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Upcoming Lectures

At the moment we are inviting more excellent speakers for our future DANDRITE lectures. The upcoming lectures will be announced as soon as possible.

Suggestions for speakers are welcomed to the seminar committee.

Previous Lectures

DANDRITE Lecture - 14 June 2017

Lecture on The good and the bad of NMDA receptor induced calcium signaling

By Hilmar Bading
Dept. of Neurobiology and Interdisciplinary Center for Neurosciences (IZN), University of Heidelberg, Germany

Where: Building 1170, room 347 (Aud. 6), 8000 Aarhus C

The dialogue between the synapse and the nucleus controls activity-driven gene transcription and is vital for virtually all adaptive responses in the nervous system including the build-up of a neuroprotective shield, the formation of memories, but also unwanted adaptations such a chronic pain or addiction. Calcium signals generated by synaptic activity and the opening of synaptic NMDA receptors and voltage-gated calcium channels serve as initiators of this communication pathway. They also mediate the propagation along the synapse-to-nucleus axis, although additional protein-based transport processes, such as the ERK-MAP kinase cascade, play a role (Hagenston and Bading, 2011). Nuclear calcium transients represent an important signaling endpoint in synapse-to-nucleus communication and function as master switch for adaptations-associated transcription. Blockade of nuclear calcium signaling in hippocampal neurons eliminates ‘acquired neuroprotection’, an activity-driven form of adaptation in which neurons that have been electrically activated are more resistant to harmful, cell death-inducing conditions. Similarly, the consolidation of memories and their extinction, as well as the development of chronic pain in mice is critically dependent on nuclear calcium signaling (Bading, 2013). In my presentation I will outline the features of the synapse-to-nucleus communication axis, discuss its genomic targets, and summarize how in neurodegenerative conditions this transcription-promoting axis is being antagonized by a cell death promoting signaling pathway activated by extrasynaptic NMDA receptors (Hardingham and Bading, 2010; Bading, 2017).

Speaker host:
Group leader Poul Henning Jensen, DANDRITE, Department of Biomedicine

Joint DANDRITE & Kjeldgaard Lecture - 25 April 2017

Lecture on The first steps in vision: cell types, circuits and repair

By Botond Roska
Friedrich Miescher Institute for Biomedical Research (FMI), Basel, Switzerland

Where: In the AIAS Auditorium, building 1632, 2nd floor, Høegh-Guldbergs gade, 8000 Aarhus C
The lecture takes place Tuesday 25 April 2017, from 13:15-14:00

Botond Roska received an MD in Budapest, Hungary, and a PhD at the University of California, Berkeley. After being a Harvard Junior Fellow at Harvard University he started his research group, eleven years ago, at the FMI. He investigates neuronal circuits in the retina, thalamus, and visual cortex; he is interested in using the gained knowledge to understand the circuit basis of neurological diseases and to design new therapies. He is the recipient of the prestigious 2016 Cogan Award from the Association of Research in Vision and Ophthalmology.

Speaker host:
Keisuke Yonehara, DANDRITE, Department of Biomedicine

Joint DANDRITE & Kjeldgaard Lecture - 1 December 2016

Lecture on "Neurogenetic aging studies in C. elegans"

By Patrick Laurent
University of Brussels, Belgium

Where: 1324-011 Twin-Auditorium
The lecture takes place Thursday 1 December 2016 13.15-14.00


To be announced

Speaker host:
Anne von Philipsborn, DANDRITE, Department of Molecular Biology and Genetics

DANDRITE Lecture - 29. November 2016

New insights into motor neuron disease from novel, animal and cellular models

By Kevin Eggan       
Harvard Department of Stem Cell and Regenerative Biology, Harvard University

Where:AIAS 1632-201
29/11 at 1 p.m.


