Caltech Launches Major Bioscience Initiative with $18 Million Donation from Eli Broad

PASADENA--Eli Broad, one of Southern California's most prominent civic and business leaders, has teamed with the California Institute of Technology to create a center for the biological sciences which will drive technological and scientific innovation and solidify Southern California's role as a leader in the biotechnology industry.

Broad has donated $18 million to create the Broad Center for the Biological Sciences, which will provide 100,000 square feet of space for 10 new Caltech research groups to work at the cutting edge of the biological sciences. The contribution is part of a $100 million campaign by Caltech to increase its historical strength in the biological sciences. The gift was announced on Tuesday, September 15 at a press conference held at Caltech's Athenaeum.

"Advances in the biological sciences will have the single greatest impact on human experience in the coming century," said Broad. "I want Southern California to be a leader in this critically important field, and Caltech is uniquely qualified to spearhead this remarkable new initiative."

Broad's gift is the largest donation so far in Caltech's new Biological Sciences Initiative, which aims at raising $100 million for new faculty and resources. A total of $56 million has been raised since the initiative was announced in May of this year.

The Initiative comes at a time when the scientific community is clearly directing greater resources to fundamental discovery in the biological sciences. With many new and promising biological and medical advances on the horizon, Caltech officials feel that augmenting the resources available to biological research will have a direct impact on high-tech ventures in the Los Angeles/Pasadena area as well as breakthroughs in the health field.

"Eli's gift will insure that Caltech remains at the biological forefront as we enter the new century," said David Baltimore, president of Caltech and a Nobel Prize-winning biologist.

"I see great strides ahead in the manipulation of genes in myriad areas from medicine to information technology to agriculture," Baltimore added. "We are entering the post-genomic age."

The new building will be located in the northwest quadrant of campus near the Beckman Institute. As the cornerstone capital project of the Biological Sciences Initiative, the building will provide crucial infrastructure in the Institute's new capabilities for magnetic imaging, structural chemistry, and mammalian genetics.

"The biological sciences are being touted as the economic engine of the 21st century," said Mel Simon, chair of the Caltech Division of Biology. "This gift is going to lead to significant contributions toward our country's economic well-being as well as our physical well-being."

In addition to the new building, the initiative also sets as its goal the hiring of a dozen new professors, the creation of new disciplines and new approaches within existing disciplines, the support of new graduate fellowships and postdoctoral positions, and the creation of new MD/PhD programs. The Biological Sciences Initiative is being co-chaired by Caltech trustees Camilla Chandler Frost and Benjamin M. Rosen.

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Robert Tindol
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Mechanism of cell suicide determined by Caltech, MIT researchers

PASADENA—Biologists at MIT and Caltech have uncovered the chemical details of a mechanism that cells use to commit suicide. The work appears in the August 28 issue of the journal Science.

According to David Baltimore, president of Caltech and a Nobel Prize-winning biologist, his lab at MIT has succeeded in describing how roundworms known as nematodes kill off unwanted cells. The work is especially interesting, Baltimore says, because human beings have very similar proteins to those causing cell suicide in nematodes and, in fact, his lab can often substitute human proteins for the same results.

"All cells contain the machinery to commit suicide," Baltimore said prior to publication of the paper. "You can see this in a wide variety of events, such as a tadpole's resorption of its tail, local ischemia in a stroke victim's brain, and tissue destruction after a heart attack.

"Cell suicide is also one of the great protections against cancer." According to the current paper in Science, a common type of apoptosis, or cell suicide, involves three stable proteins found in nematode cells. These proteins are normally quiet, but can be readily triggered by death signals in such a way that the cell digests itself.

The three proteins are known as CED-3, CED-4, and CED-9. None of these proteins alone will kill cells, the research shows, but the three interact in such a way that CED-4 can signal CED-3 to begin the destruction process, while CED-9 acts as an inhibitor to CED-4.

The general outline of this particular pathway of apoptosis was discovered by MIT professor Robert Horvitz some years ago, but the details have never been understood until now, Baltimore says.

