Research uncovers new facts about odor detection in insects; findings could lead to more effective repellents

PASADENA, Calif.--If you think it doesn't do much good to swipe the fly that's going after the potato salad, guess again. You may be discouraging the fly's colleagues from taking up the raid.

New evidence shows that a stressed fly emits an odor that makes other flies avoid the space in which the stressful event occurred. Reporting in an advance on-line publication of the September 15 issue of the journal Nature, California Institute of Technology professors David Anderson and Seymour Benzer, along with Professor Richard Axel of Columbia University, discuss their findings about how flies may communicate information about their internal state to one another.

According to the authors, the act of shaking or shocking flies causes a repellent odor to be emitted that contains carbon dioxide as one of its active components. The research involved the fruit fly, Drosophila melanogaster, which has been used for decades in genetics experiments. However, the mechanism could be more widespread.

"We showed that CO2 is itself a potent repellent for Drosophila," says Anderson, a professor of biology at Caltech and also a Howard Hughes Medical Institute investigator.

The researchers also succeeded in mapping the initial neural circuitry that leads to CO2 avoidance. The team, led by Caltech postdoctoral scholar Greg Suh, found that CO2 activates a single class of sensory neurons in the fruit flies, and that these neurons seem to be dedicated to the sole task of responding to this odor. By inhibiting the synapses of these neurons using fancy genetic trickery, the researchers were able to block the ability of flies to avoid CO2, in behavioral experiments.

"These results show that there is probably a genetically determined, or 'hard-wired' circuit mediating CO2 avoidance behavior in the fly," Anderson says.

But even though the research is primarily aimed at furthering the understanding of the neural circuitry underlying innate behaviors, there might also be practical results. For one, the fact that mosquitoes are attracted to their warm-blooded hosts by CO2 exhalations has been known for years.

Although fruit flies are repelled by CO2, while mosquitoes are attracted to it, "given the evolutionary conservation of olfactory mechanisms in insects, if we learn about the molecular details involved in CO2 sensing in fruit flies, it could potentially lead to repellents that act by interfering with the reception of CO2," Anderson adds.

Such a repellent could be of benefit in third-world countries where mosquitoes are vectors of diseases like malaria--or even in the United States, where the mosquito-borne West Nile virus has been a serious health concern this year.

Robert Tindol

Caltech Professor Awarded Stein and Moore Award for Insights Into the Life Cycle of Cells

PASADENA, Calif.-- Ubiquitin is a small protein that has a very big job. Or jobs, to be more accurate. Indeed, the ubiquitin system is central to--literally--just about everything significant that goes on inside cells, and to a lot of intercellular business as well. Once unknown and, until the 1980s, unheralded, the ubiquitin system is now one of the major areas of study in cell biology, biochemistry, and genetics, and the point of convergence for many disparate disciplines.

For their cofounding of the ubiquitin field, Alexander Varshavsky of the California Institute of Technology and Avram Hershko of the Technion-Israel Institute of Technology have been named corecipients of the Protein Society's 2005 Stein and Moore Award. Presented annually, the award was given to the pair in recognition of their "revolutionary work in discovering the ubiquitin system of protein degradation, its mechanisms, and its significance to living cells."

Varshavsky is the Smits Professor of Cell Biology at Caltech; Hershko is the distinguished professor of biochemistry at the Technion. The Stein and Moore Award is another in a long line of prestigious awards presented to the pair for their groundbreaking work.

"I am grateful to receive the Stein and Moore Award," says Varshavsky, "in part because the people who won it before us are such an illustrious company in our profession: Anfinsen, Neurath, Rossman, Fersht, Sigler, to cite just a few of them. The award is named after two great scientists, Stein and Moore, whose work in the 1950s and 1960s laid the foundations of modern protein chemistry."

The ubiquitin system is central to an incredible variety of biological processes: the cell cycle, cell growth and differentiation, embryogenesis and later development, programmed cell death, signal transmission, all kinds of DNA transactions (including DNA repair and replication), the immune response, the functions of the nervous system--the list goes on and on.

