First Graduates of Rothschild-Weizmann Program for Excellence in Science Teaching; A Hormone Ensures its Future; Unraveling Batten Disease

First Graduates of Rothschild-Weizmann Program for Excellence in Science Teaching

Twenty-six science teachers have completed advanced studies in the Rothschild-Weizmann Program for Excellence in Science Teaching and will be awarded MSc degrees in science teaching from the Feinberg Graduate School of the Weizmann Institute of Science. This unique program, the first of its kind in Israel, is designed for high-school science teachers. In the upcoming year, about 100 will be enrolled in the two-year program.

The program is based on the belief that the best way to improve science education is to groom excellent teachers. Thus, the Rothschild-Weizmann Program invites top science teachers to participate. In cooperation with Weizmann Institute scientists, an intensive study program was put together in which the students deepen their knowledge in all fields of science, meet with scientists and visit their labs, learn about the latest scientific advances, gain new approaches to teaching, participation in Institute research on science education, and receive opportunities to lead new educational initiatives.

The Rothschild-Weizmann Program, supported by the Caesarea Edmond Benjamin de Rothschild Foundation, was established three years ago at the initiative of Weizmann administration and the Institute’s Department of Science Teaching. Heading the program, which is offered through the Feinberg Graduate School, are Prof. Shimon Levit of the Faculty of Physics and Prof. Bat Sheva Eylon, Head of the Science Teaching Department.

“Program alumni can influence the educational system on many levels,” says Prof. Eylon. “A teacher can work within his or her own school, in the community or on a national level; he or she can participate in the development of educational materials or spread ideas though interactions with fellow teachers.” To further this goal, Rothschild-Weizmann Program graduates are offered a continuing program that focuses on creating and leading new educational initiatives in conjunction with the Department of Science Teaching and the Davidson Institute of Science Education.

A Hormone Ensures its Future

Scientists reveal the structure of a brain area where hormones that regulate vital body processes pass into the blood

Much of the body’s chemistry is controlled by the brain – from blood pressure to appetite to food metabolism. In a study published recently in Developmental Cell, a team of scientists led by Dr. Gil Levkowitz of the Weizmann Institute’s Department of Molecular Cell Biology has revealed the exact structure of one crucial brain area in which biochemical commands are passed from the brain cells to the bloodstream and from there to the body. In the process, they discovered a surprising new role for the “hormone of love,” showing that it helps to direct the development of this brain structure.

The area in question, the neurohypophysis, is an interface between nerve fibers and blood vessels located at the base of the brain. Here, some of the major brain-body interactions take place: Hormones released from nerves into the blood vessels regulate a series of vital body processes, including the balance of fluids and uterine contractions in childbirth.

Although the neurohypophysis has been studied for more than a century, the scientists in the Weizmann Institute-led study developed new genetic tools that enabled them to examine the exact three-dimensional arrangement of this brain structure and clarify the cellular and molecular processes leading to its formation. Since the human neurohypophysis is exceedingly complex, the scientists performed the research on live embryos of zebrafish. These fully transparent embryos offer a unique model for studying the vertebrate brain, lending themselves to genetic manipulation with relative ease and enabling researchers to observe the actual formation of a neurohypophysis under a microscope.

The study revealed a surprising new function for the hormonal messenger oxytocin, dubbed the “hormone of love” because, in addition to controlling appetite and such female reproductive behaviors as breastfeeding, it is also involved in mother-child and mate bonding. The scientists showed that oxytocin, one of the two major hormones secreted in the adult neurohypophysis, is involved in the development of this brain area while in the embryo. At this stage, the oxytocin governs the formation of new blood vessels. “The messenger helps to build the road for transmitting its own future messages,” says Dr. Levkowitz. Developmental Cell highlighted the study’s findings in a preview headlined, “The Hormone of Love Attracts a Partner for Life.”

The results provide an important advance in basic research because they shed light on fundamental brain processes, but in the future they might also be relevant to the treatment of disease. Since the neurohypophysis is one of only a few portions of the brain able to regenerate after injury, an understanding of how it is formed may one day help achieve such regeneration in other parts of the central nervous system.

The research was conducted in Dr. Levkowitz’s lab by PhD student Amos Gutnick and Dr. Janna Blechman. The Weizmann scientists worked in collaboration with Dr. Jan Kaslin of Monash University, Australia; Drs. Lukas Herwig, Heinz-Georg Belting, and Markus Affolter of the University of Basel, Switzerland; and Dr. Joshua L. Bonkowsky of the University of Utah, United States.

Dr. Gil Levkowitz’s research is supported by the Dekker Foundation; the Kirk Center for Childhood Cancer and Immunological Disorders; and the Irwin Green Alzheimer’s Research Fund. Dr. Levkowitz is the incumbent of the Tauro Career Development Chair in Biomedical Research.

Unraveling Batten Disease

Experiments with a yeast gene reveal what goes wrong in a degenerative childhood disease

Waste management is a big issue anywhere, but at the cellular level it can be a matter of life and death. A Weizmann Institute study published in the Journal of Cell Biology has revealed what causes a molecular waste container in the cell to overflow in Batten disease, a rare but fatal neurodegenerative disorder that begins in childhood. The findings may form the basis for a therapy for this disorder.

In Batten disease, an insoluble yellow pigment accumulates in the brain’s neurons, causing these cells to degenerate and ultimately die. Patients gradually become disabled, losing their vision and motor skills and suffering mental impairment; they rarely survive beyond their early twenties. It’s been known for a while that the disorder is caused by a mutation in the gene referred to as CLN3, but the role of this gene in the cell was unknown. This role has now been discovered in the Weizmann Institute study, explaining the molecular dysfunction in Batten disease.

The research was conducted in the laboratory of Prof. Jeffrey Gerst of the Department of Molecular Genetics by Rachel Kama and postdoctoral fellow Dr. Vydehi Kanneganti, in collaboration with Prof. Christian Ungermann of the University of Osnabrueck in Germany. All the studies were performed in yeast, as the yeast equivalent of the mammalian CLN3 gene has been conserved almost intact in the course of evolution, making them ideal models for study. In fact, so similar are the yeast and the mammalian genes that when the researchers replaced a missing copy of the yeast gene with a working copy of mammalian CLN3, normal functioning of the yeast cell was restored.

The experiments showed that the yeast equivalent of CLN3 is involved in moving proteins about the cell – the scientific term is “protein trafficking.” The gene activates an enzyme of the kinase family, which, in turn, launches a series of molecular events regulating the trafficking. When the yeast CLN3 is mutated, this trafficking is disrupted. As a result, certain proteins accumulate abnormally in the lysosome, the cell’s waste-recycling machine, instead of being transported to another destination. At some point the lysosome is filled beyond capacity; it then interferes with molecular signaling and other vital processes in the neuron, eventually killing the cell.

A great deal of research must still be performed before this finding benefits humans, but the clarification of the CLN3 function is precisely what might help develop a new therapy. Replacing the defective CLN3 in all the brain’s neurons is a daunting challenge, but replacing its function – for example, by activating the relevant kinase by means of a drug – should be much more feasible.

Prof. Jeffrey Gerst’s research is supported by the Miles and Kelly Nadal and Family Laboratory for Research in Molecular Genetics; the Hugo and Valerie Ramniceanu Foundation; the Y. Leon Benoziyo Institute for Molecular Medicine; the Yeda-Sela Center for Basic Research; and the estate of Raymond Lapon. Prof. Gerst is the incumbent of the Besen-Brender Professorial Chair of Microbiology and Parasitology.