scietalk göttingen 2011 programm

Approaches in Molecular Biology and Experimental Medicine

ProgrammScieTalk Göttingen 2011Von Studenten. Für Studenten.

ScieTalk Göttingen 201108. Juni 2011, 10.15 - 18.00 UhrHörsaal der PsychiatrieVon-Siebold-Str. 5 ScieTalk

...about Life Sciences!

Let’s talk...

4342 ScieTalk – Göttingen© Creative Commons – Daniel Schwen

3MF www.ScieTalk.btS-eV.de

Content

Greetings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5

Program . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7

The btS - About us . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8

Keynote Speaker . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

Abstracts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

Poster . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25

Map of the area . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31

Sponsors and Mediapartners . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32

Imprint . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33

54 ScieTalk – Göttingen

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Greetings

„Dear participant“

Welcome to the ScieTalk in Göttingen 2011! We wish you a pleasant time at the congress and hope you will enjoy many interesting new insights into various research fields of Molecular Biology and Experimental Medicine.

The ScieTalk was established by the btS, Germany`s largest network of Life Sciences students, as an innovative congress for and by students. We want to give young scientists the chance to present their ideas and projects in a relaxed atmosphere. The best talk and the best poster will be awarded with the ScieAward from the Deutsche Bildung!

Giving a talk, presenting a poster or taking part in lively discussions about re-sults, conclusions or new ideas makes YOU to be the most important part of the ScieTalk!

If you have any questions, remarks or suggestions, please do not hesitate to ask one of the many btS members within the congress area.

We are looking forward to a lively exchange, enjoy the day!


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In über 50 Ländern und über alle Kontinente hinweg vernetzen Mitarbeiter von B. Braun täglich ihr Wissen und ihre Erfahrung zum Thema Gesundheit – mit Kollegen und Kunden. Zum Beispiel in unseren „Centers of Excellence“. Fachübergreifend entwickeln dort Teams aus Spezialisten die Produkte und Technologien von morgen. Ein verlässlicher Stamm aus Know-how, auf den wir jederzeit von jedem Ort zugreifen können. Zum Vorteil unserer Kunden. Denn selbst unsere kleinste Einheit nutzt immer die Kraft der ganzen Familie. Effizient. Leistungsstark. Und das seit mehr als 170 Jahren. Sharing Expertise, made by B. Braun.

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Program

Time Program Speaker

10.15 - 10.30 ScieTalk-Opening Forum

10.30 - 11.00 Key-Note-Lecture Prof. Dobbelstein

11.00 - 11.30 StudTalk1: Vesicle recycling in vivo Annette Denker

11.30 - 12.00 Coffee Break

12.00 - 12.30

StudTalk2: A genome-wide screen for modifiers of polyglutamine-induced neurotoxicity in Drosophila melanogaster

Hannes Voßfeldt

12.30 - 13.00

StudTalk3: Isolation of internalizing anti-leukemic scFv-antibodies from naive Phage Display Libraries for targeted immunotherapy

Jenny Fitting

13.00 - 14.00 Lunch Break & Best Poster Voting

14.00 - 14.30 Key-Note-Lecture Dr. Guan

14.30 - 15.00

StudTalk4: Identification and further characterization of pro-invasive microparticles in macrophage-induced breast cancer invasion

Kerstin Menck

15.00 - 15.30StudTalk5: Antibody based cancer therapy - inducing suicide program selective in cancer cells

Franziska Hartung

15.30 - 16.00 Coffee Break

16.00 - 16.30

StudTalk6: Molecular Predictors for the Response to Nilotinib Treatment After Acquired Imatinib Failure In Ph+ Chronic Myeloid Leukemia

Mridul Agrawal

16.30 - 17.00

StudTalk7: Monocolonal Antibody Fusion-Proteins for Diagnosis and Treatment of Mesangioproliferative Glomerulonephritis

Pamela Bogner

17.00 - 17.30 Key-Note-Lecture Dr. Rizzoli

17.30 - 17.45 Best Poster & Best Talk Award


The btS - About us

Die btS-Idee

Let Life Sciences meet you!

