January 13, 2015

The 2015 CeMM PhD Program - Apply Now!

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The 2015 CeMM PhD Program is now open for applications. For our next program starting in October 2015 we are looking for exceptionally motivated PhD candidates with a keen interest in genomics and medicine and an ability and desire to work in a team.

The 2015 CeMM PhD program will focus on two thematic areas: infection and cancer. These thematic areas are built on the pillars of epigenetics, bioinformatics and systems biology, chemical biology and the mechanism of action of drugs, high-throughput genetics, genomics and proteomics, and molecular and cell biology. Future CeMM PhD students will have an opportunity to work at the cutting edge of interdisciplinary molecular medicine research and will be trained by the entire CeMM and associated faculty to become one of the scientists shaping the future of molecular medicine.

January 13, 2015

2015 CeMM PhD Program - Apply Now

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The 2015 CeMM PhD Program is now open for applications. For our next program starting in October 2015 we are looking for exceptionally motivated PhD candidates with a keen interest in genomics and medicine and an ability and desire to work in a team.

The 2015 CeMM PhD program will focus on two thematic areas: infection and cancer. These thematic areas are built on the pillars of epigenetics, bioinformatics and systems biology, chemical biology and the mechanism of action of drugs, high-throughput genetics, genomics and proteomics, and molecular and cell biology. Future CeMM PhD students will have an opportunity to work at the cutting edge of interdisciplinary molecular medicine research and will be trained by the entire CeMM and associated faculty to become one of the scientists shaping the future of molecular medicine.

January 08, 2015

Horizon Discovery acquires the CeMM spin out company Haplogen Genomics

Today it was announced that the UK life science company Horizon Discovery Group plc acquired Haplogen Genomics GmbH, a wholly subsidiary of Haplogen GmbH, the first CeMM spinout company. Haplogen’s scientific roots lie in the haploid genetics technology developed by CeMM Adjunct Principal investigator Thijn Brummelkamp while he was a fellow at the Whitehead Institute for Biomedical Research of the M.I.T. This technology greatly enhances the ability to genetically inactivate and modify genes in human cells. Together with CeMM Principal Investigators Sebastian Nijman and Giulio Superti-Furga the company was founded to generate a collection of human mutant cell lines to bolster functional genomics research at CeMM but also in the wider academic community. Those tools allow direct functional testing of a wide range of biological and medical processes in human cell lines and can often replace or reduce animal experimentation by relevant biological experiments. Georg Casari, once Head of Technology Transfer at CeMM has headed the company since its foundation in 2010. A first collection was published in Nature Methods in 2013 and other paper illustrating the power of CRISPR/Cas9 genome engineering in haploid cells appeared last month in Genome Research. The haploid cell genetics is used at CeMM also to understand resistance to cancer drugs (see Winter et al. Nature Chem Biol 2014).

The deal includes a € 7.6 M upfront payment, part in cash and part in Horizon equity, plus a potential performance-related payment of up to € 5 M in future years. The money will first be used to pay off creditors such as the AWS, the Austria Wirtschaftsservice GmbH, a bank for the promotion and financing of companies. CeMM, that owned 5% of the company, will continue to have access to the haploid genetics technology and will receive royalties on cell lines established during the public–private partnership that laid the foundation for the company. With the sale of the genomics branch of the company, Haplogen will focus its future efforts on its drug discovery and development activities. 

CeMM’s Scientific Director Giulio Superti-Furga comments: “I am tremendously proud that an initiative generated at CeMM is not only a scientific, but also a business success. Our vision of synergies between public and private for the efficient generation of human mutant cells has panned out well and fast. The toolbox is propelling CeMM’s research.” 

References:

Essletzbichler P, Konopka T, Santoro F, Chen D, Gapp BV, Kralovics R, Brummelkamp TR, Nijman SM, Bürckstümmer T. Megabase-scale deletion using CRISPR/Cas9 to generate a fully haploid human cell line. Genome Res. 2014 Dec;24(12):2059-65

Bürckstümmer T, Banning C, Hainzl P, Schobesberger R, Kerzendorfer C, Pauler FM, Chen D, Them N, Schischlik F, Rebsamen M, Smida M, Fece de la Cruz F, Lapao A, Liszt M, Eizinger B, Guenzl PM, Blomen VA, Konopka T, Gapp B, Parapatics K, Maier B, Stöckl J, Fischl W, Salic S, Taba Casari MR, Knapp S, Bennett KL, Bock C, Colinge J, Kralovics R, Ammerer G, Casari G, Brummelkamp TR, Superti-Furga G, Nijman SM. A reversible gene trap collection empowers haploid genetics in human cells. Nat Methods. 2013 Oct;10(10):965-71.