"We did all of this with proteins from a nematode where the pathway was first found, but the proteins all have human homologs," Baltimore says. These are Apaf-1, which is very similar to CED-4; Bcl-2, which is a homolog of CED-9; and mammalian cysteine protease zymogens that are analogous to CED-3.

Therefore, the cascade of reactions in nematode cells could very well resemble the manner in which the human body can cause cancerous cells to self-destruct. The work was supported by the National Institutes of Health. In addition to Baltimore, the authors are Xiaolu Yang and Howard Y. Chang. Yang is currently at the University of Pennsylvania.

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Robert Tindol
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New Study Shows How Axons Find Their Way Home

Pasadena--Like a commuter trying to get to work during rush hour, a growing axon must thread its way through a throng of other axons that are headed in many different directions in the developing brain. Axons are the wire like extensions of nerve cells that carry electrical signals from one place to another in the brain, and during development they must navigate across long distances (many centimeters) to reach their correct address within the brain. If the axon gets lost, brain circuits cannot form normally, and, like the commuter showing up at the wrong office, the axon may not be able to do its job. So how do axons find their way? A report published in the July 24 issue of the journal Science. by Drs. Susan Catalano and Carla Shatz of the University of California at Berkeley, sheds light on how axons home in on their correct targets.

Traditionally, scientists studying the mechanisms of axon navigation thought in terms of molecular guidance cues. Molecules located in specific places in the brain can tell a growing axon "grow here," "don't grow there," or "make a left turn here." The collective distribution of these molecules in the developing brain forms a pathway that the axon can follow to get to the right place. But Catalano and Shatz suspected that the situation might be more complicated than that. The brain is too complicated, and the genome too small, for there to be a molecular address at every possible target location in the brain. They suspected that there might be another potential source of guidance cues for the growing axons: electrical activity itself. They decided to block electrical activity within the developing brain with a neurotoxin made by the Japanese puffer fish, and their suspicions were confirmed: in the absence of activity many axons fail to find their way to the correct address. Instead they become confused and wander into other regions they normally bypass. Dr. Susan Catalano, now at the California Institute of Technology, offers this analogy: "If the growing axon is like a car, then the highway pavement and traffic signals would be like the guidance molecules. Demonstrating that neural activity is critical for axon navigation is like adding a Global Positioning System into the mix; its a whole new level of information that the axon can potentially use to guide its way toward the appropriate target."

Catalano and Shatz studied axons that grow out from nerve cells located in a brain structure called the thalamus. During development these axons must navigate toward their correct target, the neocortex. The thalamus is a vital way station within the brain; all of the information coming from the sensory organs (such as the eyes, ears, and skin surface) passes through the thalamus on its way to the neocortex. The neocortex is the highly folded layer of neurons on the surface of the brain that is responsible for such functions as language processing; in other words, it is the brain structure that makes us uniquely human. The connections from the thalamus to the cortex are not randomly organized: specific groups of nerve cells within the thalamus (called nuclei) connect up to specific areas of the neocortex. This precise organization, or "map", is critical for proper brain function. In order to form this circuit correctly during development, groups of axons coming from specific places within the thalamus must navigate across the vast expanse of neocortex. They must bypass incorrect areas of the neocortex and choose just the right area to connect with, but without electrical activity, the axons become lost.

How might electrical activity produce this effect? While that is not currently known, clues can be found in studies of other regions in the brain. Previous work from Dr. Shatz's lab has shown that very early in development when the axons from the eye are still navigating toward their targets in the brain, waves of electrical activity sweep across the retina. This means that axons that are nearest neighbors are electrically active at the same time. Simultaneous activity could alter the molecular environment of the pathway through which the axons grow and allow cohorts of axons to keep together during navigation.

Ever since the pioneering work of Nobel laureates David Hubel and Torsten Wiesel, it has been known that the pattern of electrical activity carried by different sets of axons can influence the physical shape of the axons themselves. During the last phases of development, axons from the thalamus form many branches as they spread out through the neocortex to make their final sets of connections. These branches are literally shaped like the branches of a tree, and hence are called the "terminal arbor." Changes in the axon's pattern of electrical activity can change the shape of the tree that forms; less activity results in a shrunken, knarled axon tree. Surrounding axons with normal levels of activity form many more branches that grow into the shrunken tree's territory, just like their counterparts in nature that grow into the sunlit space created when a neighbor falls.