„Was willst Du eigentlich nach Deinem Studium machen?“ Diese manchmal et- was unangenehme Frage wurde wahrscheinlich jedem von Euch schon häufi-ger gestellt. Eine klare Antwort wissen jedoch nur die wenigsten, da bei den meisten nur recht vage Vorstellungen über die berufliche Zukunft existieren. Genauso wie vielen von Euch erging es 1996 auch einer kleinen Gruppe von Life Sciences Studenten und Doktoranden in Köln, die daraufhin beschlossen, die btS zu gründen.

btS bundesweit

Die btS ist in 25 Städten vertreten.

Aus dieser Handvoll Studenten hat sich in den letzten 15 Jahren die größte Studenteninitiative der Life Sciences entwickelt. Mittlerweile sind wir mit über 700 Mitgliedern in 25 deutschen Universitätsstädten aktiv. Unser Ziel ist, Euch fernab von Vorlesungen und Seminaren einen Einblick in die reale Welt der Life Sciences zu geben. Außerdem möchten wir Euch den Übergang vom Studium in die Berufswelt erleichtern, indem wir jedes Semester verschiedenste Veranstal-tungen organisieren, die Euch unter anderem einen Überblick über die zahlrei-chen Karrieremöglichkeiten geben.

Unser vielfältiges Programm reicht von Vortragsreihen und Podiumsdiskus-sionen über Exkursionen bis hin zu Workshops, in denen Ihr Eure Soft Skills erweitern könnt. Aber auch zahlreiche Projekte auf europäischer Ebene sowie außergewöhnliche Events wie zum Beispiel das jährliche ScieKickIn, ein Fußballturnier zwischen Life Sciences Unternehmen und Forschungsinstituten, gehören zu unserem Programm. Bei der ScieCon, Deutschlands ältester Firmenkontaktmesse der Life Sciences, erhaltet Ihr spannende Einblicke in die spätere Berufswelt und natürlich ist der ScieTalk, der kostenlose studentische Wissenschaftskongress der btS, nicht zu vergessen! Diesen erlebst Du heute live vor Ort!

Your Life Sciences Career!

Biowissenschaften I Chemie I Pharmazie I Medizin

FirmenkontaktmesseViele Firmen – Ein Weg – Dein Job

www.ScieCon.info

ScieCon NRW 201126. Oktober – Audimax Ruhr-Universität-Bochum NRW 2011

Mit freundlicher Unterstützung von:

Let’s Start it!


Your Life Sciences Career!

Biowissenschaften I Chemie I Pharmazie I Medizin

FirmenkontaktmesseViele Firmen – Ein Weg – Dein Job

www.ScieCon.info

ScieCon NRW 201126. Oktober – Audimax Ruhr-Universität-Bochum NRW 2011

Mit freundlicher Unterstützung von:

Let’s Start it!


Keynote Speaker


Prof. Dr. Matthias Dobbelstein

Molecular Oncology

Short Portrait:

Prof. Dobbelstein is the head of the Division of Molecular Oncology in Göttingen since 2005. He received his Dr. med. 1993 in Munich and spent several years as postdoctoral fellow at Princeton University (USA) before he became group leader in Marburg and took up his first position as a Professor for Molecular Oncology 2004 at the University of Southern Denmark.

His major research interest is the cellular response of cancer cells to DNA damage, e. g. upon chemotherapy. This includes the activation of the “guardian of the genome”, the tumor suppressor p53, and its homologues. These transcription factors prevent uncontrolled cell proliferation and can drive cells into apoptosis. They are themselves regulated by a complex network of modulators.

In his presentation, however, Matthias Dobbelstein will not focus on specific research topics, but on general aspects and specific steps of an academic career in the life sciences. Participants are encouraged to bring up questions on whether and how they would like to pursue such a professional development at universities and academic research institutions.