Winter GE, Radic B, Mayor-Ruiz C, Blomen VA, Trefzer C, Kandasamy RK, Huber KV, Gridling M, Chen D, Klampfl T, Kralovics R, Kubicek S, Fernandez-Capetillo O, Brummelkamp TR, Superti-Furga G. The solute carrier SLC35F2 enables YM155-mediated DNA damage toxicity. Nat Chem Biol. 2014 Sep;10(9):768-73. 

January 07, 2015

Giulio Superti-Furga´s group discovered a key component of the nutrients sensing machinery of cells

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In order to decide whether to grow and proliferate or to break down and recycle, cells need to sense if the required nutrients are available. A central role in this context is played by the mechanistic target of rapamycin (mTOR) pathway that integrates the presence of growth factors, energy levels, glucose and amino acids to modulate cellular responses, such as protein and lipid synthesis. Past studies have demonstrated that the presence of amino acids is a crucial factor for mTOR activation. Despite this, the precise mechanisms by which amino acid levels are sensed are still poorly understood. In collaboration with Keiryn Bennetts group at CeMM, Lukas Huber and his team at the Biocenter of the Medical University Innsbruck and Cesare Indiveri´s lab at the University of Calabria, the Superti-Furga group with first author Manuele Rebsamen now succeeded in identifying the member 9 of the solute carrier family 38 (SLC38A9) as a key factor, that mediates mTOR activation. The study contributes to elucidate one of the mechanisms by which the cell recognizes the presence of amino acids and thereby controls mTOR activity. Manuele Rebsamen: “SLC38A9 is the first protein to be shown to physically and directly bind both amino acids and the machinery controlling mTOR function, suggesting it could act as sensor. Giulio Superti-Furga: “The finding may lead to new opportunities to interfere with the mTOR pathway by targeting SLC38A9 in situation where aberrant mTOR activation is thought to promote pathological conditions such as cancer and metabolic disorders.”

The study was realized in collaboration with Keiryn Bennett´s group at CeMM, Lukas Huber and his team at the Biocenter of the Medical University Innsbruck and Cesare Indiveri´s lab at the University of Calabria has been published advanced online in Nature, on January 7th, 2015.

The study has been funded by the Austrian Academy of Sciences, European Research Council, European Union, EMBO, Vienna Science and Technology Fund and the Austrian Science Fund, the Italian Ministry of Instruction University and Research.

November 25, 2014

Launch of Genom Austria

In a press conference on November 25th, 'Genom Austria' was announced as a joint Citizen Science Project of CeMM, the Medical University of Vienna, and the PersonalGenomes.org foundation. Genom Austria will explore the scientific, educational, philosophical, ethical, and social implications of personal genome sequencing. Following the model of Harvard’s Personal Genome Project, Genom Austria provides qualifying volunteers the opportunity to sequence their personal genomes and to share the data with the public. An important aim is to start a public debate on the opportunities and risks associated with whole genome information and contribute to the genomic literacy of as many Austrians as possible, particularly young people. Genom Austria is backed by an outstanding team of experts from biology, medicine, ethics, sociology and other disciplines, and it is under the patronage of Margit Fischer, chairwoman of the Science Center Network foundation and wife of the Austrian National President. For more information, please visit the project websites.

November 24, 2014

How influenza virus causes bacterial superinfection

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Viruses can predispose the host to bacterial superinfection, and secondary pneumonia is considered to play a major role in the morbidity of seasonal as well as pandemic influenza. Despite the significant clinical and socioeconomic impact, the molecular mechanisms of how influenza virus causes superinfection have been poorly understood. Scientists from Andreas Bergthaler´s Group at CeMM now succeeded in finding a new molecular mechanism, which may explain why influenza virus infections increase the susceptibility to bacterial pneumonia. Their discovery of a novel crosstalk between the antiviral molecule interferon and the enzyme Setdb2, which weakens the antibacterial response has been published advanced online on November 24th, 2014 in the scientific journal Nature Immunology.

During seasonal flu epidemics, respiratory infections with influenza virus lead to a sudden onset of high fever, cough, headache, runny nose, sore throat and other signs of fatigue and general discomfort. High-risk groups such as very young, elderly or chronically ill people may develop severe disease, which results in approximately 500.000 deaths annually (WHO). These severe influenza cases are often associated with secondary bacterial infections, so-called superinfections. Past studies suggested that the virus is not the primary cause of disease. Instead, the trigger for disease seems to be the suppression of the immune system by the virus. 

