Virtual Research Institute Needed to Unlock RNA’s

Ten years on from the human genome project, RNA (ribonucleic acid) has stolen some of DNA's limelight. The basic ingredient of our genes, DNA long outshone the other form of genetic material in our cells, RNA. RNA was seen as a simple stepping stone in the cell's gene-reading activities.
Research over the last decade has shown RNA to be a remarkable molecule and a multi-talented actor in heredity. It is thought to be a major participant in the chemical reactions that led to the origins of life on Earth -- the 'RNA World' hypothesis. RNA also controls genes in a way that was only recently discovered: a process called RNA interference, or RNAi. Medical researchers are currently testing new types of RNAi-based drugs for treating conditions such as macular degeneration, the leading cause of blindness, and various infections, including those caused by HIV and the herpes virus.
"RNA could bring significant advances to the diagnosis, treatment and prevention of many human diseases," said Professor Jörg Vogel from the University of Würzburg, Germany, who co-chaired the report. "In the global context, it's surprising that Europe doesn't have many centres specifically funded for and dedicated to it, particularly in comparison to the US. We strongly recommend creating a network of RNA centres, linked together as a Europe-wide 'virtual institute'. A first step could involve calls through the European Commission and national funders. "
The virtual RNA institute would be made up of locally-funded, multidisciplinary centres with a critical mass of strong research groups in disciplines such as biology, biochemistry, chemistry, genetics, bioinformatics, biophysics, structural analysis, microbiology, plant sciences and clinical medicine. This environment could be well-suited to promoting superior training of a generation of young scientists, PhD students and postdoctoral researchers. They could also help deliver dedicated education programmes for RNA research, which are currently lacking.
A particular area where an increasing demand in the future can be foreseen is, as in almost all other areas of life science, bioinformatics. "A new generation of bioinformaticians needs to be trained to meet future demand, in RNA research and in many other areas of the life sciences," continues Professor Vogel.
New models for public funding of infrastructure and resources for promising compounds to be used in the clinic should be developed. The financial burden for taking basic compounds and developing them into drugs could be shared by academic-industrial partnerships.
'RNA World: a new frontier in biomedical research' reviews the high pace of discovery in RNA research and gives a 5-10 year outlook of how both basic RNA research and its use in clinical practice should develop. Nine thematic priority areas were identified to address new and promising opportunities for biomedical, biotechnological, pharmaceutical and clinical RNA research

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Rare Hybrid Cell Key to Regulating the Immune System

"This is actually the first cell we know of that has this type of appearance in nature," Dr. Andrew Mellor, molecular geneticist and immunologist who co-directs MCG's Immunotherapy Discovery Institute, said of the cell that looks like a dendritic cell and a B cell but isn't really either.
The discovery of this rare hybrid could have implications for the efficacy of new therapies that manipulate these two cell types to treat diseases such as cancer and rheumatoid arthritis.
When MCG scientists first reported the human equivalent of this cell in Science in 2002, they called it a subset of the dendritic cell that clusters in high exposure areas such as the gut but also roams the body, looking for invaders like a virus or cancer. Dendritic cells show their find to T cells, telling them to ignore or attack by bringing trash-eating macrophages, natural killer cells and the like into the fight.
What seemed most unique about the subset is its ability to express indoleamine 2,3 dioxygenase, or IDO, to turn off T cells. IDO is an enzyme used by fetuses and tumors alike to escape the immune response.
The new studies show that is only part of the cells' distinctiveness. The cells also have the identifying markings of B cells, known for their ability to make antibodies against invaders. In fact, they found the IDO-presenting cells came from the same precursor cell as B cells. But, when the scientists looked at mice missing B cells, they still found the IDO-producing cells. Hence, the cell didn't need to produce antibodies to turn off T cells.
In reality, IDO-expressing cells have properties of both cells, said Burles A. Johnson III, an MCG M.D.-Ph.D. student and first author of the paper published in the Proceedings of the National Academy of Sciences. "It looks like a B cell and it's not. It looks like a dendritic cell and it is and it isn't," Johnson said.
While their studies are in mice, the cells also are in humans, showing up in some unfortunate places such as the drainage system for tumors, melanoma or even HIV where they likely help the diseases survive.
They also may be showing up in new dendritic cell therapies designed to strengthen the immune response to cancer. If the therapies happen to include some IDO-expressing cells, those could end up helping the cancer, said Mellor, the paper's corresponding author. "All you need is a few of these cells in your dendritic cell vaccine and you don't get stimulation any more, you get suppression," Mellor said.
Their confusing face could also cause hybrids to be lost in B cell-depleting therapies designed to lessen the immune system's attack on joints in rheumatoid arthritis. "These therapies may also deplete IDO-expressing cells and decrease therapy effectiveness because you are eliminating cells that are there to help you," Johnson said.
"This gives us new insight into why these therapies might not be working as well as we think they might," Mellor added. Long-term goals include figuring out how to manipulate the hybrid's activity to benefit patients.
The research was funded by the National Institutes of Health and the Germany-based pharmaceutical company Boehringer-Ingelheim. Mellor is a Georgia Research Alliance Eminent Scholar in Molecular Immunogenetics.