Dr. rer. nat. Kaomei Guan-Schmidt

Cardiology / Stem cell research

Short Portrait:

Dr. Kaomei Guan-Schmidt studied Biology and Cell Biology in Peking and came to Germany in 1995. Her research group is part of the Heart Research Center Göttingen and the main focus of her research is the generation of pluripotent stem cells (which can differentiate into all types of body cells) from somatic (“normal”, finally differentiated) cells. These re-programmed stem cells could be used in the future for stem cell-based therapies in cell death related diseases like myocardial infarction. For this scientific purpose, her group established several cell culture and animal models and she is one of the few German scientists who are allowed to import human embryonic stem cells.

In 2006 Dr. Guan-Schmidt´s Nature publication “Pluripotency of spermatogonial stem cells from adult mouse testis” attracted the attention of scientist all over the world and she was honored with science awards for outstanding research.


Dr. Silvio O. Rizzoli

STED Microscopy of Synaptic Function

Short Portrait:

Silvio Rizzoli obtained his PhD degree in the lab of William Betz at the Department of Physiology and Biophysics at the University of Colorado (USA). He came to Göttingen in 2004 and worked as a postdoctoral fellow with Reinhard Jahn at the Neurobiology Department of the Max Planck Institute for Biophysical Chemistry. In 2007 he became group leader at the European Neuroscience Institute (ENI) in Göttingen and his group “STED Microscopy of Synaptic Function” is part of the Cluster of Excellence “Microscopy at the Nanometer Range”.

Dr. Rizzoli`s research is focused on the investigation of synaptic vesicle function, especially synaptic vesicle recycling. For this purpose, his group takes advantage of the increased imaging resolution provided by stimulated emission depletion (STED) microscopy. He published numerous high impact papers in the field of synaptic vesicles.


...about Life Sciences!

Let’s talk...

Cutting-Edge Technologies in Molecular Life Sciences

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Bewirb Dich jetzt unter www.ScieTalk.btS-eV.deAbstract Submission Deadline: 31. Juli

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ScieTalk NRW 201123. November 2011 Schloß Münster10.00 - 17.00 Uhr ScieTalk


Umfassende Infos aus erster Hand

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Abstracts


Synaptic Vesicle Recycling in vivo

Annette Denker, [email protected] Georg-August-Universität Göttingen

Abstract:

It has been assumed for decades that neurotransmitter release constitutes the function of all synaptic vesicles. Strikingly however, although presynaptic terminals can contain up to hundreds of thousands of vesicles, the majority fail to release in vitro even under stimulation conditions well above the physiological range. Vesicle use in vivo may therefore be rather limited.

To investigate this issue, a fluorescent marker was injected into living animals. Upon injection, the animals were allowed to behave freely for a defined amount of time. During this time, synaptic activity was monitored by dye uptake into recycling synaptic vesicles. This was followed by dissection, fixation and investigation by high-resolution microscopy to determine the number of vesicles used in vivo. The preparations employed spanned nine species (e.g., insects, nematodes, fish, amphibians, birds and mammals).

For all organisms and conditions tested, only a minority (~1-5%) of the vesicles were recycled even over several hours. We therefore conclude that the majority of vesicles might not function in neurotransmitter release in vivo.


A Genome-wide Screen for Modifiers of Polyglutamine-induced Neurotoxicity in Drosophila Melanogaster

Hannes Voßfeldt, [email protected] Georg-August-Universität Göttingen/Universitätsklinikum Aachen

Abstract:

Spinocerebellar ataxia type 3 (SCA3) or Machado-Joseph disease (MJD) belongs to the group of polyglutamine (polyQ) neurodegenerative diseases and is the most prevalent autosomal dominant cerebellar ataxia worldwide. A highly variable polyglutamine tract is thought to confer toxicity upon the otherwise unrelated proteins causing polyQ diseases. Apart from the glutamine extension, the physiological function and cellular context of these proteins and their interaction partners appear to be crucial for the specific pathogenesis and course of the disorders. In order to elucidate the molecular disease mechanisms triggered by trinucleotide repeats, we intended to identify genetic interactors enhancing or suppressing polyQ toxicity. Therefore, we targeted expression of a human Ataxin-3-derived polyQ transgene to the Drosophila compound eye. The resulting photoreceptor degeneration induced a rough eye phenotype (REP) in adult flies. Eye-specific silencing of specific genes (all fly genes with a human homolog, ca. 8,000 genes) by RNAi was utilized to identify genetic interactors of the REP. Changes in the observed REP are likely to originate from the knockdown of the RNAi target. Thus, silenced candidate genes are capable of modifying polyQ-induced neurotoxicity. The gene products we discovered in this manner represent various biological pathways and molecular functions. We conducted secondary investigations with this set of candidate genes to gain more insight into the mode and quality of the interactions. Our results are likely to shed further light on the molecular pathogenesis of Machado-Joseph disease and the role of Ataxin-3 and its modulator proteins in this process.


Isolation of Internalizing Anti-leukemic scFv-Antibodies from Naive Phage Display Libraries for Targeted Immunotherapy

Jenny Fitting, [email protected] RWTH, Aachen

Abstract:

Acute myelogenous leukemia (AML) is a cancer of the myeloid line of blood cells and is characterized by an uncontrolled overproduction of non-functional blast cells in the peripheral blood. Standard chemotherapeutic treatment still results in a therapy-associated mortality of more than 20% and a five-year survival rate that ranges from 15% for the elderly to 50% for younger patients. In addition, this treatment poorly discriminates between malignant and healthy cells resulting in severe off-target effects. Thus, the need for specific therapies that target the tumor cells through the recognition of tumor-specific surface antigens is evidently given. Using the Phage Display Technology, we have gene-rated a panel of highly-specific antibody fragments (scFv) to a human AML-de-rived cell line without any cross reactivity to healthy blood cells. The identified AML-binders were characterized in their binding affinity and tumor cell inter-nalization behavior, providing the basis for antibody-based fusion proteins for target-oriented leukemia therapy.


Identification and Further Characterization of Pro-invasive Microparticles in Macrophage-induced Breast Cancer Invasion

Kerstin Menck, [email protected] Georg-August-Universität Göttingen

Abstract:

Solid human tumors are composed of neoplastic epithelial cells as well as the surrounding tumor stroma. One of the stroma components are tumor-associ-ated macrophages, which are known to play a role in tumor progression. We could already show that the co-culture of human macrophages with the breast cancer cell line MCF-7 increases tumor cell invasion. However, the molecular mechanism behind this pro-invasive crosstalk could not be revealed so far. Hence, recent research activities have focused on the possible role of plasma- membrane derived microparticles (MP) for the intercellular communication.

Electron microscopy revealed that MCF-7 cells release intact MP (T-MP) into the cell culture supernatant under basal conditions. It could be demonstrated that T-MP were able to increase tumor cell invasion whereas stimulation with platelet-derived MP (P-MP) did not show any effect. By fluorescent labeling, an uptake of T-MP, but not P-MP, by the tumor cells could be visualized. Studies of the T-MP uptake kinetic into human macrophages revealed an incorporation of T-MP within the first hours after stimulation.

In order to identify possible candidate proteins which mediate their pro-inva-sive phenotype, T-MP were characterized by Western Blot indicating an enrich-ment of the glycoprotein EMMPRIN on T-MP. The results show that MP are a part of both arms of the tumor cell-macrophage loop and mediate tumor cell invasion. The pro-invasive phenotype of T-MP seems to be associated with the enrichment of pro-invasive factors such as EMMPRIN as well as with a specific recognition and uptake by their target cells.