In addition, the ubiquitin system has become the cornerstone of cancer research. The relevance of the ubiquitin system to cancer cannot be overstated: a large number, if not a majority, of oncoproteins (proteins that, when mutated or overexpressed, can cause a normal cell to become cancerous) and tumor suppressors have been found to be either components or targets of the ubiquitin system. Studies by Varshavsky and coworkers in the 1980s, and particularly their discoveries of the first physiological functions of the ubiquitin system (in the cell cycle, DNA repair, transcriptional regulation, protein synthesis, and stress responses), eventually led, through the work by many laboratories, to the current preeminence of the ubiquitin system in cancer research.

By the late 1980s, the definitive and profoundly complementary advances by the laboratories of Hershko and Varshavsky transformed the realm of intracellular protein degradation from a relative backwater to a broad and dynamic subject of great importance.

Varshavsky is a member of the National Academy of Sciences, and has received a number of scientific awards, including the Gairdner Award, the Lasker Award, the Sloan Prize, the Hoppe-Seyler Award, the Merck Award, the Wolf Prize, the Horwitz Prize, the Max Planck Research Award for Biosciences and Medicine, the Pasarow Award, the Massry Prize, and the Wilson Medal.

The Protein Society is the leading international society devoted to furthering research and development in protein science. Varshavsky and Hershko will be presented their award at the society's annual symposium, to be held in Boston in 2005.-

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Fish, Frog, and Fly Share a Molecular Mechanism to Control Embryonic Growth

PASADENA, Calif. — Oriented cell division is a fundamental process in developing organisms, whether you are a worm, a fruit fly--or a human. As an embryo begins to grow, cells divide again and again, from the single fertilized egg to the countless cells present at birth. These cell divisions are not haphazard; instead, they are often precisely oriented, playing an important role in building an embryo of the right size and shape, and with the right body "parts"--the control of cell division also plays a central role in placing cells in the proper positions to build organs that will contain the correct cell types.

The orientation of cell divisions has been well studied in invertebrates, especially in Caenorhabditis elegans (worm) and Drosophila melanogaster (fruit fly), but relatively little has been known about oriented cell division in vertebrates. Now for the first time, researchers at the California Institute of Technology report that the molecular machinery that underlies oriented cell division in invertebrates serves a similar but twofold purpose in the development of the vertebrate embryo. For one, it is responsible for orienting cell division, or mitosis. For another, it's responsibile for the movements that elongate the round egg into the vertebrate body plan; that is, the shape of the particular animal. The research appears in the August 5 edition of the journal Nature (

The researchers are recent graduates Ying Gong '04 and Chunhui Mo '03, working with Scott Fraser, the Anna L. Rosen Professor of Biology and director of the Biological Imaging Center. Using the zebrafish, a card-carrying vertebrate, as their animal model, the researchers first marked certain cells with fluorescent proteins. Then, using a four-dimensional confocal microscope, they were able to follow the motions of these cells in real time, as the body plan of the zebrafish took shape during development, or gastrulation. The researchers found that cells in dorsal tissue divide in an oriented fashion, with one of the two daughter cells from each division moving towards the head, and the other towards the future tail. They were able to determine that such oriented cell division is a major driving force for the extension of the body axis--the growth of the embryo into the animal's final shape.

By combining their advanced imaging tools with molecular biological techniques, the researchers were able to show that the driving force for these oriented divisions is the Wnt "pathway," a ubiquitous cascade of specific proteins that trigger cellular function. Research over the past decade has shown that the Wnt pathway controls the patterns, fates, and movements of cells in both vertebrates and invertebrates. One major branch of this biochemical communication network is the planar cell polarity (PCP) pathway. In previous work from the Fraser lab and their collaborators, the PCP pathway has been shown to guide the tissue motions that convert the spherical frog embryo into the familiar shape of the elongated tadpole. This is a key process in the life of the frog, termed convergent extension. Each cell attempts to "elbow between" the row of cells to its left or its right. "This simple motion has a profound effect on the length and width of the embryo," says Fraser; "think of a band marching shoulder to shoulder on a football field. If half of the rows of marchers merged with the adjacent row, the band would be half as wide and twice as long."

The trio of researchers explored the effects in fish embryos of altering the many proteins in the Wnt-PCP signaling pathway, including some of the potential signals and co-receptors (proteins called Silberblick/Wnt11, Dishevelled, and Strabismus). They were expecting to see an alteration in the convergent-extension motions. Instead, what they found was a major alteration in the orientation of cell division. When they blocked the Wnt pathway, cell division did not take place along the head-tail axis, but randomly. In normal fish embryos, the oriented divisions lengthened the body axis by nearly twofold. With randomization, though, a short and squat embryo was created.