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Cell Survival Protein Discovery Rewrites Immune System Story

A discovery by Walter and Eliza Hall Institute researchers in Melbourne, Australia, reported in the journal Science, is set to rewrite a long-held belief about how the body's immune system establishes its memory.

The findings of Dr Ingela Vikstrom and Associate Professor David Tarlinton, from the institute's Immunology division, centre on immune cells called B cells that produce the antibodies which fight infection.

"B cells and antibody production are the key to the success of all currently used vaccines for immunity in humans," said Associate Professor Tarlinton. "It is therefore critical that we continue to develop our knowledge of the molecular interactions that lead to immune function, which are still only vaguely understood."

Memory B cells are essential for the long-lived immunity that arises after immunisation. To develop into memory cells, B cells have to survive the natural process of apoptosis, or programmed cell death, that occurs following a large immune response.

Associate Professor Tarlinton and Dr Vikstrom study the so-called pro-survival proteins that regulate B cell survival and are therefore responsible for instructing these cells whether to live or die.

Dr Vikstrom said that B cell memory arises in temporary cellular structures called germinal centres that develop in response to activation of the immune system.

"We used genetic and pharmacological methods to identify which pro-survival molecules were essential for the process of 'instructing' these cells to establish germinal centres, as well as instructing activated B cells to proliferate and differentiate into memory B cells," Dr Vikstrom said.

"We studied two well-known pro-survival proteins called Bcl-xL and Mcl-1, which we knew were involved in the process. It surprised us to find that, contrary to popular belief, Mcl-1 is the essential pro-survival protein required for creation and maintenance of B cell memory."

The finding contradicts the widely accepted theory in immunology circles that Bcl-xL is the major pro-survival protein responsible for sustaining the development of memory B cells.

The findings build on a paper Associate Professor Tarlinton and Dr Vikstrom published earlier this year in Proceedings of the National Academy of the Sciences, with institute researchers Dr Andrew Lew and Dr Emma Carrington. Using a molecule that blocked the action of Bcl-xL, the study revealed that Bcl-xL was not necessary for the development of germinal centres and memory B cells, indicating that another pro-survival protein -- now shown to be Mcl-1 -- was the key to survival.

Mcl-1 is known to be an important survival protein for cancers. Associate Professor Tarlinton said the discovery could have repercussions for cancer treatment, as cancerous cells often arise from unregulated cell growth caused by defects in the apoptotic pathway. It could also have implications for the treatment of autoimmune disease and inhibiting transplant rejection.

"All cells have the potential to undergo apoptosis, so developing our understanding of the major proteins responsible for this process will have applications to all cell types in the body," he said.

The work was supported by the National Health and Medical Research Council, the Leukaemia and Lymphoma Society, and the US National Institutes of Health.

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Clue to Unusual Drug-Resistant Breast Cancers Found

Researchers at the University of Illinois at Chicago College of Medicine have found how gene expression that may contribute to drug resistance is ramped up in unusual types of breast tumors. Their findings may offer new therapy targets.

 

The study is published in the Oct. 8 issue of the Journal of Biological Chemistry, where it is designated a paper of the week.

Approximately 70 percent of breast cancers express the estrogen receptor. These "ER-positive" tumors usually respond to hormone-related therapies, such as tamoxifen or aromatase inhibitors. But not always.

"We were interested in a subset of ER-positive tumors that are unusually aggressive and also drug-resistant," said Jonna Frasor, assistant professor of physiology and biophysics at the UIC College of Medicine and principal investigator of the study.

