星空娱乐频道

2013年8月2日星期五

Genetics: More than merely a mutated gene

In the current issue of PLoS Genetics, Michigan State University genetic scientists have begun to understand how the rest of the genome interacts with such mutations to cause the differences we see among individuals.

"It's been known for a while that genetic mutations can modify each other's effects," said Ian Dworkin, MSU associate professor of zoology and co-author of the paper. "And we also know that the subtle differences in an individual's genome -- what scientists call wild type genetic background -- also affects how mutations are manifested."

Dworkin and Sudarshan Chari, zoology doctoral student and the paper's lead author, wanted to know how common it was for wild type genetic background to alter the way genetic mutations interact with each other. This is the first time that it's been examined in a systematic manner, Dworkin added.

Using the fruit fly genome, the researchers found that wild type genetic background affected the outcomes of interactions between genetic mutations about 75 percent of the time. This could have huge implications in how scientists construct genetic networks -- maps of how genes interact with each other.

"It may be that some crucial portions of genetic networks are missing," he said. "It also seems that network descriptions are more fluid than we thought."

Fruit flies have been called humans with wings, genetically speaking, due to their similarities. By focusing on wings and a genetic mutation that alters them, the researchers demonstrated the influence of wild type genetic background was actually quite common.

The broader implication for humans is that even for diseases with a simple genetic basis, variation in the genome may matter for both understanding and treatment, Dworkin said.

This new insight explains how, in an example like breast cancer, every woman's genetic background is likely influencing how the mutation is expressed, causing different disease outcomes. The research also may help explain why some people benefit from a specific treatment for a disease, while others get no benefits or become resistant to a drug after a short time.

It's likely that most diseases with a suspected genetic component, such as cancer, asthma or Parkinson's, involve reactions between more than one set of genes. For Dworkin and Chari, the next step is to tease apart the intricacies of what's happening.

"Is it just the two pairs of genes that are interacting?" Dworkin asked. "Or is it that the two genes are interacting and then many other genes are modifying that reaction? This will help us understand how much complexity is involved."

The research is funded by the National Science Foundation grant number MCB 0922344.

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Baby owls spotted sleeping like baby humans

Aug. 2, 2013 — Baby birds have sleep patterns similar to baby mammals, and their sleep changes in the same way when growing up. This is what a team from the Max Planck Institute for Ornithology and the University of Lausanne found out working with barn owls in the wild. The team also discovered that this change in sleep was strongly correlated with the expression of a gene involved in producing dark, melanic feather spots, a trait known to covary with behavioral and physiological traits in adult owls. These findings raise the intriguing possibility that sleep-related developmental processes in the brain contribute to the link between melanism and other traits observed in adult barn owls and other animals.

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Sleep in mammals and birds consists of two phases, REM sleep ("Rapid Eye Movement Sleep") and non-REM sleep. We experience our most vivid dreams during REM sleep, a paradoxical state characterized by awake-like brain activity. Despite extensive research, REM sleep's purpose remains a mystery. One of the most salient features of REM sleep is its preponderance early in life. A variety of mammals spend far more time in REM sleep during early life than when they are adults. For example, as newborns, half of our time asleep is spent in REM sleep, whereas last night REM sleep probably encompassed only 20-25% percent of your time snoozing.

Although birds are the only non-mammalian group known to clearly engage in REM sleep, it has been unclear whether sleep develops in the same manner in baby birds. Consequently, Niels Rattenborg of the MPIO, Alexandre Roulin of Unil, and their PhD student Madeleine Scriba, reexamined this question in a population of wild barn owls. They used an electroencephalogram (EEG) and movement data logger in conjunction with minimally invasive EEG sensors designed for use in humans, to record sleep in 66 owlets of varying age. During the recordings, the owlets remained in their nest box and were fed normally by their parents. After having their sleep patterns recorded for up to five days, the logger was removed. All of the owlets subsequently fledged and returned at normal rates to breed in the following year, indicating that there were no long-term adverse effects of eves-dropping on their sleeping brains.

