Titia de Lange to receive 47th Rosenstiel Award

Professor Titia de Lange

The 47th Lewis S. Rosenstiel Award for Distinguished Work in Basic Medical Research has been awarded to Professor Titia de Lange of Rockefeller University for her studies on the protection of chromosome ends (telomeres) from degradation and rearrangement. Professor de Lange will receive the award on April 12, 2018 at Brandeis University where de Lange will present a public lecture.

Dr. de Lange’s laboratory identified and characterized the roles of proteins that compose the shelterin complex, which binds specifically to the special telomeric DNA sequences and maintains the stability of these ends.  Dr. de Lange’s work has shown that the shelterin complex and the unusual telomere-loop structure of telomere DNA prevent these ends from being detected as broken chromosome ends and thus protect telomeres from being degraded and rearranged as are the ends at chromosome breaks.  De Lange’s work has further shown that disabling different components of shelterin triggers different cellular alarms designed to detect broken and degraded DNA ends and leads to lethal chromosome rearrangements such as the fusion of chromosomes.  In addition, her lab has gained critical insights into the mechanisms of cellular response to the presence of DNA damage and recently has defined processes that lead to massive chromosome rearrangements (chromothripsis) associated with many human cancers.

She is the Leon Hess Professor and director of the Anderson Center for Cancer Research at Rockefeller University, as well as an American Cancer Society Research Professor.  Her honors include: the Life Sciences Breakthrough Prize, the Rosalind E. Franklin Award from the National Cancer Institute, the Vilcek Prize in Biomedical Sciences, election as a foreign member of the US National Academy of Sciences and as Fellow of the American Academy of Arts and Sciences.

The Rosenstiel Award has had a distinguished record of identifying and honoring pioneering scientists who subsequently have been honored with the Lasker and Nobel Prizes.  Professor de Lange joins a long list of past awardees.

Rosenstiel Award lectures on Mar 22 to honor Susan Lindquist

James Haber, Director of the Rosenstiel Center, writes:

The 46th annual Rosenstiel Award for Distinguished Work in Basic Medical Research was awarded last October to Susan Lindquist (MIT), one of the most inventive and influential life scientists of our generation.  Sue tragically passed away a few weeks thereafter; in her honor we have arranged a symposium to celebrate her lab’s great legacy.  The Award talks will be held in next Wednesday, March 22, in Gerstenzang 123 from 3:30 PM to 5:30 PM, followed by a reception open to all in the Shapiro Science Center atrium.  We hope you will all come to honor Sue Lindquist and to be edified by the excellent work carried out by her former colleagues.

Angelika Amon  (Massachusetts Institute of Technology)
“The Remarkable Scientific Life of Susan Lindquist”

Leah Cowen (University of Toronto)
“Harnessing Evolution to Thwart Microbial Drug Resistance and Treat Infectious Disease”

Daniel Jarosz (Stanford University)
“Remembering the Past: A New Form of Protein-Based Inheritance”

Sandro Santagata (Brigham and Women’s Hospital)
“Heat Shock Factor (HSF1): A Powerful Driver of Malignancy”

Susan Lindquist

 

Yoshinori Ohsumi to Receive Rosenstiel Award Wednesday, April 6

ohsumi220Biologist Yoshinori Ohsumi will receive the 45th Rosenstiel Award for Distinguished Work in Biomedical Science this Wednesday, April 6th at 4:00 pm in Gerstenzang 123. At that time, he will present a lecture titled, “Lessons from yeast: Cellular recycling system, autophagy”.

Ohsumi is a cell biologist and professor at the Tokyo Institute of Technology’s Frontier Research Center in Japan. He is one of leading experts in the world on autophagy, a process that allows for the degradation and recycling of cellular components. The Rosenstiel Award is being given to Ohsumi in recognition of his pioneering discoveries in autophagy.

Learn more about Professor Ohsumi and his research at BrandeisNow.