While the role of electrical activity in the final stages of thalamic axon branch formation had been well established, the possibility that the same process might be crucial in early development during axon navigation remained uninvestigated until now. The clinical implications of this are potentially alarming: drugs such as nicotine, which can affect electrical activity within the brain, have the potential to disrupt circuit formation in a developing infant's brain at very early stages, when the major circuits of the brain are being formed. The possibility that developing brains are vulnerable to disruption by activity-altering agents at such early times suggests important areas for future research.

Brain cells attuned to visual nearness and farness interact to allow judgments of size, research shows

PASADENA—Evolution has been benevolent to humans and other primates in providing us with eyes that can judge the size of nearby objects.

With a visual feature known as "size constancy," we can pretty accurately judge whether the furry thing walking across our field of view is the size of a mouse or the size of a lion, regardless of its distance and whether we recognize the object. Where survival of the species is concerned, the advantage of having size constancy is pretty obvious: it helps us identify dinner, but at the same time helps us stay off someone else's menu.

But the precise neurological nature of size constancy has never been well understood. If we are seeing our very first lion and the lion is walking away from us, then his image in our field of vision is getting smaller and smaller. Distance cues and stereoscopic vision are at play, but what is really happening in our brains? Is the third dimension added on at a late stage in visual processing, or are the images of lions at varying distances actually analyzed at the very first stage of visual perception?

New research from the California Institute of Technology shows that the latter is the case. Our brains need information for object and three-dimensional scaling, and this information is common to all visual cortical areas of the brain.

In the July 24 issue of Science, Caltech biology professor John Allman and his colleagues write that brain cells involved in vision tend to be apportioned to picking up farness or nearness. In working with rhesus monkeys trained to follow dots of varying size on a moving TV monitor, the researchers have found that the monkeys use their nearness and farness cells in tandem.

"The perception of depth is the product of the interaction of the two opposed tendencies, near and far," says Allman. "There are many systems in the body, and several in the visual system, which work by the precise counterbalancing of two opposed tendencies.

"For color perception, for example, you have opposition between black and white, red and green, and blue and yellow," he adds. "So our results show that depth perception is also a fundamental opposition."

Thus, the basic idea is that ability to judge the size of objects is embedded in the primary visual center as a code of opposed interaction of "nearness" and "farness" cells. Therefore, the neurons are pooled for depth perception; lab work with monkeys earning rewards for correct depth identification bears this out.

In addition to Allman, the authors are Jozsef Fiser of the University of Southern California; and Allan C. Dobbins and Richard M. Jeo of the Caltech Division of Biology.

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Robert Tindol
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Professor Jose Alberola-Ila Named 1998 Pew Scholar

PASADENA–The California Institute of Technology is pleased to announce that José Alberola-Ila, assistant professor of biology, has been named a 1998 Pew Scholar as part of the Pew Scholars Program in Biomedical Sciences. The $200,000 award will support Alberola-Ila's research over the next four years.

Alberola-Ila joined the Caltech faculty in 1997. His research focuses on one of the most important signal transduction pathways in the immune system and has used transgenic techniques as well as clever and creative chemical approaches to resolve some important issues regarding the pathway's involvement in the immune response.

"His addition to our Division of Biology greatly strengthens Caltech's immunology program," said David Baltimore, president of Caltech, in his endorsement of Alberola-Ila. "Dr. Alberola-Ila studies the intracellular signals that regulate T cell development and function and thus control how T cells respond to tumors and pathogens . . . He will pursue this research with T cells at Caltech, where, I am happy to say, he and I will have adjacent research labs."

Alberola-Ila is an honors graduate of the University of Valencia (MD 1987) and the University of Barcelona (PhD in cellular biology/immunology 1992). He specialized in immunology as a resident physician at the Hospital Clinic Barcelona, Servei d'immunologia, from 1988 to 1992, and was a senior research fellow in immunology at the University of Washington's Howard Hughes Medical Institute from 1992 to 1997.