Following up on earlier observations that these aggressive ER-positive tumors express genes that respond both to estrogen and inflammatory factors called cytokines, Frasor and her colleagues focused on the gene for a drug-transporter protein which is believed to pump chemotherapy drugs out of tumor cells, making them resistant.

It is unexpected to find estrogen and inflammatory proteins seemingly working together to drive the cancer's aggressiveness, says Madhumita Pradhan, a student in Frasor's lab and first author of the paper. In many cases, estrogen is known to be protective against inflammatory processes, Pradhan said.

The researchers showed that in breast cancer cells, an inflammatory protein called NFĸB and the estrogen receptor act together to increase expression of the transporter gene. And they were able to show how.

An area on a gene called a promoter acts as an on/off switch that determines whether the gene is transcribed and the protein it encodes is produced. The promoter has spaces called response elements, where molecules can attach and help to turn the switch on or off.

"We found that the estrogen receptor gets recruited to the promoter of this gene," Frasor said. "Once there, the ER allows NFĸB to be recruited to its own response element. Once the second molecule binds, it actually stabilizes the ER and the gene is turned on to a much greater extent than with the ER alone."

This novel mechanism could have important implications in the treatment of breast cancers in which inflammation and estrogen can promote cancer progression, Frasor said.

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Scientists Trick Bacteria Into Embedding Small Molecules in Cell Wall

The finding, described online in the journal ACS Chemical Biology this week, represents the first time scientists have engineered the cell wall of a pathogenic "Gram-positive" bacteria -- organisms responsible not only for Staph infections but also pneumonia, strep throat and many others. The discovery could pave the way for new methods of combating the bacteria responsible for many of the most infectious diseases.

The team engineered one end of their small molecules to contain a peptide sequence that would be recognized by the bacteria. In Staphylococcus aureus, an enzyme called sortase A is responsible for attaching proteins to the cell wall.

"We sort of tricked the bacteria into incorporating something into its cell wall that it didn't actually make," said David Spiegel, a Yale chemist who led the study. "It's as if the cell thought the molecules were its own proteins rather than recognizing them as something foreign."

The scientists focused specifically on the cell wall because it contains many of the components the cell uses to relate to its environment, Spiegel said. "By being able to manipulate the cell wall, we can in theory perturb the bacteria's ability to interact with human tissues and host cells."

The team used three different small molecules in their experiment -- including biotin, fluorescein and azide -- but the technique could be used with other molecules, Spiegel said, as well as with other types of bacteria. Another advantage to the new technique is that the scientists did not have to first genetically modify the bacteria in any way in order for them to incorporate the small molecules, meaning the method should work on naturally occurring bacteria in the human body.

Staph infections, such as the drug-resistant MRSA, have plagued hospitals in recent years. More Americans die each year from Staphylococcus aureus infections alone than from HIV/AIDS, Parkinson's disease or emphysema.

Being able to engineer the cell walls of not only Staphylococcus aureus but a whole family of bacteria could have widespread use in combating these illnesses, Spiegel said, adding that any number of small molecules could be used with their technique. "For example, if we tag these bacteria with small fluorescent tracer molecules, we could watch the progression of disease in the human body in real time." The molecules could also be used to help recruit antibodies that occur naturally in the bloodstream, boosting the body's own immune response to diseases that tend to go undetected, such as HIV/AIDS or cancer.

"This technique has the potential to help illuminate basic biological processes as well as lead to novel therapeutics from some of the most common and deadly diseases affecting us today," Spiegel said.

Other authors of the paper include James Nelson, Alexander Chamessian, Patrick McEnaney, Ryan Murelli and Barbara Kazmiercak (all of Yale University).

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Transgenic Corn Suppresses European Corn Borer, Saves Farmers Billions

Transgenic corn's suppression of the European corn borer has saved Midwest farmers billions of dollars in the past decade, reports a new study in Science.

Research conducted by several Midwest universities shows that suppression of this pest has saved $3.2 billion for corn growers in Illinois, Minnesota, and Wisconsin over the past 14 years with more than $2.4 billion of this total benefiting non-Bt corn growers. Comparable estimates for Iowa and Nebraska are $3.6 billion in total, with $1.9 billion accruing for non-Bt corn growers.