Given that the same PCP pathway is involved in controlling cell division in the invertebrates, C. elegans and D. melanogaster, and the vertebrate zebrafish, the results suggest that the pathway has an evolutionary conserved role. That is, that across a wide variety of animal species, such pathways share a common function, perhaps reflecting a common origin in the biological past.

"The amazing thing about these studies is that they show that the many varied mechanisms that can create the long and narrow body plan of a fish, frog, or fly come under a common molecular control mechanism," Fraser says. "Work in frog embryos from John Wallingford (formerly of UC Berkeley, currently at University of Texas, Austin) and Richard Harland (UC Berkeley) have established a link between these motions and neural tube defects (such as craniorachischisis and spina bifida). Our new experiments have already prompted a new round of collaborative experiments to determine if the same molecular pathway controls convergent extension, cell division, or both in mammals. The answers to these questions promise new insights into the underlying cause for some of the devastating birth defects seen in humans. "

MEDIA CONTACT: Mark Wheeler (626) 395-8733

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New Class of Reagents Developed by Caltech Chemical Biologists for In Vivo Protein Tracking

PASADENA, Calif.--One of the big problems in biology is keeping track of the proteins a cell makes, without having to kill the cell. Now, researchers from the California Institute of Technology have developed a general approach that measures protein production in living cells.

Reporting in the July 26 issue of the journal Chemistry and Biology, Caltech chemistry professor Richard Roberts and his collaborators describe their new method for examining "protein expression in vivo that does not require transfection, radiolabeling, or the prior choice of a candidate gene." According to Roberts, this work should have great impact on both cell biology and the new field of proteomics, which is the study of all the proteins that act in living systems.

"This work is a result of chemical biology—chemists, and biologists working together to gain new insights into a huge variety of applications, including cancer research and drug discovery," says Roberts.

"Generally, there is a lack of methods to determine if proteins are made in response to some cellular stimuli and what those specific proteins are," Roberts says. "These are two absolutely critical questions, because the behavior of a living cell is due to the cast of protein characters that the cell makes."

Facing this problem, the Roberts team tried to envision new methods that would enable them to decipher both how much and what particular protein a cell chooses to make at any given time. They devised a plan to trick the normal cellular machinery into labeling each newly made protein with a fluorescent tag.

The result is that cells actively making protein glow brightly on a microscope slide, much like a luminescent Frisbee on a dark summer night. Importantly, these tools can also be used to determine which particular protein is being made, in much the same way that a bar code identifies items at a supermarket checkout stand.

To demonstrate this method, the team used mouse white blood cells that are very similar to cells in the human immune system. These cells could be tagged to glow various colors, and the tagged proteins later separated for identification.

Over the next decade, scientists hope to better understand the 30,000 to 40,000 different proteins inside human cells. The authors say they are hopeful that this new approach will provide critical information for achieving that goal.

The title of the paper is "A General Approach to Detect Protein Expression In Vivo Using Fluorescent Puromycin Conjugates." For more information, contact Heidi Hardman at

Robert Tindol

Caltech Nobel Laureate Ed Lewis Dies

PASADENA—Edward Lewis, winner of the 1995 Nobel Prize for his groundbreaking studies of how genes regulate the development of specific regions of the body, died Wednesday, July 21, 2004, at Huntington Hospital in Pasadena after a long battle with cancer. He was 86.

A member of the California Institute of Technology faculty since 1946, Lewis spent his life working on the genetics of the fruit fly, with special attention to the fundamental ways in which the genes relate to embryonic development. The work had profound implications for a basic understanding of the genetic regulation of development in humans. At the time of his death he was the Morgan Professor of Biology, Emeritus, and until very recently maintained an active schedule in his campus laboratory.

In a book published on Lewis earlier this year, author and longtime collaborator Howard Lipshitz wrote that Lewis's scientific research was "the bridge linking experimental genetics as conducted in the first half of the 20th century, and the powerful molecular genetic approaches that revolutionized the field in its last quarter." Lipshitz also lauded Lewis's much less widely known work on the understanding of radiation and cancer, and the closely related issues concerning nuclear-weapons testing policy.