Rosenstiel Award 2012- Dr. Steven J. Elledge

The 2012 Rosenstiel award is being awarded to Dr. Steven J. Elledge of Harvard University and the Howard Hughes Medical Institute for his seminal contributions towards understanding the eukaryotic DNA damage response[1] [2] .
Cells are constantly challenged by damage to their DNA. It of no surprise therefore, that both prokaryotic and eukaryotic cells have evolved sophisticated and remarkably complex responses to deal with damaged DNA. It is for elucidating these mechanisms that Dr. Elledge is being honored with the Rosenstiel award this year.
Dr. Elledge’s interest with the DNA damage response began as a graduate student at MIT in the laboratory of Graham Walker, where he identified and cloned genes involved in DNA repair mechanism known as the SOS reponse in the bacterium E.coli[3, 4] . It was during this time that Dr. Elledge also invented an extremely useful molecular biology tool known as ‘phasmids’ which allowed for the ability to rapidly clone E.coli genes by packaging them in phages[5].
After MIT, Dr Elledge began his postdoctoral work at Stanford University where he discovered the Ribonucleotide reductase(RNR) genes in budding yeast[6, 7]. These genes are induced following DNA damage to promote the synthesis of deoxyribonucleotides which helps facilitate DNA repair. Dr. Elledge followed up on this work as a professor at Baylor University by a series of important papers that shed light on how cells arrest division after DNA damage. Most notably in 1994, his group identified the Rad53 checkpoint kinase that is activated after DNA damage and contributes to cell cycle arrest [8]. In 1998, his group also identified the mammalian homolog of Rad53 (Chk2) [9, 10].In 1999, the Elledge group reported that the DNA damage checkpoint in yeast occurs in two parallel pathways laying the foundation of our understanding of the DNA damage checkpoint[11]. More recently, work from the Elledge lab identified novel factors in the DNA damage response by performing a siRNA screen in mammalian cells[12].
Dr Steve Elledge has been an investigator of the Howard Hughes Medical Institute since 1993. In 2003 he moved to Harvard Medical School as Professor in the Departments of Genetics and as a Geneticist in the Department of Medicine, Brigham and Women’s Hospital. Dr. Elledge was elected in 2003 to both the U.S. National Academy of Sciences and the American Academy of Arts and Sciences. In addition to the Rosenstiel award, he has received the DAMD Breast Cancer Innovator Award (2003), the National Academy of Sciences Award in Molecular Biology (2002), the John B. Carter, Jr. Technology Innovation Award (2002), and the Paul Marks Prize for Cancer Research (2001[2]).

Editor’s Note: On Mar 20, 2013, Elledge was named to receive a 2013 Canada Gairdner International Award.

1. Brownlee, C., Biography of Stephen J. Elledge. Proc Natl Acad Sci U S A, 2004. 101(10): p. 3336-7.
2. Haber, J.E., The 2005 Genetics Society of America Medal. Steven J. Elledge. Genetics, 2005. 169(2): p. 506-7.
3. Elledge, S.J. and G.C. Walker, Proteins required for ultraviolet light and chemical mutagenesis. Identification of the products of the umuC locus of Escherichia coli. J Mol Biol, 1983. 164(2): p. 175-92.
4. Elledge, S.J. and G.C. Walker, The muc genes of pKM101 are induced by DNA damage. J Bacteriol, 1983. 155(3): p. 1306-15.
5. Elledge, S.J. and G.C. Walker, Phasmid vectors for identification of genes by complementation of Escherichia coli mutants. J Bacteriol, 1985. 162(2): p. 777-83.
6. Elledge, S.J. and R.W. Davis, Identification of the DNA damage-responsive element of RNR2 and evidence that four distinct cellular factors bind it. Mol Cell Biol, 1989. 9(12): p. 5373-86.
7. Elledge, S.J. and R.W. Davis, DNA damage induction of ribonucleotide reductase. Mol Cell Biol, 1989. 9(11): p. 4932-40.
8. Allen, J.B., et al., The SAD1/RAD53 protein kinase controls multiple checkpoints and DNA damage-induced transcription in yeast. Genes Dev, 1994. 8(20): p. 2401-15.
9. Hirao, A., et al., DNA damage-induced activation of p53 by the checkpoint kinase Chk2. Science, 2000. 287(5459): p. 1824-7.
10. Matsuoka, S., M. Huang, and S.J. Elledge, Linkage of ATM to cell cycle regulation by the Chk2 protein kinase. Science, 1998. 282(5395): p. 1893-7.
11. Sanchez, Y., et al., Control of the DNA damage checkpoint by chk1 and rad53 protein kinases through distinct mechanisms. Science, 1999. 286(5442): p. 1166-71.
12. Adamson, B., et al., A genome-wide homologous recombination screen identifies the RNA-binding protein RBMX as a component of the DNA-damage response. Nat Cell Biol, 2012. 14(3): p. 318-28.