Despite lacking significant eye movements (a trait common to owls), the owlets spent large amounts of time in REM sleep. "During this sleep phase, the owlets' EEG showed awake-like activity, their eyes remained closed, and their heads nodded slowly," reports Madeleine Scriba from the University of Lausanne (see video in the link below). Importantly, the researchers discovered that just as in baby humans, the time spent in REM sleep declined as the owlets aged.

In addition, the team examined the relationship between sleep and the expression of a gene in the feather follicles involved in producing dark, melanic feather spots. "As in several other avian and mammalian species, we have found that melanic spotting in owls covaries with a variety of behavioral and physiological traits, many of which also have links to sleep, such as immune system function and energy regulation," notes Alexander Roulin from the University of Lausanne. Indeed, the team found that owlets expressing higher levels of the gene involved in melanism had less REM sleep than expected for their age, suggesting that their brains were developing faster than in owlets expressing lower levels of this gene. In line with this interpretation, the enzyme encoded by this gene also plays a role in producing hormones (thyroid and insulin) involved in brain development.

Although additional research is needed to determine exactly how sleep, brain development, and pigmentation are interrelated, these findings nonetheless raise several intriguing questions. Does variation in sleep during brain development influence adult brain organization? If so, does this contribute to the link between behavioral and physiological traits and melanism observed in adult owls? Do sleep and pigmentation covary in adult owls, and if so how does this influence their behavior and physiology? Finally, Niels Rattenborg from the Max Planck Institute for Ornithology in Seewiesen hopes that "this naturally occurring variation in REM sleep during a period of brain development can be used to reveal exactly what REM sleep does for the developing brain in baby owls, as well as humans."

Video: http://www.frontiersinzoology.com/imedia/2039187711104100/supp2.mp4

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Embedded Systems Freescale aims rugged Cortex-M0+ home appliances

2013/08/02

Freescale is offering 5V ARM Cortex-M0+ microprocessors for higher electromagnetic noise immunity.

Called the Kinetis E series, they are inteded to displace 8 and 16-bit processors from dishwashers, refrigerators, home and building control systems, motor control fans, industrial converters and other equipment commonly operating in high-noise environments.

“Historically, 32-bit MCUs have been associated with lower voltage operation and considered unreliable in electromagnetically harsh environments such as factories or even many households,” said Brandon Tolany, v-p of Freescale MCU business development. “Kinetis E series MCUs have advanced electromagnetic compatibility [EMC] and electrostatic discharge [ESD] protection features designed to support compliance with industrial-grade reliability and temperature requirements.”

The argument is that one 32bit processor can replace multiple less-capable chips, and cost is kept down by giving the Kinetis E series large-pitch packaging options so single-layer board designs can be implemented.

Hardware features and pre-certified, fault-tolerant software routines are available to help designers meet the IEC 60730 Class B safety standard for household appliances, which is mandatory in European markets.

Design support comes through the FRDM-KE02Z Freescale Freedom development platform, Processor Expert software, as well as a software development kit providing access to sample software libraries.

Cortex-M0+ is also supported by IAR Embedded Workbench and the Keil MDK-ARM microcontroller development kit, and additional resources include middleware and software libraries, said Freescale.

Kinetis KE02 MCU features:
Electrical fast transient/electrostatic discharge (EFT/ESD) protection
Flash, RAM, register, watchdog and clock tests
2.7 to 5.5V and -40 to 105°C operating range
20MHz ARM Cortex-M0+ core
Single-cycle 32×32 multiplier
Single-cycle I/O access
Up to 64kbyte flash
256byte EEPROM
Up to 4kbyte RAM

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Business Renesas takes the medicine

2013/08/02

Renesas is slimming down, focussing and increasingly looking to foundries.

Last year the company narrowly escaped being taken over by New York private equity company KKR.

Now that it has ben saved from that fate by the Japanese government, Renesas is looking to implement some of the productivity improvement measures which KKR would have undoubtedly introduced.

Renesas has reduced headcount from 48,000, when it merged with NEC Electronics in April 2010, to 33,000 now.