Transgenic corn is engineered to express insecticidal proteins from the bacterium Bacillus thuringiensis (Bt). Bt corn has become widely adopted in U.S. agriculture since its commercialization in 1996. In 2009, Bt corn constituted 63 percent of the U.S. crop.
Corn borer moths can't distinguish between Bt and non-Bt corn, so females lay eggs in both types of fields. Once eggs hatch in Bt corn, young borer larvae feed and die within 24 to 48 hours.

The major benefit of planting Bt corn is reduced yield losses, and Bt acres received this benefit after the growers paid Bt corn technology fees. But as a result of areawide pest suppression, non-Bt acres also experienced yield savings without the cost of Bt technology fees, and thus received more than half of the benefits from growing Bt corn in the region.

"We've assumed for some time that economic benefits were accruing, even among producers who opted not to plant Bt hybrids," said co-author of the study Mike Gray, University of Illinois Extension entomologist and professor in the Department of Crop Sciences. "However, once quantified, the magnitude of this benefit was even more impressive."

Over the past several years, entomologists and corn producers have noticed very low densities of European corn borers in Illinois. In fact, Illinois densities have reached historic lows to the point where many are questioning its pest status, Gray said.

"Since the introduction of Bt corn, initially targeted primarily at the European corn borer, many entomologists and ecologists have wondered if population suppression over a large area would eventually occur," Gray said. "As this research shows, areawide suppression has occurred and dramatically reduced the estimated $1 billion in annual losses caused previously by the European corn borer."

This information also provides incentives for growers to plant non-Bt corn in addition to Bt corn.

"Sustained economic and environmental benefits of this technology will depend on continued stewardship by producers to maintain non-Bt maize refuges to minimize the risk of evolution of Bt resistance in crop pest species," Gray said.

This study titled, "Areawide Suppression of European Corn Borer with Bt Maize Reaps Savings to Non-Bt Maize Growers," will appear in the October 8 edition of Science. The lead researcher is Bill Hutchison of the University of Minnesota. Collaborating authors include Eric Burkness and Roger Moon of the University of Minnesota, Paul Mitchell of the University of Wisconsin, Tim Leslie of Long Island University, Shelby Fleischer of Pennsylvania State University, Mark Abrahamson of the Minnesota Department of Agriculture, Krista Hamilton of the Wisconsin Department of Agriculture, Trade and Consumer Protection, Kevin Steffey and Mike Gray of the University of Illinois, Rick Hellmich of USDA-ARS, Von Kaster of Syngenta Seeds Inc., Tom Hunt and Bob Wright of the University of Nebraska, Ken Pecinovsky of Iowa State University, Tom Rabaey of General Mills Inc., Brian Flood of Del Monte Foods and the late Earl Raun of Pest Management Company.

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HUMAN-LIKE BRAIN FOUND IN WORM

Brain structures directly related to the human brain have just been identified in a marine ragworm, according to a paper published in the latest issue of the journal Cell.

The discovery means that the origins of the human brain can now be traced back at least 600 million years, when we last shared a common ancestor with this species,Platynereis dumerilii, a relative of the common earthworm.

"This worm lives in self-made tubes, explores its environment actively for food, and shows signs of learning behavior," lead author Raju Tomer told Discovery News. "Therefore, we thought this ragworm would be the ideal candidate to look for the counterparts of vertebrate higher brain centers in invertebrates."

Tomer, a scientist at the European Molecular Biology Laboratory (EMBL), and his colleagues suspect that other invertebrates, such as insects, spiders, crustaceans and velvet worms likely also possess the brain structures, called "mushroom bodies," which correspond to our cerebral cortex. The cerebral cortex is a part of the human brain involved in memory, learning, thought, language, consciousness and more.

Tomer and his team used a new technique they developed, called "cellular profiling by image registration," to investigate a large number of genes in the marine ragworm's compact brain. The method enabled the scientists to determine each cell's molecular fingerprint, and to define cell types according to the genes they express, rather than just based on their shape and location, as was done before.

"The development and patterning mechanisms of annelid mushroom bodies and vertebrate brains are too similar to be explained by independent origins," Tomer said. "They must share a common evolutionary precursor, though less complex, which evolved in the last common ancestor more than 600 million years ago."

Co-author Detlev Arendt, also at EMBL, told Discovery News that the sea floor at that time must have been covered with various food sources. In order for organisms to explore these foods, it would have been "advantageous to evolve a brain center that was able to integrate the different smells and ultimately learn what is good and what is bad food."