Elledge wins Rosenstiel Award

Professor Stephen J. Elledge of the Harvard Medical School and the Howard Hughes Medical Institute has been awarded the 42nd Rosenstiel Award For Distinguished Work in Basic Medical Science  for “elucidating how eukaryotic cells sense and respond to DNA damage”. He identified key DNA damage response genes both in yeast and mammalian cells, showed how the pathway is activated by DNA lesions, and made key contributions to defining the cascade of phosphorylation events that enforces cell cycle arrest and controls DNA repair. Dr. Elledge’s work is also marked by the development of powerful research tools to uncover the network of genes involved in sensing and repairing DNA damage. His pioneering work laid the foundation for our current understanding of how failures in DNA damage sensing relate to the medically important field of genome instability.

The Rosenstiel Award consists of a cash prize and a medal, to be awarded at a dinner at Brandeis on March 14, 2013.

 

2012 Rosenstiel Award Recipient, Dr. Nahum Sonenberg

2012 Rosenstiel Award Lecture
Thursday, March 29, 2012, 4:00 PM
Gerstanzang 123

The 2012 Rosenstiel award winner, Dr. Nahum Sonenberg of McGill University, is a well-deserving recipient of this honor. Dr. Sonenberg received his Ph.D. in 1976 at the Weizman Institute of Science.  He then worked with Aaron Shatkin, where he discovered the translation initiation factor responsible for binding the 5’ cap of mRNA, eukaryotic Initiation Factor 4E (eIF4E); He has studied translation ever since.  Although his lab focuses on understanding how the cell achieves precise control of translation initiation, this line of investigation has led to discoveries affecting a wide variety of systems.  His lab has made key discoveries in cancer, obesity, virology, memory consolidation and how translation control plays a role in regulating these disparate processes.

In 1988, the Sonenberg lab made the groundbreaking discovery (Nature 1988, http://www.ncbi.nlm.nih.gov/pubmed/2839775) that the uncapped viral mRNA from poliovirus recruits the ribosome to internal regions of the 5’ untranslated region (UTR).  These sites have since been renamed internal ribosomal entry sites (IRESs). This finding was exciting since eukaryotic translation initiation typically requires the 5’ cap on an mRNA for eIF4E binding which subsequently recruits translation initiation machinery.  Until this time, the only mechanism of translation initiation was through the binding of eIF4E to the 5’ cap of mRNAs.  Sonenberg’s discovery that some mRNA has a mechanism to bypass the need for eIF4E binding and thereby avoiding translation control mechanisms started a new line of investigation in the translation field.  Along with discovering IRESs, this paper established an in vitro and an in vivo assay to study cap-independent translation initiation.  These assays are still used widely to test for IRES activity of mRNA UTRs.

Since that initial discovery, it has been found that many viruses contain IRES sequences in the UTR of mRNA that direct translation of viral proteins.  Some viruses, including poliovirus, are able to hijack eukaryotic translation machinery by cleaving factors necessary for canonical cap-dependent translation initiation, but dispensable for IRES translation. In this way, viral mRNAs are able to outcompete eukaryotic mRNAs for ribosome binding and in many cases become the most abundant transcript being translated.

Since the discovery of viral IRESs, many labs, including the Sonenberg lab, have discovered that some cellular genes also use IRESs to bypass the typical translation initiation control mechanisms. These genes are capable of translating even when the cell is actively shutting down translation.  One such cellular IRES-containing mRNA is the insulin receptor message, the IRES I study in the Marr lab.  Using assays similar to those first used in the 1988 paper published by the Sonenberg lab, I am exploring the necessity for the various initiation factors and IRES sequences required for efficient translation of insulin receptor in Drosophila melanogaster and mammalian cells.

The discovery that Dr. Sonenberg made in 1988 is only one example of the elegant research his lab has produced and continues to pursue.

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