In the same timeframe, it has reduced fixed costs by 20% representing about $2 billion.

The company’s break-even point is now at about $3.6 billion.

Renesas’ focus is now on energy conservation, the environment, power efficiency and the fusion of control and IT.

‘We are working with the automotive industry on efforts to create next-generation self-driving smart cars,’ says Renesas.

‘In the industrial/networking and general-purpose fields we are aiming to by growing our business through motor solutions with power efficiency, ‘ says Renesas, ‘we are expanding kit solutions and platform solutions. Until now the semiconductor business model has centered on supplying individual MCUs, analogue devices, and power semiconductor products. Demand is growing for a model in which customers are provided with kit solutions consisting of combinations of MCUs, analogue devices, and power semiconductor devices optimized for their products.’

Renesas will continue to operate the Naka factory, Kawashiri factory, and Saijo factory sites as its main front-end production facilities. Other front-end facilities will be either scaled back or consolidated as Renesas looks increasingly to foundries. ‘As we scale back the facilities we operate ourselves, we plan to strengthen our relationships with foundries/subcontractors as strategic partners’ says Renesas.

‘Already, the number of company executives, units, and business divisions in the Renesas Group has been reduced substantially, as we move forward with efforts to slim down the organization to achieve speedier decision-making’ says the company.

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Business Spansion completes Fujitsu deal; expands NAND business

2013/08/02

Spansion, the NOR flash specialist, has completed its acquisition of Fujitsu’s microcontroller and analogue business.

Spansion is paying $110 million for the business plus $38 million for inventory.

Spansion had Q2 sales of $195.1 million, gross margin of 29.4%, an operating loss of $600,000 and a net loss of $3.2 million.

Thr company is moving into NAND and had $22 million in sales of NAND chips and ‘strong design win momentum.’

The company has $305 million cash.

“We remain the embedded market leader for NOR Flash memory, delivered sequential improvements in margins and profit, and saw strong NAND momentum,” says John Kispert, CEO of Spansion, “we remain confident of our long-term vision and strategy as we enhance our Flash memory product portfolio, protect our IP and add new microcontroller and analog IP and products.”

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Monster galaxies lose their appetite with age

Aug. 1, 2013 — Our universe is filled with gobs of galaxies, bound together by gravity into larger families called clusters. Lying at the heart of most clusters is a monster galaxy thought to grow in size by merging with neighboring galaxies, a process astronomers call galactic cannibalism.

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New research from NASA's Spitzer Space Telescope and Wide-field Infrared Survey Explorer (WISE) is showing that, contrary to previous theories, these gargantuan galaxies appear to slow their growth over time, feeding less and less off neighboring galaxies.

"We've found that these massive galaxies may have started a diet in the last 5 billion years, and therefore have not gained much weight lately," said Yen-Ting Lin of the Academia Sinica in Taipei, Taiwan, lead author of a study published in the Astrophysical Journal.

Peter Eisenhardt, a co-author from NASA's Jet Propulsion Laboratory in Pasadena, Calif., said, "WISE and Spitzer are letting us see that there is a lot we do understand -- but also a lot we don't understand -- about the mass of the most massive galaxies." Eisenhardt identified the sample of galaxy clusters studied by Spitzer, and is the project scientist for WISE.

The new findings will help researchers understand how galaxy clusters -- among the most massive structures in our universe -- form and evolve.

Galaxy clusters are made up of thousands of galaxies, gathered around their biggest member, what astronomers call the brightest cluster galaxy, or BCG. BCGs can be up to dozens of times the mass of galaxies like our own Milky Way. They plump up in size by cannibalizing other galaxies, as well as assimilating stars that are funneled into the middle of a growing cluster.

To monitor how this process works, the astronomers surveyed nearly 300 galaxy clusters spanning 9 billion years of cosmic time. The farthest cluster dates back to a time when the universe was 4.3 billion years old, and the closest, when the universe was much older, 13 billion years old (our universe is presently 13.8 billion years old).

"You can't watch a galaxy grow, so we took a population census," said Lin. "Our new approach allows us to connect the average properties of clusters we observe in the relatively recent past with ones we observe further back in the history of the universe."