Antibody Based Cancer Therapy –Inducing Suicide Program Selective in Cancer Cells

Franziska Hartung, [email protected] Georg-August-Universität Göttingen

Abstract:

Antibody-based cancer therapy uses the high specificity of antibodies to selec-tively destroy cancer cells. Therefore, a chief factor for an efficient antibody-based cancer therapy is the targeted antigen. The potassium channel KV10.1 (ether-á-go-go) seems to be a promising target. Outside of the CNS the chan-nel is not detected in normal tissues, but more than 75 % of tumor cells from different origins have been tested positive for KV10.1 expression. As a surface protein KV10.1 can be easily targeted by blocking agents or specific antibodies.

We designed a single-chain antibody (scFv) which binds to the pore region of KV10.1. ScFv antibodies offer several advantages in comparison to whole antibodies, like better tissue penetration or easier production. We generated a fusion construct consisting of KV10.1-specific scFv antibody and tumor necrosis factor-related apoptosis inducing ligand (TRAIL). TRAIL is as part of the immu-ne system and is involved in the elimination of transformed cells, e.g. cancer cells. Binding of TRAIL to its death receptors induces the apoptotic signaling cascade. The antibody-TRAIL fusion allows as tumor-specific targeting and se-lective apoptosis induction in cancer cells.

KV10.1-specific scFv62-TRAIL fusion protein was expressed in CHO-K1 cells and analyzed on cancer cells. After sensitization with cytotoxic drugs, scFv62-TRAIL induced apoptosis only in KV10.1-positive prostate cancer cells, but not in non-tumor cells nor in tumor cells lacking KV10.1 expression. In co-cultures scFv62-TRAIL fusion protein also induced apoptosis in bystander KV10.1-negative cancer cells in a paracrine manner, while normal prostate epithelia cells were not affected.

In summary, KV10.1 represents a novel therapeutic target for cancer. We could design a strategy that selectively kills tumor cells based on a KV10.1-specific antibody.


Molecular Predictors for the Response to Nilotinib Treatment After Acquired Imatinib Failure in Ph+ Chronic Myeloid Leukemia

Mridul Agrawal, [email protected] Ruprecht-Karls-Universität Heidelberg

Abstract:

A switch to the 2nd generation tyrosine kinase inhibitor (TKI) nilotinib has been proven to be effective in case of resistance or intolerance to imatinib for the majority of patients with Ph+ chronic myeloid leukemia (CML) in chronic phase (CP). Besides mutations in the BCR-ABL kinase domain and various BCR-ABL-independent mechanisms, TKI efficacy is dependent on intracellular drug levels, which is influenced by the efflux transporter protein MDR1.

In order to allow risk stratification and prediction of treatment outcome, we sought to elucidate molecular markers, e.g. MDR1 gene expression, BCR-ABL transcript burden, BCR-ABL mutation status and common SNPs in the MDR1 gene regarding their potency to predict therapy-related endpoints, such as MMR, complete cytogenetic response (CCyR), and progression-free survival (PFS) du-ring second line therapy with nilotinib in imatinib-resistant CML-CP patients.

Imatinib resistant patients in chronic phase CML treated with nilotinib (n=83) were investigated in a phase II study. BCR-ABL mutations were detected by D-HPLC and direct sequencing. MDR1 and BCR-ABL mRNA expression levels were determined by qRT-PCR using LightCycler™ technology, normalized against beta-glucuronidase (GUS) expression and standardized according to the inter-national scale (IS). MDR1 SNPs were analysed by direct sequencing. Log-rank tests were performed to compare the time to MMR, CCyR, and PFS.

Our data reveal that high pre-treatment expression levels of MDR1 serve as a favourable predictor for MMR, CCyR and PFS of imatinib resistant chronic phase CML patients within the first two years of treatment with nilotinib. Further, MDR1 SNPs at positions 1236 and 2677 were significantly associated with high-er gene expression. These findings might allow prediction of treatment out-come and therefore further tailor the individualized second line therapy in CML.