The Pew Charitable Trusts, a national philanthropy based in Philadelphia, support nonprofit activities in the areas of conservation and the environment, culture, education, health and human services, public policy, and religion. Through their grant making, the Trusts seek to encourage individual development and personal achievement, cross-disciplinary problem solving, and innovative, practical approaches to meet the changing needs of society.

Founded in 1891, Caltech has an enrollment of some 2,000 students, and a faculty of about 280 professorial members and 284 research members. The Institute has more than 19,000 alumni. Caltech employs a staff of more than 1,700 on campus and 5,300 at JPL.

Over the years, 26 Nobel Prizes and four Crafoord Prizes have been awarded to faculty members and alumni. Forty-three Caltech faculty members and alumni have received the National Medal of Science; and eight alumni (two of whom are also trustees), two additional trustees, and one faculty member have won the National Medal of Technology. Since 1958, 13 faculty members have received the annual California Scientist of the Year award. On the Caltech faculty there are 75 fellows of the American Academy of Arts and Sciences; and on the faculty and Board of Trustees, 68 members of the National Academy of Sciences and 46 members of the National Academy of Engineering.

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Sue Pitts McHugh
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Professor Bruce Hay Named 1998 Ellison Medical Scholar

PASADENA–The California Institute of Technology is pleased to announce that Bruce Hay, assistant professor of biology, has been named a 1998 Ellison Medical Scholar as part of the Ellison Medical Foundation New Scholars in Aging Program. The $200,000 award will support Hay's research over the next four years.

While Hay's work is centered on the study of the regulation of cell death in Drosophila, the topic of the present grant focuses on the development and application of genetic techniques to build sophisticated tools for identifying the relevant proteins that could be drug targets.

Caltech's president, David Baltimore, in endorsing Hay's investigation of apoptosis, a genetically regulated form of cell death that is critical for the normal development and adult function of multicellular organisms, said that "understanding what happens when apoptosis is inappropriately activated is important for investigating the neuronal cell loss associated with acute brain injuries such as stroke, and in degenerative, age-related diseases such as Alzheimer's disease."

Hay received a BA in biology from Claremont McKenna College in 1982 and a PhD in neuroscience from the University of California, San Francisco, in 1989. He held postdoctoral fellowships in the departments of physiology and biochemistry at the University of California, San Francisco, from 1990 to 1991 and in the department of molecular and cellular biology at the University of California, Berkeley, from 1991 to 1996. He joined the Caltech faculty in 1996.

The Ellison Medical Foundation has been established by a gift from Mr. Laurence J. Ellison to support biomedical research (including basic biology, epidemiology, and clinical investigation) on aging. The Ellison Medical Foundation New Scholars in Aging Program is designed to support new investigators of outstanding promise in the basic biological and clinical sciences relevant to understanding aging processes and age-related diseases and disabilities. The award is intended to provide the significant support to new investigators needed to permit them to become established in the field of aging.

Founded in 1891, Caltech has an enrollment of some 2,000 students, and a faculty of about 280 professorial members and 284 research members. The Institute has more than 19,000 alumni. Caltech employs a staff of more than 1,700 on campus and 5,300 at JPL.

Over the years, 26 Nobel Prizes and four Crafoord Prizes have been awarded to faculty members and alumni. Forty-three Caltech faculty members and alumni have received the National Medal of Science; and eight alumni (two of whom are also trustees), two additional trustees, and one faculty member have won the National Medal of Technology. Since 1958, 13 faculty members have received the annual California Scientist of the Year award. On the Caltech faculty there are 75 fellows of the American Academy of Arts and Sciences; and on the faculty and Board of Trustees, 68 members of the National Academy of Sciences and 46 members of the National Academy of Engineering.

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Sue Pitts McHugh
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Adhesive substance at nerve synapses is importantin memory and learning, research shows

PASADENA—A sticky molecule found at the junctions of brain cells may be a crucial chemical ingredient in learning and memory, neuroscientists have discovered.

In the current issue of the journal Neuron, Erin Schuman and her students at the California Institute of Technology report that a calcium-dependent family of molecules known as cadherins plays a significant role in chemically joining the synapses (the junctions of nerves). Neuroscientists believe that the environment of the synapses is where memories are stored.