Spitzer and WISE are both infrared telescopes, but they have unique characteristics that complement each other in studies like these. For instance, Spitzer can see more detail than WISE, which enables it to capture the farthest clusters best. On the other hand, WISE, an infrared all-sky survey, is better at capturing images of nearby clusters, thanks to its larger field of view. Spitzer is still up and observing; WISE went into hibernation in 2011 after successfully scanning the sky twice.

The findings showed that BCG growth proceeded along rates predicted by theories until 5 billion years ago, or a time when the universe was about 8 billion years old. After that time, it appears the galaxies, for the most part, stopped munching on other galaxies around them.

The scientists are uncertain about the cause of BCGs' diminished appetites, but the results suggest current models need tinkering.

"BCGs are a bit like blue whales -- both are gigantic and very rare in number. Our census of the population of BCGs is in a way similar to measuring how the whales gain their weight as they age. In our case, the whales aren't gaining as much weight as we thought. Our theories aren't matching what we observed, leading us to new questions," said Lin.

Another possible explanation is that the surveys are missing large numbers of stars in the more mature clusters. Clusters can be violent environments, where stars are stripped from colliding galaxies and flung into space. If the recent observations are not detecting those stars, it's possible that the enormous galaxies are, in fact, continuing to bulk up.

Future studies from Lin and others should reveal more about the feeding habits of one of nature's largest galactic species.

JPL manages the Spitzer Space Telescope mission for NASA's Science Mission Directorate, Washington. Science operations are conducted at the Spitzer Science Center at the California Institute of Technology in Pasadena. Data are archived at the Infrared Science Archive housed at the Infrared Processing and Analysis Center at Caltech. Caltech manages JPL for NASA. For more information about Spitzer, visit http://spitzer.caltech.edu and http://www.nasa.gov/spitzer .

JPL managed and operated WISE for NASA's Science Mission Directorate. Edward Wright is the principal investigator and is at UCLA. The mission was selected competitively under NASA's Explorers Program managed by the agency's Goddard Space Flight Center in Greenbelt, Md. The science instrument was built by the Space Dynamics Laboratory in Logan, Utah. The spacecraft was built by Ball Aerospace & Technologies Corp. in Boulder, Colo. Science operations and data processing take place at the Infrared Processing and Analysis Center at the California Institute of Technology in Pasadena. Caltech manages JPL for NASA. More information is online at http://www.nasa.gov/wise and http://wise.astro.ucla.edu and http://jpl.nasa.gov/wise .

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Arctic sea-ice loss has widespread effects on wildlife

Aug. 1, 2013 — With sea ice at its lowest point in 1,500 years, how might ecological communities in the Arctic be affected by its continued accelerating melting over the next decades? Penn State University Professor of Biology Eric Post and an international team of scientists tackle this question by examining relationships among algae, plankton, whales, and terrestrial animals such as caribou, arctic foxes and walrus; as well as the effects of human exploration of previously inaccessible parts of the region.

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"Arctic sea ice has declined by more than 86,000 square kilometers -- a space slightly larger than the state of South Carolina -- per year," Post said. "That's an area of critical habitat for many species and the rate of loss is increasing." Post added that an acceleration of this rate likely will be due, in part, to the loss the white surface provided by ice that reflects sunlight -- thereby causing a cooling effect. The highly reflective ice, Post added, will be replaced by a much-less-reflective, darker surface of open water -- and the effect will be accelerated warming and accelerated melting.

A domino effect of sea-ice melting on terrestrial animals, Post explained, could happen through a disruption in the food chain. Sea-ice algae and sub-ice plankton, which together account for 57 percent of the total annual biological production in the Arctic Ocean, already are being immediately affected by sea-ice melting because ice loss triggers a significant change in the blooming times of these organisms. Likewise, land adjacent to areas of sea-ice loss will experience significant surface warming inland from the coastline, affecting soil conditions and plant growth. Post and his colleagues hypothesize that, while invertebrate ocean-dwelling animals -- such as zooplankton that feed on algae and phytoplankton in the seas -- already are being affected, larger terrestrial animals such as caribou could find their land-dwelling food sources disrupted, as well, due to temperature changes affecting plant communities inland.

