The Fondation pour la science is a non-profit, private entity. Its aim is to promote the Weizmann Institute of Science in Belgium and to support its research projects via appropriate public relations activities as well as selective fund raising, in particular in the form of sponsorships, donations and legacies.

One of the Foundation’s regular activites is the sponsoring of promising students attending Belgian secondary schools, who qualify for participation in the annual 4 weeks International Scientific Summer School (ISSI) on the Weizmann Institute of Science campus, before continuing their tertiary education in science. This year two promising young women have been selected.

The Foundation is chaired by Mr Christian Hendboeg.
Mrs Diane Culer, Prof. Pierre Klees, Prof Maurice Sosnowski, Mr Paul de Schietere de Lophem, Mr Eric Hemeleers and Mr Roland Louis are directors.
The Belgian Foundation was founded in 2006, replacing the Belgian Committee, which had been established in 1973 by Prof. Georges Schnek, who also served as the first Secretary General until 1979. He was succeeded by Mr Louis Culer, who held this position for 20 years until 1999, followed by Prof. Marc van Montagu until June 2006.

Among the former Chairmen of the Committee were the former Belgian Prime Minister Theo Lefèvre (1973-1975), Prof. Piet de Somer, Rector of the “Katolieke Universiteit Leuven” (1975-1980) and Prof. Jean Brachet (1980-1972). Two Nobel Laureates, Prof. Christian de Duve and Prof. Ilya Prigogine, were members of the Academic Council.

When Male and Female Brain Connections Break Down Differently

A link in a worm nervous system that is broken in maturing females, but not in males, may shed light on the sex-linked nature of certain mental conditions

Depression, schizophrenia, Alzheimer’s disease and other neurological and psychiatric disorders tend to strike one sex more than the other; and for reasons that remain unknown, they sometimes even produce different symptoms in women and men. A study comparing brain circuits in the two sexes of worms, conducted by researchers at the Weizmann Institute of Science, has identified a molecular mechanism that could help explain how the sex differences in human brain disorders come about.

The tiny, one-millimeter-long worm called Caenorhabditis elegans is an excellent model for studying brain circuitry: Its relatively simple nervous system contains a total of 302 neurons, and it’s the only organism whose entire set of neuronal connections in the brain has so far been mapped out for both sexes. At birth these connections are the same in the two sexes, but the circuitry starts to diverge when the worms mature sexually. Dr. Meital Oren-Suissa of Weizmann’s Neurobiology Department and her team thought that identifying the mechanisms of this divergence in the worm’s nerve circuitry could shed light on sex-related differences in the human brain, particularly the ones that may be linked to psychiatric disorders.

Dr. Dr. Meital Oren-Suissa and Dr. Yehuda Salzberg

In experiments led by Dr. Yehuda Salzberg, the scientists focused on a particular connection between two neurons that allow the worm to sense its environment. This connection is known to be present in both sexes in juvenile worms, but as they mature sexually, it is retained in males but disappears in females. How does this difference in wiring emerge from a common template? (Side note: The female worms are also called hermaphrodites because they produce both eggs and sperm, but their nervous system is genetically female.)

Cancer cells turn out to have memories. But these are unreliable and can end up causing trouble

Much as our earliest memories go into making our grown-up personalities, the cells in our bodies have “memories” that shape their identities. Cellular memories remind our skin cells to stay skin and bone cells to stay bone – even as these cells divide again and again. A team of scientists at the Weizmann Institute of Science recently investigated this cellular memory in cancer cells. Their findings may help us better understand the kinds of “memory loss” that help drive cancer.

Prof Amos Tanay of the Institute’s Mathematics and Computer Science, and Biological Regulation Departments explains that as a general rule, cancers start with genetic mutations, “but these can only partially explain the changes that cancer cells undergo as they divide and turn deadly.” Epigenetics – memory mechanisms that give our cells their identities by telling some genes to be expressed and others to be stably repressed – also get modified by cancer. This much was clear, but little else has been clear about if and how cancer cells change epigenetics to their benefit. For example, is this memory randomly lost or damaged in cancer, or could it be modified more directly as cells take on more cancerous features? Even if the process is random, Tanay wondered whether the deterioration of epigenetic memories would still push cancer forward, something in the way that random genetic mutations eventually conspire to turn cells deadly in the disease. Tanay and research student Zohar Meir decided to find out.

(l-r) Prof. Amos Tanay, Dr. Zohar Mukamel, Zohar Meir, Aviezer Lifshitz and Elad Chomsky

To probe cancer cell memory, Tanay and Meir developed a modern version of a classic elegant experiment. In the 1940s, Salvador Luria and Max Delbrück investigated a question about genetic mutations in bacteria. In the experiment, the scientists asked why, when bacteria are grown in the lab and challenged with viral infection, some cells can survive while others die. Did the cells have a “memory” of the infection that granted their progeny resistance? Luria and Delbruck grew colonies, each from a single bacterial cell, and after many generations they tested the colonies’ ability to survive a viral infection. The results were striking: Most of the colonies couldn’t resist viruses at all. But a small subset, each comprising millions of progeny all from the same bacterium, were nearly completely resistant. This led Luria and Delbruck — and soon after the entire new field of molecular biology – to understand some basic mechanisms of genetic heritability and to zoom in on DNA as the major carrier of genetic information.

Bacteria Could Provide Us with the Next Antivirals

Bacteria Could Provide Us with the Next Antivirals

Virus-fighting viperins, part of the human immune system, turn out to have bacterial counterparts that might boost the fight against human disease

By tracking the evolution of what may be our oldest means of fighting off viral infection, a group at the Weizmann Institute of Science has uncovered a gold mine of antiviral substances that may lead to the development of highly effective antiviral drugs. These substances are made by virus-fighting enzymes known as viperins, which were previously known to exist only in mammals, and have now been found in bacteria. The molecules produced by the bacterial viperins are currently undergoing testing against human viruses such as the influenza virus and COVID-19. The study was published today in Nature.

A New Approach to Tailoring Cancer Therapy: Tapping into Signaling Activities in Cancer Cells

Matching drugs to tumors may lead to personalized treatment and new therapies


Lung cancer samples: Far left untreated. Lung cancer tissue failed to respond when exposed to a microtubule inhibitor drug (left) or to a drug that enhanced the apoptosis-inducing pathway (middle). But when the two drugs were applied together to the same tissue, the cancer cells died (right)

Choosing the right drug for each cancer patient is key to successful treatment, but currently physicians have few reliable pointers to guide them in designing treatment protocols. Researchers at the Weizmann Institute of Science and Broad Institute of MIT and Harvard have now developed a new method for selecting the best drug therapy for a given tumor based on assigning scores to the cells’ internal messaging activities. In addition to helping physicians choose from a list of existing treatments, the method can help identify new molecular targets for the development of future drugs. In fact, the researchers have already used it to single out a gene that can be targeted for effectively treating breast cancers with a BRCA mutation. The study was recently published in Nature Communications.

Which Came First?

An experiment in reconstructing primordial proteins solves a long-standing riddle


The characteristic (HhH)2 fold and its binding to the minor groove of a modern DNA molecule. How did the first ones form?

What did the very first proteins look like – those that appeared on Earth around 3.7 billion years ago? Prof. Dan Tawfik of the Weizmann Institute of Science and Prof. Norman Metanis of the Hebrew University of Jerusalem have reconstructed protein sequences that may well resemble those long-lost ancestors of modern proteins, and their research suggests a way that these primitive proteins could have played a role in forming the earliest living cells. Their findings were published in the Proceedings of the National Academy of Sciences (PNAS).