This first pre-brain probably then consisted of a group of densely packed cells that received and processed very basic information about food and the environment. The structure may have enabled our ancestors crawling over the sea floor to identify food sources, move towards them, and then later to integrate previous experiences into learning.

When French biologist Felix Dujardin first observed the mushroom bodies in invertebrates in 1850, he proposed that these structures bestowed insects with a certain degree of free will control over their instinctive actions. Dujardin's theories have since been largely validated.

Subsequent research has established that the mushroom bodies, which look a bit like mushrooms, serve as a center for associative learning and memory formation, activities that are very similar to those of the cerebral cortex.

"Our cerebral cortex functions by associating sensory information, such as smell, sound and vision, with events, and by storing these associations as memories by modifying the connection strength of neurons," Tomer explained.

"These stored memories then form the basis for making right decisions in the future. Similar mechanisms are found in invertebrates as well, where mushroom bodies are known to be largely responsible for associative learning."

He doubts, however, that invertebrates think and feel just as we do, since their brains are small and lack the "immensely large number of neurons" present in the human brain.

In the future, the scientists hope to further investigate worm brains, and those of other invertebrates, to better determine how they work and to help figure out what the brain of the last common ancestor of vertebrates and these worms might have looked like.

"Our ultimate goal is to reconstruct and understand the evolution of brains in animals, to trace their neuronal composition and their function from the very beginning of animal evolution to something as complex as today's human brain," Arendt said.

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New twists in double helix discovery story are uncovered

Cold Spring Harbor, NY -- The story of the double helix's discovery has a few new twists. A new primary source -- a never-before-read stack of letters to and from Francis Crick, and other historical materials dating from the years 1950-76 -- has been uncovered by two professors at the Watson School of Biological Sciences at Cold Spring Harbor Laboratory (CSHL).

The letters both confirm and extend current knowledge of the circumstances surrounding the epoch-making discovery of DNA's elegant double-helical structure, for which Crick, James D. Watson (now CSHL's chancellor emeritus) and Maurice Wilkins were awarded the Nobel Prize in 1962. Unlike the structure itself, which amazed even its discoverers in its simplicity, the story of the discovery has revealed a complex tangle of people, ambitions and institutional politics behind the process of scientific investigation.

"It's primarily the insights these new letters provide about the personalities of the discoverers that people will find most fascinating," says Alex Gann, Ph.D., who along with Jan Witkowski, Ph.D., uncovered the new Crick materials and co-authored a paper on them that appears in the journal Nature Sept. 30.

Following the publication of landmark works including Watson's confessional The Double Helix in 1968 and Horace Freeland Judson's The Eighth Day of Creation 11 years later, most historians have been content to believe that the archives had been fully explored and would not reveal much more about the double helix story. But 34 of the newfound letters are between Crick and Wilkins and draw attention to what Gann and Witkowski have described as Wilkins' "tortured soul" during the critical period 1951-53, when Watson and Crick were alternately put on, taken off and then restored to an effort to discover DNA's structure.

"We are really between forces which may grind all of us into little pieces," Wilkins wrote to Crick in one letter. As Witkowski explains, "Maurice Wilkins on the one hand wanted to be open - he believed science should be open and was all in favor of cooperation, the exchange of ideas and data; but on the other hand, he was also mindful of his own career: he knew he had to get results and publish papers." As the upstarts Watson and Crick, then unknowns, jockeyed for permission at Cambridge to explore the DNA structure problem, Wilkins, at King's College, was already well engaged in experimentation that would prove vital in determination of the solution. Wilkins' boss at King's, John Randall, hired Rosalind Franklin and had, unknown to Wilkins, assured her that she was in "sole charge" of the DNA work at King's. This led to conflicts between Franklin and Wilkins, who assumed he and Franklin would be partners.

This was but the beginning of a series of now historic misunderstandings. Between the lines of the newly discovered Crick letters with Wilkins, one grasps, on Wilkins' end, the anguish, and on Crick's, what at times comes across as the self-assurance and jocularity of the player possessing superior position.

This is but a fraction of the newly found letters, which were uncovered unexpectedly in the midst of an archival collection of materials donated to Cold Spring Harbor by Sydney Brenner, the distinguished molecular biologist and Nobel laureate, who worked alongside Crick following discovery of the double helix. The two shared an office at Cambridge from 1956 to 1977. Coincidentally, the CSHL Press has just released a new biography of Brenner by Errol Friedberg.