Monoclonal Antibody Fusion-Proteins for Diagnosis and Treatment of Mesangioproliferative Glomerulonephritis

Pamela Bogner, [email protected] RWTH Aachen

Abstract:

Glomerulonephritis (GN) describes the most important group of chronic inflammatory renal diseases, accounting for nearly 27 percent of all cases of end-stage kidney failure. Mesangioproliferative GN, a chronic, slowly progressive form of GN, is characterized by increased mesangial proliferation and/or matrix accumulation in the glomeruli due to antibody-dependent activation of the classical complement pathway. Because there is currently no specific therapy available, further research into the immunopathology of mesangioproliferative GN is absolutely desirable. A stable mouse model, corresponding to the well-established anti-Thy 1.1 nephritis rat model could open up a large field of therapeutic options in transgenic mouse models.

Using the Phage Display technology we generated a set of highly-specific single-chain (scFv)-antibodies directed against murine mesangial cells and used them as fusion partner for construction of scFv-Fc-fusion proteins. Detailed characterization and cross-reactivity controls with other co-located cell types underline the functionality of our antibodies as the first in vitro murine mesangial cell markers. The in vivo application of the fusion proteins will provide detailed insight into new therapeutic approaches against GN.


Poster


Markus Döring

Tel. 0551/49702 - 517Mobil 0151 / 145 348 [email protected]


The Kinase MK2 in the DNA Damage Response of Leukemic Cells to Ara-C-treatment

Veena Jagannathan, [email protected] IMPRS, Georg-August-Universität Göttingen

Poster:

Nucleoside analogs represent one of the most commonly used class of chemo-therapeutic agents for the treatment of various kinds of cancers. Ara-C is one such example of a nucleoside analog, widely used for the treatment of acute leukemia. After its incorporation in the DNA, Ara-C causes stalled replication forks and activates the S-phase cell cycle checkpoint. However, little is known about the role of different mediators involved in this checkpoint activated by Ara-C. In a siRNA screen performed by our lab to identify kinases involved in the UV induced damage response, MK2 came up as one of the strongest candi-dates. Here we investigated the role of this kinase in the response of leukemic cells to Ara-C treatment. Time course experiments performed indicate a criti-cal role of this kinase in the later stages of the checkpoint activated by Ara-C. Further studies performed with Ara-C and MK2 inhibition suggest that MK2 might regulate the activity of the checkpoint kinases Chk1 and Chk2. While MK2 seems to positively regulate the activity of Chk2 and increase the levels of its phosphorylated form, the opposite is observed for Chk1. In addition to this, MK2 is also involved in controlling the cellular survival in response to the DNA damage by Ara-C. Furthermore, results from similar inhibition experiments also show that MK2 might mediate its actions by phosphorylating and thus inacti-vating the Cdc25 phosphatases and cyclin- dependent kinases, thereby regu-lating the cell-cycle progression. Based on our findings, we propose a model in which MK2 activity connects apoptosis in response to Ara-C, via three possible mechanisms: (a) inactivation of Cdc25 phosphatases and hence collapse of replication forks due to enhanced incorporation of Ara-C; (b) activation of Chk2 and initiation of apoptotic pathways; and (c) inactivation of Chk1 and inhibition of DNA repair pathways.


Influence of Osmolality and Sodium/Potassium Ratio on Morphology and Productivity of Aspergillus Niger

Judith Mönch-Tegeder, [email protected] Technische-Universität Braunschweig

Poster:

Aspergillus niger is an important organism for the biotechnological production of organic acids and enzymes. One of the most startling and often uncont-rollable characteristics of this filamentous organism is its complex morphology, ranging from dense spherical pellets to viscous mycelia depending on culture conditions.

It was reported for different organisms that elevated concentrations of salt can induce several physiological responses like an altered morphology and enhanced productivity. To investigate the effect of the Na+/K+ ratio on A. niger morphology and productivity several experiments in shaking-flasks and 2L-bioreactors were conducted. The shaking flask experiments indicated an enhanced productivity for the model product β-fructofuranosidase at surplus of Na+-Ions. An optimum for the osmolality and the sodium-potassium-ratio was determined. The results of these experiments were validated by 2L-bioreactor-cultivations.