Using a superinfection model of influenza virus and streptococci, Bergthaler´s group could now show that interferon, which plays a central role in the antiviral response, induces the enzyme Setdb2. Subsequently they found that Setdb2 blocks the expression of antibacterial genes such as the chemoattractant Cxcl1, which is crucial for the recruitment of immune cells to the lungs and the control of bacterial infections. This mechanism may avoid excessive inflammation during viral infection. At the same time, however, it renders the organism more vulnerable to bacterial superinfection. Future research aims to elucidate the complex molecular interplay between the virus, Setdb2, the bacteria and the immune system. This may open new potential therapeutic avenues for patients at risk of superinfections.

Setdb2 mediates virus-induced susceptibility to bacterial superinfection.

Christopher Schliehe, Elizabeth K. Flynn, Bojan Vilagos, Udochuku Richson, Savitha Swaminanthan, Berislav Bosnjak, Lisa Bauer, Richard K. Kandasamy, Isabel M. Griesshammer, Lindsay Kosack, Frank Schmitz, Vladimir Litvak, James Sissons, Alexander Lercher, Anannya Bhattacharya, Kseniya Khamina, Anna L. Trivett, Lino Tessarollo, Ildiko Mesteri, Anastasiya Hladik, Doron Merkler, Stefan Kubicek, Sylvia Knapp, Michelle M. Epstein, David E. Symer, Alan Aderem and Andreas Bergthaler. Nature Immunology AOP, Doi: 10.1038/ni.3046 

The study has been funded by  CeMM, the Austrian Academy of Sciences (ÖAW), the Austrian Science Fund (FWF), the German Academic Exchange Service (DAAD), the Swiss Foundation for Grants in Biology and Medicine (SSMBS), the Swiss National Science Foundation (SNF) and the US National Institutes of Health (NIH).

November 24, 2014

Human Proteome Day

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As a follow-up to the publications on the initial draft of the human proteome that appeared in Nature in May this year, Bernhard Küster and Akhilesh Pandey were invited to CeMM to present their key research findings. As part of their presentations, the speakers described the broad range of applications of their research, such as the use of protein identification to aid forensic teams at crime scenes, or a large-scale malarial study in India. They also discussed the future of this research field, including the aim to produce a more refined map of the human proteome and also the development of proteogenomic centers to complement upcoming organism-wide sequencing  efforts.

The presentations were followed by an interactive and lively round table discussion on the next frontier in human proteome research, and what it may mean for us to perform research in a post-proteomic era. Karl Mechtler (Head of Mass Spectrometry & Protein Chemistry at the IMP), Thomas Helbich (Professor of Radiology at the Medical University of Vienna), Keiryn Bennett (Head of Mass Spectrometry &  Proteomics at CeMM) and Giulio Superti-Furga (Scientific Director at CeMM) joined the two speakers on the panel.

November 19, 2014

Biallelic loss-of-function mutation in NIK causes a primary immunodeficiency with multifaceted aberrant lymphoid immunity

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The team of Kaan Boztug, Principal Investigator at CeMM and Assistant Professor at the Department of Pediatrics and Adolescent Medicine of the Medical University of Vienna discovered the molecular origin of a new rare disease and succeeded in deciphering the essential role of the NFkB-inducing kinase (NIK) for an efficient immune response in humans. The findings have been published online, on November 19th, 2014, in the open access journal Nature Communications. 

Primary immunodeficiencies are inherited disorders resulting in malfunction of the immune system. The identification of the molecular defects underlying these disorders is crucial not only to diagnose patients and enable targeted therapies, but also highlights essential components and pathways in human immunity in general. The research team under the supervision of Kaan Boztug has now uncovered a novel, rare form of primary immunodeficiency, and identified a loss-of-function mutation in the gene NIK as the underlying genetic cause for this disorder.

In their publication, first author Katharina Willmann and her colleagues at CeMM and the Medical University decipher the essential role of NFkB-inducing kinase (NIK), a central kinase involved in non-canonical NFkB signaling, for an efficient immune response in humans. Usually, the signaling molecule NIK is expressed in lymphoid cells of the immune system. However, the variant they found in the patients is enzymatically inactive and therefore unable to transmit signals necessary to mount an appropriate immune response. Human NIK deficiency not only leads to defective B-lymphocytes that cannot produce antibodies appropriately. The scientists discovered that also T-lymphocytes, which specialize in memorizing and recognizing specific pathogens, as well as the so-called natural killer cells, which specialize in killing virus infected body cells, were affected in their functions. Together, these defects have a profound and devastating effect on the defense mechanisms of the patients.