Born May 20, 1918, in Wilkes-Barre, Pennsylvania, Lewis as an adolescent became interested in the genetics of the fruit fly, Drosophila melanogaster, which was already being touted as an excellent animal for research by Caltech's Thomas Hunt Morgan. Lewis performed genetics experiments on Drosophila while just a freshman in high school, and after taking a bachelor's degree in 1939 at the University of Minnesota, came to Caltech for a doctorate and remained at the Institute for the rest of his life, save for four years in the U.S. Army Air Force during World War II, when he worked as a meteorologist.

Lewis published several research papers while still a college student, and soon after the war was a recognized expert in the field of fly genetics. Returning to Caltech in 1946 as an instructor, he was named an assistant professor in 1948, earned tenure the following year, and became a professor of biology in 1956. He was named the Thomas Hunt Morgan Professor of Biology in 1966 and retained the chair until his retirement from active faculty duties in 1988.

In a campus article appearing in 1957, Lewis described his success in causing the flies to mutate with four wings (they normally have two). "We now have a working model for picturing the genetic control of development," he said. His prognostication was indeed correct, and nearly four decades later the Nobel Committee, in awarding Lewis the Nobel Prize in physiology or medicine, cited his triumph in identifying and classifying "a small number of genes that are of key importance in determining the body plan and the formation of body segments." The Nobel Committee also lauded Lewis for his discovery of "how genes were arranged in the same order on the chromosomes as the body segments they controlled."

In the same article, Lewis discussed his good fortune in becoming an active geneticist at a revolutionary time in biology. After the war, the gene was still treated as an abstract entity because the techniques needed to ascertain its molecular nature were yet to be developed, he explained. "You could begin to try to see how a gene is constructed, even though DNA hadn't yet been determined to be the hereditary material. The laws of genetics had never depended upon knowing what the genes were chemically and would hold true even if they were made of green cheese."

Although the modern techniques of molecular biology were yet to be invented, Lewis was never reticent about using novel methods to better understand the genetics of the fly. He created his four-winged mutants by bombarding the flies with x-rays, thereby playing a key role in discovering and explaining the role of homeotic genes--that is, genes that influence how the undifferentiated cells in a fertilized embryo separate into a head and a tail end, and how the eyes, legs, antennae, and other organs all form in their correct positions. These genes are "highly conserved," as geneticists say, because the genes are similar in all organisms and play a role in the development of all animals, from fruit flies to mice to humans.

"Ed was the bridge between the pioneers of Drosophila work--Morgan, Bridges, and Sturtevant--to modern developmental biology," said David Baltimore, president of Caltech and also a Nobel Prize-winning biologist. "Ed saw that even a lowly fruit fly could be a key to understanding the mysterious process of how a fertilized egg turns into a fully developed organism."

Lewis became a legend on the Caltech campus, and when he returned home after his 1995 Nobel Prize was announced—he had been attending a scientific conference in Switzerland at the time—was celebrated for his 60 years of dedication to his work and his classical approach to individual research in an era when "big science" increasingly became the more prominent model.

Lewis is survived by his wife of 57 years, Pam Lewis; and two sons, Keith Lewis of Redwood City, California, and Hugh Lewis of Bellingham, Washington.

Robert Tindol

Neuroscientists Demonstrate New Way to Control Prosthetic Device with Brain Signals

PASADENA, Calif.—Another milestone has been achieved in the quest to create prosthetic devices operated by brain activity. In the July 9 issue of the journal Science, California Institute of Technology neuroscientists Sam Musallam, Brian Corneil, Bradley Greger, Hans Scherberger, and Richard Andersen report on the Andersen lab's success in getting monkeys to move the cursor on a computer screen by merely thinking about a goal they would like to achieve, and assigning a value to the goal.

The research holds significant promise for neural prosthetic devices, Andersen says, because the "goal signals" from the brain will permit paralyzed patients to operate computers, robots, motorized wheelchairs—and perhaps someday even automobiles. The "value signals" complement the goal signals by allowing the paralyzed patients' preferences and motivations to be monitored continuously.

According to Musallam, the work is exciting "because it shows that a variety of thoughts can be recorded and used to control an interface between the brain and a machine."

The Andersen lab's new approach departs from earlier work on the neural control of prosthetic devices in that most previous results have relied on signals from the motor cortex of the brain used for controlling the limb. Andersen says the new study demonstrates that higher-level signals, also referred to as cognitive signals, emanating from the posterior parietal cortex and the high-level premotor cortex (both involved in higher brain functions related to movement planning), can be decoded for control of prosthetic devices.