"These cadherins may form a sort of zipper-like structure at the junction of the presynaptic cell and the postsynaptic cell," says Schuman, who is a Howard Hughes Medical Institute investigator and assistant professor of biology at Caltech

"We show in this study that these molecules participate in making the synapses bigger and stronger, a process called 'long-term potentiation' that may be involved in memory storage."

According to Schuman's graduate student Lixin Tang, who is coauthor of the paper, the new research involves turning off the cadherins to see what happens to long-term potentiation when the synapses have to do without them.

"It has been known for some time that cadherins are important during early development," says Tang. "But they are also expressed well into adulthood. So we were interested in seeing what would happen when cadherin was disrupted in the adult brain."

The researchers shut off the cadherins in the hippocampuses of adult mice and rats with various antibodies targeting various adhesion sites, as well as with inhibitory peptides. The results showed that long-term potentiation was significantly reduced when the cadherins were temporarily inactivated at synapse junctions.

However, the overall signal transmission of the synapses and their structural integrity were unchanged by the antibodies. This would indicate that the cadherins are used very specifically by the nerves for changing the strength of synapses, but not for the basic transmission of nerve impulses.

Finally, the inhibitory peptides were indeed effective in shutting down long-term potentiation, but only if they were introduced at the beginning of long-term potentiation. When the peptides were introduced about 30 minutes afterward, they had no effect.

This suggests that there may be factors other than the cadherins involved in long-term potentiation, and that these factors cannot be blocked by the peptides, Schuman explains. Like the antibodies, the peptides have no effect on baseline signal transmission or structural integrity when they disrupt the cadherins.

Also, it is known that calcium transiently leaves the synaptic junction during nerve impulses. And further, cadherins require calcium in order to stick together. Therefore, a possibility to explain the selective effect of the peptides on long-term potentiation initiation is that calcium leaving the junction during synaptic activity transiently destabilizes the cadherin bonds, thus allowing the blocking action of the peptides.

Schuman and colleagues find that elevating the concentration of calcium in the extracellular solution protects the cadherins from the inhibitory peptides. This suggests that cadherins might be able to work as "activity sensors" outside nerve cells by monitoring changes in calcium and then changing their binding to one another.

Taken together, the new results suggest that the cadherins are important in changing synapses in ways thought to be important to learning and memory. In addition to Schuman and Tang, the authors of the paper also include Chou P. Hung, who graduated from Caltech in 1996.

The research was supported by the Howard Hughes Medical Institute.

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Robert Tindol
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Parent that takes care of offspring tends to outlive the other parent, study shows

PASADENA--The parent who stays home to take care of the kids may be getting a good deal healthwise. New primate research from the California Institute of Technology shows that a primary caregiver tends to live longer than the other parent.

In a statistical study of 10 primate species, including humans, apes, and various Old and New World monkeys, the Caltech researchers show that the parent that cares for the offspring is significantly longer lived than the mate, regardless of gender. Titi monkey males of South America, for example, which take care of the baby after the mother has given birth, outlive their mates by 20 percent.

"The numbers show that if there is a difference in role, the sex doing the bulk of the care is likely to survive longer," says John Allman, a Caltech biology professor who is lead author of the study.

"This follows from the fact that it takes a lot of energy to raise a big-brained offspring like a human or an ape or a monkey," he adds. "The sex not caring for the infants will not be as crucial for the survival of the species."

The size of the brain is the key, Allman says. Species with big brains mature slowly and have only one baby at time, and these babies depend on their parents for a long time.

"Big brains are very expensive," Allman says. "They are costly in terms of time, energy and anatomical complexity. This reduces the reproductive potential of the parents because extra-special care must be provided to insure that this reduced number survive to reproductive age."

In an article appearing in the current issue of the journal Proceedings of the National Academy of Science, Allman and his coauthors outline their data from the 10 species of primates. To determine the lifespans of males and females that have borne offspring, the researchers analyzed the data from zoo populations, field studies, laboratory research, and human historical and demographic documents.