By identifying the signaling molecule NIK as a crucial player in a functional immune defense, the team of Kaan Boztug uncovered a central molecular mechanism of the human immune system. These findings will not only help to understand signaling in the human immune system better but will, in the long run, also enable scientists to develop molecular therapeutic approaches.

Publication: Biallelic loss-of-function mutation in NIK causes a primary immunodeficiency with multifaceted aberrant lymphoid immunity. Katharina L. Willmann, Stefanie Klaver, Figen Doğu, Elisangela Santos-Valente, Wojciech Garncarz, Ivan Bilic, Emily Mace, Elisabeth Salzer, Cecilia Domínguez Conde, Heiko Sic, Peter Májek, Pinaki P. Banerjee, Gregory I. Vladimer, Sule Haskoloğlu, Musa Gökalp Bolkent, Alphan Küpesiz, Antonio Condino-Neto, Jacques Colinge, Giulio Superti-Furga, Winfried F. Pickl, Menno C. van Zelm, Hermann Eibel, Jordan S. Orange, Aydan Ikincioğulları & Kaan Boztug. DOI:10.1038/ncomms6360

November 18, 2014

Obituary Max L. Birnstiel

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Max L. Birnstiel 2007 in Vienna with his scientific son and grandson Meinrad Busslinger and Giulio Superti-Furga

It is with great sadness that we learn of the decease of Prof. Dr. h.c. mult. Max L. Birnstiel, of Wollerau, Switzerland. Max Birnstiel was the founding director of the Institute of Molecular Pathology (IMP) in Vienna and can be held responsible for kicking off the renaissance of the life sciences in Austria in the last 25 years. As a mentor of the CeMM director Giulio Superti-Furga, who in the late eighties had followed him as a PhD student together with his PhD supervisor Meinrad Busslinger, from Zurich to Vienna, Max Birnstiel provided important advice for the making and leadership of CeMM. Max Birnstiel will long remain a towering figure in molecular biology. Trained at the ETH in Switzerland with Frey-Wissling, he moved to Caltech to work with James Bonner. In 1966, together with his wife Margaret Chipchase, he first purified ribosomal RNA genes from vertebrates. He moved to Edinburgh where he physically isolated the histone genes of the sea urchin, before the invention of molecular cloning. Ernst Hadorn called him to the University of Zurich where for 15 years he led a world-renowned research program that determined gene-regulatory processes of eukaryotes. He was recruited by Boehringer Ingelheim and Genentech to conceive and lead the new IMP in Vienna, as a rather risky and innovative experiment, recruiting internationally and fostering world-class basic research in molecular biology in an environment that initially was a waste-land. He insisted on having the biochemical institutes of Vienna University to settle next to the IMP, to create the nucleus of the Vienna Biocenter. During his period as head of the IMP, he founded Intercell, a successful pioneering biotechnology company that helped put Vienna on the world map of research and business excellence in the life sciences. In his life, Max Birnstiel has earned numerous awards, prizes and honorary doctorates. He was a member of numerous academies, including the Austrian Academy of Sciences and the United States Academy of Sciences, as a foreign associate. In recognition of his pioneering work and immense contributions, the Austrian community of life scientists gave him the Achievement Award Medal during the EMBanniversary meeting in July 2014. In no possible way can the importance of Max L. Birnstiel for the life sciences in general, and for the Austrian molecular biology, be overstated. He will be dearly missed.  

November 03, 2014

10 Year Anniversary of the MedUni Vienna

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It is our great pleasure to congratulate the Medical University of Vienna on their 10 year anniversary! The Medical University of Vienna is one of our key research partners and plays a major role in the education and scientific development of CeMM’s PhD students, and postdoctoral fellows. We truly value the strong collaborative relationship with our neighbours, and we would like to thank the rectorate, our collaborators and the administrative staff of the Medical University of Vienna for their cooperation. Several members of CeMM Faculty are also affiliated with the Medical University and thus represent a successful “marriage” of ideas and objectives. In recent years we have published a number of co-authored papers in top journals and have shared some very promising research results. We are looking forward to continuing this successful relationship on many more collaborative projects to come.

Giulio Superti-Furga, Director CeMM