The morphology of A. niger was examined by microscope and an automated image analytic methods using the open source software Image.


Reconstitution of Both Steps of S. Cerevisiae Splicing with Purified Components

Zbigniew Warkocki, [email protected] Max-Planck-Institut für biophysikalische Chemie

Poster:

The spliceosome is a protein-rich ribonucleoprotein (RNP) machine that catalyses intron removal from pre-mRNA in a two step reaction. To investigate the catalytic steps of splicing, we established, for the first time, an in vitro splicing complementation system using purified yeast spliceosomal components of defined composition. Spliceosomes were stalled prior to step 1 using extract from a temperature-sensitive mutant of Prp2, an essential DEAH box helicase which acts prior to step 1 of splicing.

The composition of the prp2Δ spliceosome was defined by mass spectrometry and RNA analyses and the complexes shown to catalyze both steps of splicing when supplemented with native and/or recombinant proteins. Efficient catalysis of step 1 required purified recombinant Prp2, Spp2 and Cwc25 proteins, demonstrating a previously unknown role for the latter in promoting step 1 of splicing. Our data demonstrate that Prp2 facilitates catalytic activation of the spliceosome by inducing rearrangements, including destabilization of SF3a/b proteins, that likely expose the branchsite sequence prior to step 1. Our new approach paves the way for future ultrastructural and biophysical studies to dissect spliceosome activation and catalysis.


The Same Synaptic Vesicles Drive Active and Spontaneous Release

Benjamin Wilhelm, [email protected] Georg-August-Universität Göttingen

Poster:

Synaptic vesicles fuse with the neuronal plasma membrane to release their neurotransmitter contents both upon the arrival of action potentials (active release) and at rest (spontaneous release). It has been assumed for almost six decades that identical vesicles exocytose in both cases. This assumption has been used to generate the quantal (vesicular) release theory. However, several recent studies report to find evidence for a seperate pool maintaining spontaneous release. We tested here this controversial issue by combining several fluorescence imaging assays (FM dye imaging, antibody labeling of synaptotagmin via both conventional and super-resolution microscopy and pHluorin imaging) and we suggest that the same vesicles participate in active and spontaneous release.


Map of the area

Universitätsklinikum Göttingen Von-Siebold-Str. 5 37075 Göttingen

ScieTalk GöttingenHörsaal der Psychiatrie


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Media Partners

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Biotechnologische Studenteninitiative e.V.

Organizer: Biotechnologische Studenteninitiative e.V. c/o BIOCOM Projektmanagement GmbH Brunnenstr. 128 13355 BerlinTelefon: 030/26492121 Vereinsregisternummer: VR12830 (Amtsgericht Köln) www.btS-eV.de

Project Management/V.i.S.d.P.: Finances:Bastian Behrens Christopher Nötzel [email protected] [email protected]

Federal Board: Graphic & Layout: Hans Kleine-Brüggeney it’s FR!TZ / Heiko [email protected] [email protected]

Marketing: Homepage: Milena Schöneke Anna Cicholas [email protected] [email protected]

Scientific Coordination: Christian Veltkamp [email protected]

Disclaimer/Haftungshinweis:Die Biotechnologische Studenteninitiative e.V. übernimmt weder Haftung noch Garantie dafür, dass die in diesem Programmheft bereitgestellten Informationen vollständig, richtig und in jedem Fall aktuell sind. Dies gilt insbesondere für alle Abstracts, die von den Teilnehmern des ScieTalk 2011 eingereicht wurden. Für die wissenschaftliche Richtigkeit und rechtlichen Konsequenzen sind ausschließlich die namentlich genannten Verfasser der Abstracts verantwortlich. Nachdruck, auch auszugsweise, ist nur nach Zustimmung der Redaktion und unter Quellenangabe frei.

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Notes


Let‘s talk about Life Sciences


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scietalk göttingen 2011 programm

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