The study involved three monkeys that were each trained to operate a computer cursor by merely "thinking about it," Andersen explains. "We have him think about positioning a cursor at a particular goal location on a computer screen, and then decode his thoughts. He thinks about reaching there, but doesn't actually reach, and if he thinks about it accurately, he's rewarded."

Combined with the goal task, the monkey is also told what reward to expect for correctly performing the task. Examples of variation in the reward are the type of juice, the size of the reward, and how often it can be given, Andersen says. The researchers are able to predict what each monkey expects to get if he thinks about the task in the correct way. The monkey's expectation of the value of the reward provides a signal that can be employed in the control of neural prosthetics.

This type of signal processing may have great value in the operation of prosthetic devices because, once the patient's goals are decoded, then the devices' computational system can perform the lower-level calculations needed to run the devices. In other words, a "smart robot" that was provided a goal signal from the brain of a patient could use this signal to trigger the calculation of trajectory signals for movement to be accomplished.

Since the brain signals are high-level and abstract, they are versatile and can be used to operate a number of devices. As for the value signals, Andersen says these might be useful in the continuous monitoring of the patients to know their preferences and moods much more effectively than currently possible.

"These signals could also be rapidly adjusted by changing parameters of the task to expedite the learning that patients must do in order to use an external device," Andersen says. "The result suggests that a large variety of cognitive signals could be interpreted, which could lead, for instance, to voice devices that operate by the patients' merely thinking about the words they want to speak."

Andersen is the Boswell Professor of Neuroscience at Caltech. Musallam and Greger are both postdoctoral fellows in biology at Caltech; Corneil is a former researcher in Andersen's lab who is now at the University of Western Ontario; and Scherberger, a former Caltech researcher, is now at the Institute of Neuroinformatics in Zurich, Switzerland.

Robert Tindol

"Minis" Have Mega Impact in the Brain

Embargoed: Not for Release Until 11:00 a.m. PDT Thursday, 24 June, 2004

PASADENA, Calif. — The brain is a maddeningly complex organ for scientists to understand. No assumption can remain unchallenged, no given taken as a given.

Take "minis" for example. That is, miniature excitatory synaptic events. The location where neurons communicate with each other is the synapse, the tiny gap between the ends of nerve fibers. That's where one nerve cell signals another by secreting special chemicals called neurotransmitters, which jump the gap. The synapse, and its ability to strengthen and wane, is thought to be at the heart of learning and memory. Minis, mere single, tiny packets of neurotransmitters, were always thought to have no biological significance, nothing more than "noise," or background chatter that played no role in the formation of a memory. Minis, it was thought, could be safely ignored.

Maybe not, says Mike Sutton, a postdoctoral scholar in the lab of Erin Schuman, an associate professor of biology at the California Institute of Technology, and an associate investigator for the Howard Hughes Medical Institute. Sutton, Schuman, and colleagues Nicholas Wall and Girish Aakalu report that on the contrary, minis may play an important role in regulating protein synthesis in the brain. Further, their work suggests the brain is a much more sensitive organ than originally perceived, sensitive to the tiniest of chemical signals. Their report appears in the June 25th issue of the journal Science.

Originally, Sutton et. al. weren't looking at minis at all, but at protein synthesis, the process through which cells assemble amino acids into proteins according to the genetic information contained within that cell's DNA. Proteins are the body's workhorses, and are required for the structure, function, and regulation of cells, tissues, and organs. Every protein has a unique function.

A neuron is composed of treelike branches that extend from the cell body. Numerous branches called dendrites contain numerous synapses that receive signals, while another single branch called an axon passes the signal on to another cell.

The original rationale behind the experiment was to examine how changes in synaptic activity regulate protein synthesis in a dendrite, says Sutton. His first experiment was a starting point to ask what happens when we first remove all types of activity from a cell, so he could then add it back later incrementally and observe how this affected protein synthesis in dendrites. "So we were going on the assumption that the spontaneous glutamate release--the minis--would have no impact, but we wanted to formally rule this out," he says.