"A change in population mixing could be another, indirect effect of sea-ice melting," Post said. He explained that populations of wolves and arctic foxes that currently are isolated only during the summer could become even more isolated. A longer period of the year without ice, which promotes travel between populations, could lead to a decline in crossbreeding.

However, for other species, the effect of sea-ice loss could be just the opposite: "We know that, for some species, sea ice acts as a barrier to intermixing," Post explained. "So for these species, ice loss and a lengthening of the ice-free season likely will increase population mixing, reducing genetic differentiation." Post explained that, for example, polar and grizzly bears already have been observed to have hybridized because polar bears now are spending more time on land, where they have contact with grizzlies.

While such mixing of populations is not necessarily cause for concern, Post explained, it could lead to drastic changes in disease dynamics. For example, a population that currently is a host to a certain pathogen could carry that pathogen to another, previously unexposed population. "In addition, a decrease in sea ice in arctic Canada likely will increase contact between eastern and western arctic species, promoting mixing of pathogen communities that previously were isolated," Post said. "For example, phocine distemper virus (PDV) currently affects eastern Arctic seals. But if these seals begin to mix with western arctic seals, the virus may reach other, naive populations."

Post added that greater accessibility of previously remote parts of the Arctic to human exploration could be yet another unexpected consequence of sea-ice loss. "Retreating sea ice, longer ice-free seasons, and loss of sea ice are expected to promote development of shipping lanes and increased shipping traffic in areas that formerly were rather inaccessible," Post said. "This increased marine access likely will accelerate the pace of mineral and petroleum exploration in the Arctic, which in turn could affect both terrestrial and marine animals; for example, bowhead whales and Pacific walrus."

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'Soft' approach leads to revolutionary energy storage: Graphene-based supercapacitors

Published today in Science, a research team led by Professor Dan Li of the Department of Materials Engineering has developed a completely new strategy to engineer graphene-based supercapacitors (SC), making them viable for widespread use in renewable energy storage, portable electronics and electric vehicles.

SCs are generally made of highly porous carbon impregnated with a liquid electrolyte to transport the electrical charge. Known for their almost indefinite lifespan and the ability to re-charge in seconds, the drawback of existing SCs is their low energy-storage-to-volume ratio -- known as energy density. Low energy density of five to eight Watt-hours per litre, means SCs are unfeasibly large or must be re-charged frequently.

Professor Li's team has created an SC with energy density of 60 Watt-hours per litre -- comparable to lead-acid batteries and around 12 times higher than commercially available SCs.

"It has long been a challenge to make SCs smaller, lighter and compact to meet the increasingly demanding needs of many commercial uses," Professor Li said.

Graphene, which is formed when graphite is broken down into layers one atom thick, is very strong, chemically stable and an excellent conductor of electricity.

To make their uniquely compact electrode, Professor Li's team exploited an adaptive graphene gel film they had developed previously. They used liquid electrolytes -- generally the conductor in traditional SCs -- to control the spacing between graphene sheets on the sub-nanometre scale. In this way the liquid electrolyte played a dual role: maintaining the minute space between the graphene sheets and conducting electricity.

Unlike in traditional 'hard' porous carbon, where space is wasted with unnecessarily large 'pores', density is maximised without compromising porosity in Professor Li's electrode.

To create their material, the research team used a method similar to that used in traditional paper making, meaning the process could be easily and cost-effectively scaled up for industrial use.

"We have created a macroscopic graphene material that is a step beyond what has been achieved previously. It is almost at the stage of moving from the lab to commercial development," Professor Li said.

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Stimulating brain cells can make false memories

Aug. 1, 2013 — Any crime scene investigator can tell you that memories are unreliable; the way people remember a place or event changes over time and varies between individuals. But for the mice in one lab at MIT, the accuracy of memories is even more suspect. Howard Hughes Medical Institute researchers in that lab have discovered how to alter the animals' memories by turning on neurons in the brain that are associated with the memories and updating them with new information.