The researchers were especially interested in reviewing field studies as well as zoo data to ensure that artificial effects were not skewing the data. However there is also data from natural populations of primates that supports this hypothesis.

"Female gorillas, orangutans, and chimpanzees have a proportionally larger survival advantage than human females," Allman says. But the advantage of female gorillas is not so pronounced, and this could very well have to do with the fact that male gorillas play with their offspring and take on certain other nurturing duties.

In fact, the Caltech hypothesis is not only that the caregiver who takes care of the offspring tends to outlive his/her mate, but also that the effect disappears when parents share in caregiving more or less equally.

Perhaps for this reason human males and females also have lifespans that are fairly similar in length. The current figure is about 8 percent, but does not take into consideration the fact that medical care has significantly reduced the death rate from childbirth. Swedish demographic data from the late 1700s, by contrast, shows that females lived about 5 percent longer than their mates in those days, when childbirth was a leading cause of death in women.

The demographic data of the 10 primate species shows remarkable conformity to the hypothesis. In all of the primates studied in which females are the primary caregivers-spider monkeys, gibbons, orangutans and gorillas-females live significantly longer than males. Human female live longer than males, but the difference is smaller than in these primates and the male role is larger although less than the female role in childrearing.

In the two primates studied in which females and males share caregiving more or less equally, there is no difference between the survival rates of the sexes. In the two primate studies in which males have a larger role in caring for offspring, the owl monkey and the titi monkey, males live longer than females. The effect is significant for the owl monkeys, but not for titi monkeys because of the smaller sample available for these animals.

Allman acknowledges that the results are somewhat counterintuitive: many people think that child raising is quite stressful, and if anything should shorten the life of a harried parent. But just the opposite is true.

"There's probably not one single reason that the caregiver outlives the other parent," he says. "Risk taking in males and estrogen in females are probably factors, and there may even be a beneficial hormonal or chemical change that occurs through extending care to another.

"There's evidence that greater longevity can also coincide with the taking care of an elderly parent or even a pet," he concludes.

"So it could be that taking care of others is just good for you."

The other authors of the paper are Andrea Hasenstaub, a junior majoring in mathematics and engineering at Caltech; Aaron Rosin, a former Caltech student who graduated with a degree in biology; and Roshan Kumar, another Caltech graduate, who is now a researcher at the Scripps Research Institute in La Jolla, California.

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Robert Tindol
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Biologists discover fundamental genetic principle governing blood vessel formation

PASADENA--An unsuspected but fundamental genetic rule governing the formation of the cardiovascular system has been uncovered by biologists at the California Institute of Technology. The discovery could influence the development of therapies for both cardiovascular disease and cancer.

According to Caltech biology professor and Howard Hughes Medical Institute Investigator David Anderson, the new findings arrive amid an explosion of new information about the molecular basis of blood vesveins "have to 'talk' to each other to develop properly," says Anderson. The findings may help explain how an intact circulatory system, with the correct proportion of arteries and veins, can be put into place before the heart even begins to beat. The research appears in the current issue of the journal Cell.

By "talking," Anderson is referring to the major finding of the study, which is that complementary molecules found on surfaces of primitive arteries and veins must interact with each other for proper blood vessel formation to occur.

The findings may have broad implications, Anderson suggests. "One should reconsider the molecular biology, pathology, and drug therapies of the vascular system in terms of the molecular differences between arteries and veins." It is likely, says Anderson, that arteries and veins will differ in their expression of many other genes that have yet to be discovered. Such genes may lead to the development of new artery- or vein-specific drugs, or may help to target known drugs specifically to either arteries or veins. Such advances could potentially enhance the efficacy or specificity of blood vessel-directed anticancer drugs such as those discovered by Dr. Folkman. They could also aid in the treatment of diseases that selectively affect either arteries or veins.

Specifically, the Anderson team found that a molecule known as ephrin-B2, present on developing arteries, must communicate with its receptor Eph-B4, present on developing veins. These proteins are expressed by endothelial cells, the first cells that form primitive vessel-like tubules in the embryo and that go on to form the inner lining of arteries or veins. This process appears to be a fundamental interaction for the development of the embryo. If it fails to occur, embryonic development is blocked almost as soon as the heart begins to beat.