Using several different drugs, Sutton first blocked any so-called action potentials, an electrical signal in the sending cell that causes the release of the neurotransmitter glutamate. Normally, a cell receives hundreds of signals each second. When action potentials are blocked, it receives only minis that arrive at about one signal each second. Next he blocked both the action potential and the release of any minis. "To our surprise, the presence or absence of minis had a very large impact on protein synthesis in dendrites," he says. It turned out that the minis inhibit protein synthesis, which increased when the minis were blocked. Further, says Sutton, "it appears the changes in synaptic activity that are needed to alter protein synthesis in dendrites are extremely small--a single package of glutamate is sufficient."

Sutton notes that it is widely accepted that synaptic transmission involves the release of glutamate packets. That is, an individual packet (called a vesicle) represents the elemental unit of synaptic communication. "This is known as the 'quantal' nature of synaptic transmission," he says, "and each packet is referred to as a quantum. The study demonstrates, then, the surprising point that protein synthesis in dendrites is extremely sensitive to changes in synaptic activity even when those changes represent a single neurotransmitter quantum.

"Because it's so sensitive," says Sutton, "there is the possibility that minis provide information about the characteristics of a given synapse (for example, is the signal big or small?), and that the postsynaptic or receiving cell might use this information to change the composition of that synapse. And it does this by changing the complement of proteins that are locally synthesized."

The ability to rapidly make more or fewer proteins at a synaptic site allows for quick changes in synaptic strength. Ultimately, he says, this ability may underlie long-term memory storage.

"It's amazing to us that these signals, long regarded by many as synaptic 'noise,' have such a dramatic impact on protein synthesis," says Schuman. "We're excited by the possibility that minis can change the local synaptic landscape. Figuring out the nature of the intracellular 'sensor' for these tiny events is now the big question."

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The Brain Can Make Errors in Reassembling the Color and Motion of Objects

PASADENA, Calif.—You're driving along in your car and catch a glimpse of a green SUV out of the corner of your eye. A few seconds later, you glance over, and to your surprise discover that the SUV is actually brown.

You may assume this is just your memory playing tricks on you, but new research from psychophysicists at the California Institute of Technology and the Helmholtz Institute in the Netherlands suggests that initial perceptions themselves can contain misassigned colors. This can happen in certain cases where the brain uses what it sees in the center of vision and then rearranges the colors in peripheral vision to match.

In an article appearing in this week's journal Nature, Caltech graduate student Daw-An Wu, Caltech professor of biology Shinsuke Shimojo, and Ryota Kanai of the Helmholtz Institute report that the color of an object can be misassigned even as observers are intently watching an ongoing event because of the way the brain combines the perceptions of motion and color. Because different parts of the brain are responsible for dealing with motion and color perception, mistakes in "binding" can occur, where the motion from one object is combined with the color of another object.

This is demonstrated when observers gaze steadily at a computer screen on which red and green dots are in upward and downward motion. In the center area of the screen, all the red dots are moving upward while all the green dots are moving downward.

Unknown to the observers, however, the researchers are able to control the motion of the red and green dots at the periphery of the screen. In other words, the red and green dots are moving in a certain direction in the center area of the screen, but their motion is partially or even wholly reversed on each side.

The observers show a significant tendency to mistake the motion of the red and green dots at the periphery. Even when the motion was completely reversed on the sides, the observers would see the same motion all across the screen.

According to Wu, the lead author of the paper, the design of the experiment exploits the fact that different parts of the brain are responsible for processing different visual features, such as motion and color. Further, the experiment shows that the brain can be tricked into binding the information back together incorrectly.

"This illusion confirms the existence of the binding problem the brain faces in integrating basic visual features of objects, " says Wu. "Here, the information is reintegrated incorrectly because the information in the center, where our vision is strongest, vetoes contradicting (but correct) information in the periphery."

The title of the article is "Steady-State Misbinding of Color and Motion."



Robert Tindol

Two Caltech Faculty Receive Franklin Medals

PASADENA—Two members of the California Institute of Technology faculty, chemist Harry Gray and biologist Seymour Benzer, are among this year's recipients of the prestigious Benjamin Franklin Medals.

The honor is bestowed annually by the Franklin Institute in Philadelphia to outstanding American scientists and technologists. Approaching its 180th anniversary, the Franklin Medal has been presented in the past to Albert Einstein, Samuel F. B. Morse, Alexander Graham Bell, Steven Hawking, Gordon Moore, Jane Goodall, and Noam Chomsky, among others. Past recipients have also won 103 Nobel Prizes through the years.