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The new findings, which appear in the journal Science, illustrate that a mouse can be made to fear a cage by giving it a foot shock while at the same time reactivating a memory of the cage to associate the two.

"The kinds of things that once existed only in the realm of science fiction movies like Inception and Eternal Sunshine of the Spotless Mind are now experimentally possible," says Steve Ramirez, a graduate student in the lab of HHMI investigator Susumu Tonegawa and first author of the new work.

Researchers knew that memories are stored by the brain in a small set of neurons. Understanding how this information is encoded could be key to understanding how human memory works as well as memory disorders. But identifying exactly which neurons are linked to specific memories has been technically challenging.

Ramirez and Tonegawa, along with Xu Liu, a postdoctoral fellow in Tonegawa's lab at the Massachusetts Institute of Technology, had previously developed a way to pinpoint the specific handful of neurons that are activated in the brains of mice in any particular situation. The technique relies on optogenetics, a method of controlling brain cells through bursts of light developed by HHMI early career scientist Karl Deisseroth at Stanford University. The researchers engineered brain cells to produce a light-sensitive protein whenever the neurons were activated in a new setting or situation. Then, by shining a light onto the brain through a fiber optic cable connected to the mouse's skull, they could reactivate only that subset of neurons. Even without reactivating the cells, they could determine which cells had been activated by measuring which contained the light-sensitive protein. The approach was described in a 2012 Nature paper.

More recently, the scientists wondered if they could alter the way a mouse remembered a setting by activating neurons associated with it. They chose to test this idea by attempting to change whether or not a mouse was afraid of a particular cage.

"In mice, fear can be seen as a binary behavioral output," says Ramirez. "Either the animal is exploring a box that it's interested in, and it's curious and sniffing around. Or, if it's displaying fear behavior, it's huddled in a corner not moving. So it's a very easy, very powerful readout of memory."

To see whether they could make an animal associate fear with a previously neutral setting, Tonegawa's lab group first exposed mice to one of four unique cages. Each cage had distinct flooring materials, artificial smells, and different lighting. As the mice scouted out the new room, whichever neurons were activated produced the special light-sensitive protein.

Next, the mice were moved to a second cage. This time, as the mice explored, the scientists used light to turn on the neurons that had been activated in the first cage and simultaneously shocked the feet of the mice. Then the mice were put back in the first area -- where they'd never received a shock. The mice were clearly fearful of the setting, Ramirez says, spending more than a quarter of their time frozen in place.

"We were astonished that this worked on the very first mouse we ever tried," he says. "We got the animal to be scared of an environment where technically, nothing bad had ever happened to it."

By contrast, when the mice were put in a third cage that they'd never been in before, they exhibited no fear. And in a control group of mice that had received shocks in the second cage but no neuron reactivation, the first cage never induced fear.

After the successful experiment, Tonegawa, Ramirez, and Liu looked at the details of which neurons in the brain had been responsible for inducing the memory of the first cage. The neurons, they found, were located in the dentate gyrus, part of the hippocampus. The dentate gyrus has previously been implicated in the formation of memories, and is one of the areas of the brain with the most new neuron generation during adulthood. But most evidence about its importance came from instances in which the area had been damaged and memories lost.

"This study gives us information on the basic mechanism that could be happening in the brain when memories or false memories are formed," says Ramirez. "Next, we want to see if we can do the same with not only fear memories but pleasure memories or memories of objects or memories of other mice."

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New type of protein modification may play a role in cancer and diabetes

"It appears to be an intrinsic feedback mechanism in glucose metabolism, but I suspect that its other functions throughout the cell will prove at least as interesting when they are more fully elucidated," said Benjamin F. Cravatt, chair of the Department of Chemical Physiology and member of the Skaggs Institute for Chemical Physiology at TSRI.

Cravatt and his postdoctoral fellow Raymond E. Moellering reported the finding in the August 2, 2013 issue of the journal Science.

