

A group of ecologists led by Peter J. Mumby constructed a mathematical model to investigate the effects of a series of events, each of which acted as sucker punches that damaged reef health over the 1980s. First, coral was damaged by Hurricane Allen in 1980, and shortly after, in 1983, the ecosystem was rocked by a mass die-off of the urchin Diadema antillarum, which help to maintain coral health by grazing algae growing on dead coral, allowing the reef to be recolonized by healthy new coral colonies.

As Mumby and colleagues explain this combination of events — as well as the impact of the immense Hurricane Gilbert in 1988 — left the coral vulnerable to being taken over by algae. Their analysis may offer strategies for rescuing the reef ecosystem, perhaps by promoting populations of parrotfish, which also graze algae growing on the reef.

CONTACT

Peter J. Mumby (University of Exeter, UK)

Climate: Fires affect carbon balance in boreal forest


Carbon balance in the Canadian boreal forest is driven primarily by fire disturbance rather than by climate change. The researchers claim that overall changes in climate have not yet been felt in this large boreal region, and that variations in the landscape carbon balance and vegetation dominance have so far been largely driven by increases in fire frequency.

Ben Bond-Lamberty and colleagues use a process model with three competing vegetation types to examine the effects of climate, carbon dioxide concentrations and fire disturbance on a large area of Canadian boreal forest. They report that the carbon balance between 1948 and 2005 was driven largely by changes in fire disturbance. More frequent and larger fires in the late twentieth century resulted in deciduous trees and mosses increasing production at the expense of coniferous trees. They also find that poor soil drainage decreased the variability of the landscape carbon balance, suggesting that increased climate and hydrological changes do have the potential to affect disproportionately the carbon dynamics of these areas.

CONTACT

Ben Bond-Lamberty (University of Wisconsin-Madison, Madison, WI, USA)

Tel: +1 608 265-5628; E-mail: bpbond@wisc.edu

Neuroscience: The brain in glorious Technicolor


With a combination of genetic tricks and fancy proteins, researchers have colourfully labelled hundreds of individual neurons with distinctive hues to create a ‘Brainbow’. The research, takes mapping to a new level, and results in the labelling of neurons with approximately 90 different colour combinations.

Over a hundred years ago, Ramon Y Cajal’s use of Golgi staining on nerve cells opened the gates to modern neuroscience, but until now it has been tough to map out individual cells in each neuronal circuit. Jeff Lichtman and colleagues have developed the Technicolor version of Golgi staining, Brainbow, allowing more detailed reconstructions of brain circuits. This provides a key step towards modelling how the nervous system works normally and in diseased brains.

CONTACT
Jeff Lichtman (Harvard University, Cambridge, Ma, USA)

Tel: +1 617 496 8943; E-mail: jeff@mcb.harvard.edu

Alternative rewards may reduce addiction



Nondrug rewards could be a viable alternative to addictive drugs according to a study published in Neuropsychopharmacology. This finding could have important implications for those seeking treatment for drug addiction.


Serge Ahmed and colleagues found that rats with the hallmarks of heroin addiction used the substance less when a nondrug reward in the form of food was available. They also found that more dependant rats responded more to this alternative reward. This research indicates that the addicted brain remains reactive to nondrug rewards, and challenges the belief that the transition to addiction is associated with an individual valuing a drug more and nondrug rewards less. While studies in humans are needed, this finding suggests that heroin addiction could potentially be alleviated by increasing the availability of nondrug rewards to those with an addiction.



Contact:

Serge Ahmed (Université Victor-Segalen Bordeaux 2, Bordeaux, France)

Tel: +33 557 571 566; E-mail: sahmed@u-bordeaux2.fr

Evolution: Outside-in?



Theories that explain how the ‘primordial soup’ from which the first cell formed are challenged by a new model presented by Gareth Griffiths.


The theory that all life evolved from one source — the last common ancestor — as proposed by Charles Darwin and others, enjoys considerable support among evolutionary biologists. But questions remain about how the features that comprise a cell — membrane, cytoskeleton, genetic material — evolve to form a functional cell.



Numerous models propose that the formation of cells occurred inside randomly formed compartments (called vesicles) by a process known as the ‘cytoplasm within the vesicle’ scenario. But experimental validation of this theory is limited. Gareth Griffiths now describes an alternative theory that challenges previous dogma: the ‘cytoplasm outside the vesicle’ scenario. This theory states that early cytoplasmic components evolved in fresh water, probably on a mineral rock surface that also anchored small vesicles upon which the cytoplasm evolved.



The crucial difference is that this model proposes that the cytoskeleton, which maintains the three-dimensional structure of a cell and is involved in diverse cellular functions such as motility and transport, is required before, and as part of, the mechanism that led to cell formation. This theory provides an explanation to some of the mystifying questions in evolution, such as how two of the main kingdoms of life — prokaryotes (such as bacteria) and eukaryotes (such as mammals and plants) — might have diverged.



Contact

Gareth Griffiths (European Molecular Biology Laboratory, Heidelberg, Germany)
Tel: + 49 6221 387 8267 Email: gareth-griffiths@embl-heidelberg.de