Gray, who is being recognized for his work in metalloproteins, is the Beckman Professor of Chemistry and founding director of the Beckman Institute at Caltech. A Caltech professor since 1966, he served as chair of the Division of Chemistry and Chemical Engineering from 1978 to 1984. He is a member of the National Academy of Sciences, received the National Medal of Science in 1986, and is also the recipient of the Wolf Prize and the Harvey Prize. Gray was named a foreign member of Great Britain's Royal Society, as well as a member of the American Philosophical Society.

Benzer is the Boswell Professor of Neuroscience, Emeritus, at Caltech, and a preeminent molecular biologist who has worked on phage genetics, nervous system development, and behavioral genetics of the fruit fly. He has been at Caltech since 1965. He is a member of the National Academy of Sciences. He received the National Medal of Science in 1983, and is also the recipient of the Lasker Award, the Wolf Prize, the Crafoord Prize, and the Harvey Prize. He is a member of the Royal Society and the American Philosophical Society.

Benzer and Gray will be honored in Philadelphia on April 29 at the annual Franklin Institute Awards Ceremony and Dinner, which is held in the Benjamin Franklin National Memorial.

Robert Tindol
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Researchers discover fundamental scaling rule that differentiates primate and carnivore brains

PASADENA, Calif.--Everybody from the Tarzan fan to the evolutionary biologist knows that our human brain is more like a chimpanzee's than a dog's. But is our brain also more like a tiny lemur's than a lion's?

In one previously unsuspected way, the answer is yes, according to neuroscientists at the California Institute of Technology. In the current issue of the Proceedings of the National Academy of Sciences (PNAS), graduate student Eliot Bush and his professor, John Allman, report their discovery of a basic difference between the brains of all primates, from lemurs to humans, and all the flesh-eating carnivores, such as lions and tigers and bears.

The difference lies in the way the percentage of frontal cortex mass increases as the species gets larger. The frontal cortex is the portion of brain just behind the forehead that has long been associated with reasoning and other "executive" functions. In carnivores, the frontal cortex becomes proportionately larger as the entire cortex of the individual species increases in size--in other words, a lion that has a cortex twice the size of another carnivore's also has a frontal cortex twice the size.

By contrast, primates like humans and apes tend to have a frontal cortex that gets disproportionately larger as the overall cortex increases in size. This phenomenon is known as "hyperscaling," according to Bush, the lead author of the journal article.

What this says about the human relationship to the tiny lemurs of Madagascar is that the two species likely share a developmental or structural quirk, along with all the other primates, that is absent in all the carnivores, Bush explains. "The fact that humans have a large frontal cortex doesn't necessarily mean that they are special; relatively large frontal lobes have developed independently in aye-ayes among the lemurs and spider monkeys among the New World monkeys."

Bush and Allman reached their conclusions by taking the substantial histological data from the comparative brain collection at the University of Wisconsin at Madison. The collection, accumulated over many years by neuroscientist Wally Welker, comprises painstaking data taken from well over 100 species.

Bush and Allman's innovation was taking the University of Wisconsin data and running it through special software that allowed for volume estimations of the various structures of the brain in each species. Their results compared 43 mammals (including 25 primates and 15 carnivores), which allowed them to make very accurate estimations of the hyperscaling (or the lack thereof) in the frontal cortex.

The results show that in primates the ratio of frontal cortex to the rest of the cortex is about three times higher in a large primate than in a small one. Carnivores don't have this kind of systematic variation.

The hyperscaling mechanism is genetic, and was presumably present when the primates first evolved. "Furthermore, it is probably peculiar to primates," says Allman, who is Hixon Professor of Neurobiology at Caltech.

The next step will be to look at the developmental differences between the two orders of mammals by looking at gene expression differences. Much of this data is already available through the intense efforts in recent years to acquire the complete genomes of various species. The human genome, for example, is already complete, and the chimp genome is nearly so.

"We're interested in looking for genes involved in frontal cortex development. Changes in these may help explain how primates came to be different from other mammals," Bush says.

At present, the researchers have no idea what the difference is at the molecular level, but with further study they should be able to make this determination, Allman says. "It's doable."

The article is titled "The scaling of frontal cortex in primates and carnivores." For a copy of the article, contact Jill Locantore, PNAS communications specialist, at 202-334-1310, or e-mail her at

The PNAS Web site is at

For more information on Bush and Allman's research, go to the Web site


Robert Tindol


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