The discovery actually occurred when Anderson's graduate student, Hai Wang, was performing a gene knockout experiment to see if the ephrin-B2 gene is essential for the development of the nervous system. When Wang eliminated the gene that codes for ephrin-B2 in mouse embryos, he found no nervous system defects, but did notice that there were defects in the forming vascular system and heart.

The procedure involved the substitution of a "marker" gene that makes cells turn blue where the ephrin-B2 gene would normally be turned on. The result revealed, surprisingly, that the ephrin-B2 gene was expressed in arteries but not veins. Wang then showed that the receptor for ephrin-B2, Eph-B4, was expressed on veins but not arteries. Eph-B4 and ephrin-B2 fit together in a lock-and-key-like manner, signaling each cell that the other has been engaged. This complementarity was seen on vessels throughout the developing embryo. The fact that elimination of the ephrin-B2 gene caused defects in both arteries and veins suggests that not only do arteries send a signal to veins via ephrin-B2, but that veins must also signal back to arteries. The fact that both ephrin-B2 and Eph-B4 span the cell membrane suggests that each protein may be involved in both sending and receiving a signal.

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Robert Tindol
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Caltech Announces $100 million Drive For Biological Sciences

PASADENA—The California Institute of Technology has formally announced the goal of raising $100 million in a campaign to support new initiatives in the biological sciences.

The Biological Sciences Initiative (BSI) will allow the Institute to create approximately a dozen new faculty positions in biology and related disciplines, construct a new biology building on campus, develop new joint training programs with medical schools, and target several major biological questions that can be answered only through sustained research in state-of-the-art facilities.

"We intend to keep Caltech at the forefront of research in the biological sciences," says Camilla Frost, cochair of the BSI and member of the Caltech Board of Trustees.

According to Caltech president David Baltimore, a Nobel Prize–winning biologist, the campaign is designed to strengthen Caltech's ability to advance scientific knowledge and pave the way for new technologies.

"The 21st century will be the Golden Age of biology. We will see advances in both fundamental understanding of nature and medical technology for the treatment of disease.

"Our campaign is ultimately aimed at complex questions like the nature of consciousness, how memory and learning operate at the molecular level, how cells grow and die, and how genetic networks function," Baltimore says. "To answer these questions, we need the modern resources that only a major fundraising effort can provide for Caltech."

According to Ben Rosen, the other cochair of the BSI, approximately one-third of the $100 million has already been raised.

Caltech has a long history of biological innovation. For example, Thomas Hunt Morgan, Caltech's first biology chair, early in the century demonstrated that genes are linked in a series on chromosomes and are responsible for determining hereditary traits. A few decades later, Max Delbrück began studying bacteriophages (a class of viruses that infect bacteria), and in doing so became one of the first to apply the quantitative methods of physics to the study of genes.

More recently, Caltech's Ed Lewis won the 1995 Nobel Prize, for studying how genetic mutations affect early development.

The BSI's scientific program therefore furthers the investments Caltech has made in the biological sciences since the 1920s. According to Mel Simon, chair of the Division of Biology at Caltech, the campaign will provide significant impetus for "understanding the basic principles that underlie the behavior of genetically driven systems."

"If you ask what the world will look like in the year 2050, the answer is probably that we will have mastered how complex biological systems work," says Simon. "And we will be able to repair dysfunction in our own bodies and minds and use synthetic genetic approaches to maintain a natural and sustaining environment."

Rather than singling out specific scientific goals, Simon says that the BSI is aimed at further extending the remarkable advances that have been made in the past in biology in understanding how the brain works and how human beings develop.

"This is the next step in the evolution of biology at Caltech," he says. "The BSI will enable us to go beyond descriptions of genes and genetic networks to an understanding of how they function. We will go beyond the traditional disciplines and integrate our approaches with those of our colleagues in chemistry, physics, and engineering to achieve a more intimate understanding of how biology works.

"We see a broad range of possibilities that will clearly lead to new breakthroughs and new technology."

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Robert Tindol

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