Among the new letters there are some 30 between Crick and George Gamow, dating to 1953-64. Other of his correspondents included Leo Szilard, C.P. Snow, and J. Robert Oppenheimer, among many others. The most important of the new letters, cited in the Gann-Witkowski paper, are now in the process of being digitized at the CSHL Archives (http://library.cshl.edu) to facilitate public access. Mila Pollock, Executive Director of the CSHL Library and Archives, says it is her hope that digitization will proceed so that the Crick correspondence in its entirety will be accessible to all via the Internet. The greater part of the collection resides at the Wellcome Library (http://library.wellcome.ac.uk)

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Scientists say rare plant has biggest genome yet

When it comes to genomes, size matters -- and British scientists say a rare and striking plant native to Japan is in a perilous position.
 

Researchers at Britain's Kew Botanical Gardens say the plant, Paris japonica, has the largest genome yet recorded, putting it at high risk of extinction.

"Some people may wonder what the consequences are of such a large genome and whether it really matters if one organism has more DNA than another," said Ilia Leitch, a researcher at Kew's Jodrell Laboratory. "The answer to this is a resounding 'yes'"

"Having a large genome increases the risk of extinction. The larger it is, the more at risk you are."

The vast range of genome size -- the amount of DNA -- in plants and animals has long fascinated and puzzled scientists.

With 152.23 picograms (pg) of DNA, the Paris japonica has around 15 percent more than the previous record holder, the marbled lungfish or Protopterus aethiopicus, with 132.83 pg.

It is also more than 50 times bigger than the human genome, which is 3.0 picograms. A picogram is one trillionth of a gram.

Leitch said the importance of size lies in the fact that the more DNA there is in a genome, the longer it takes for a cell to copy all of its DNA and divide.

"The knock-on effect of this is that it can take longer for an organism with a larger genome to complete its life cycle than one with a small genome," she said.

This explains why many plants living in deserts which must grow quickly after rains have small genomes enabling them to grow rapidly, while species with large genomes grow much more slowly and are not found in such harsh habitats.

Leitch said that in plants, research has shown that those with large genomes are at greater risk of extinction, are less adapted to living in polluted soils and are less able to tolerate extreme environmental conditions, factors which she said were "all highly relevant in today's changing world."

The smallest genome so far reported is in a parasite of humans and other mammals called Encephalitozoon intestinalis, which has just 0.0023 picograms of DNA.

The record holder among plants for 34 years was a species called Fritillaria assyriaca, until earlier this year when a group of Dutch scientists found that a natural hybrid of trillium and hagae, related to the herb paris, had a genome four percent larger than the fritillary at 132.50 pg.

According to Kew's scientists, this had been widely thought to be around maximum size a genome could reach until the recent discovery of the 152.23 pg Paris japonica genome.

The latest finding was reported in the Botanical Journal of the Linnean Society.

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TIFR Coming to Hyderabad | PM to lay foundation stone on october 19th

The family tree of the Tata Institute of Fundamental Research, which so far includes Mumbai, Pune and Bangalore, will soon have a fourth major branch: TIFR Hyderabad. The foundation stone will be laid by PM Manmohan Singh on October 19, as reported recently in the Times of India. TIFR Director Mustansir Barma and NCBS Director Prof. K. VijayRaghavan welcome and encourage all interested parties at NCBS to join them in Hyderabad for the event. See below for more details.
For those at NCBS who cannot make it, the PM's visit will be covered in a webcast, and food and refreshments will help to mark the occasion.

A message from Prof. Mustansir Barma, TIFR Director

Dear NCBS Colleagues:

I am very happy to inform you that the Prime Minister Dr. Manmohan Singh has consented to lay the foundation stone of the new campus of TIFR in Hyderabad at 2.30 p.m. on October 19, 2010. This will be followed by a few scientific talks. Those of you who would like to attend the function in Hyderabad, are requested to contact your Dean or Centre Director by noon on Monday, October 11, 2010. Further, in order to have the largest reach possible for the TIFR community, this historic event will be broadcast live to TIFR Mumbai, as well as to TIFR centres.

A message to All at NCBS from Prof. K. VijayRaghavan

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