In Search of New Protein Modifiers

The Cravatt laboratory has long studied the natural chemical modifications that can change the functions of proteins "on the fly," switching their biological activities on or off or otherwise altering them. The better known of these modifications include phosphorylation, the addition of a small molecule known as a phosphate group, and acetylation, the addition of an acetyl group.

In search of new protein modifiers, Cravatt and Moellering, whose postdoctoral fellowship is sponsored in part by the Howard Hughes Medical Institute and the Damon Runyon Cancer Research Foundation, decided to investigate a small molecule known as 1,3-bisphosphoglycerate (1,3-BPG). The molecule's chemical makeup suggested that it might readily react with some proteins to form semipermanent, function-altering modifications. 1,3-BPG is one of the main "intermediate" molecules produced during glycolysis, which is a core metabolic pathway that converts glucose to cellular fuel.

"1,3-BPG's intrinsic reactivity seemed odd to us, considering that it is such a central metabolite," remembered Moellering.

Moellering's initial test-tube experiments showed that 1,3-BPG does indeed react with certain lysine amino acids to modify GAPDH, the enzyme that mediates the production of 1,3-BPG. "That gave us the first indication that this reaction does happen, and that we should therefore start looking for it in cells," he said.

A Role in Glucose Metabolism

After devising new methods to detect this unique lysine modification in human cell cultures, Moellering soon found it -- on other glucose-metabolizing enzymes, as well as on proteins seemingly unrelated to glucose metabolism.

"With every step we took, the project became more interesting, because we were finding signs that this reaction occurs frequently in cells and in animal tissues, and in unexpected cellular locations, too," Moellering said.

He detected the signature of the new lysine modification not only on proteins in the main volume of the cell (the cytosol), but also in the DNA-containing cell nucleus and even on the cell's membrane compartments.

"It appears that wherever GAPDH goes within cells, it is capable of catalyzing the localized production of 1,3-BPG, which in turn reacts with nearby proteins to modify their structure and function," said Cravatt.

Moellering found that when 1,3-BPG's lysine modification occurs on glucose-metabolizing enzymes, it tends to inhibit their activities, causing a slowdown of central glucose processing and a consequent buildup of certain glucose metabolites in the processing pathway. Moellering and Cravatt suspect that these overabundant metabolites may end up being shunted into other cellular processes besides basic fuel-making -- processes that contribute to the synthesis of new molecules and even cell proliferation.

Moellering also discovered that 1,3-BPG and the modification it makes on proteins become more prevalent as glucose levels rise. Within the context of glucose metabolism, 1,3-BPG's modification thus seems to act as a "very old, maybe ancient feedback mechanism for regulating that central metabolic pathway," Moellering said.

Looking Ahead

The abnormal processing of glucose within cells features in a number of major diseases including cancer and diabetes. "Cancer cells, for example, bring in as much as 20 times more glucose than non-cancerous cells of the same type," Moellering noted. He now wants to find out whether 1,3-BPG is part of the problem in such cells. At abnormally high levels, it conceivably could help force glucose metabolism toward the runaway cell proliferation that is a hallmark of cancer.

Cravatt and Moellering also want to learn more about what 1,3-BPG's lysine modification does in the nuclei and membrane compartments of cells, where they found evidence of it. "We suspect that it works to connect glucose metabolism to other pathways, perhaps as a kind of signaling mechanism," said Moellering.

Already Moellering has uncovered evidence that there are enzymes that work to reverse 1,3-BPG's modification of lysines -- which underscores the likelihood that this modification represents a fundamental, dynamic mechanism in cells. "We'd like to discover which enzymes catalyze the removal of the modification," said Cravatt, "because then, in principle, we could use inhibitors of these enzymes to control the levels of the modification and get a better understanding of its biological functions as well as the conditions under which it occurs."

Funding for the study, "Functional Lysine Modification by an Intrinsically Reactive Primary Glycolytic Metabolite," was provided by the National Institutes of Health (CA087660), the Skaggs Institute for Chemical Biology at TSRI and the Damon Runyon Cancer Research Foundation.

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