To be announced

Speaker host:
Hanne Poulsen, DANDRITE, Department of Molecular Biology and Genetics

Joint DANDRITE & Kjeldgaard Lecture - 17 November 2016

Lecture on “Linking protein phosphorylation and degradation: How a specific phospho-signal serves as a degradation tag”

By Tim Clausen
Research Institute of Molecular Pathology (IMP), Austria

Where: AIAS auditorium (1632-201)
The lecture takes place Thursday 17 November 2016 13.15-14.00


To be announced

Speaker host:
Anne von Philipsborn, DANDRITE, Department of Molecular Biology and Genetics

Joint DANDRITE & MEMBRANES Lecture - 15 September 2016

Lecture on "The molecular landscape of Na,K-ATPase mutations: genotype/phenotype relationships in human disease"

By Dr. Kathleen J. Sweadner
Laboratory of Molecular Neurophysiology, Massachusetts General Hospital & Harvard Medical School

Where: The AIAS auditorium, building 1632, 2nd floor, Høegh-Guldbergs gade, 8000 Aarhus C
The lecture takes place Thursday the 15. Sept. 2016 from 10.15-11.00

To date, there are over 200 mutations in subunits of Na,K-ATPases that cause human diseases. Gene carriers present with a range of symptoms, however. In most cases, a clear genotype/phenotype relationship has not been found. Genomic data on random variants and human mutations in all four of the catalytic subunit isoforms show that each one has a different pattern of mutation. The structural distributions of known mutations also differ in significant ways. The evidence indicates that entire classes of mutations are missing from the known mutations. This suggests that entirely different human phenotypes and risk factors will eventually be discovered in this important gene family.

Speaker host:
Poul Nissen, DANDRITE & Dept. Molecular Biology and Genetics, Aarhus University

DANDRITE Lecture - 14 September 2016

Lecture on "Emotional Arousal and Lasting Memories"

By Dr. James McGaugh
Fellow, Center for the Neurobiology of Learning and Memory, Research Professor of Neurobiology and Behavior, 307 Qureshey Research Laboratory, University of California Irvine

Where: The AIAS auditorium, building 1632, 2nd floor, Høegh-Guldbergs gade, 8000 Aarhus C
The lecture takes place Wednesday the 14. Sept. 2016 from 15.15-16.00

James L. McGaugh’s research focuses on the neurobiological systems that regulate the formation of lasting memories.

He is Research Professor of Neurobiology and Behavior at the University of California, Irvine, and he was the founding Chair of the department and founding Director of the Center for the Neurobiology of Learning and Memory. He is a member of the U.S. National Academy of Sciences and a Fellow of the American Academy of Arts and Sciences.

He received his Ph.D. from the University of California, Berkeley and did postdoctoral study with Nobel Laureate Daniel Bovet in Rome. He has received the William James Award from Association for Psychological Science, the Karl Lashley award from the American Philosophical Society, the John P. McGovern Award from the American Association for the Advancement of Science, the Distinguished Science Award from the American Psychological Association, the Laurea Honoris Causa from the University of L’Aquila in Italy, and the Grawemeyer Award.

Speaker host:
Group Leader Sadegh Nabavi, DANDRITE - the Danish Research Institute of Translational Neuroscience, Dept. Molecular Biology and Genetics, Aarhus University


See video here of the DANDRITE Lecture by Dr. James McGaugh



DANDRITE Lecture - 27 June 2016

Lecture on "The roles of dopamine in perceptual and economic decision making"

By Armin Lak

Sir Henry Wellcome Fellow, University College London, United Kingdom

Where: Auditorium 6 (building 1170-347), Aarhus University, Dept. Biomedicine, Ole Worm’s Allé, 8000 Aarhus C
The lecture takes place Monday 27 June 2016 9.15-10.00


Dopamine neurons are known to reflect the economic value of rewards in form of reward
prediction error signals. In this talk, I will describe experiments in which we investigated how
dopamine signals emerge during learning of an economic choice task. I will then introduce a
novel behavioural paradigm for probing perceptual decisions in mice, and present experiments
in which we asked how optogenetic manipulation of dopamine neurons influences animals’
perceptual choices. Finally, I will discuss experiments in which we investigated whether
dopamine-mediated changes in animal’s choice behaviour are reflected in the activity of brain
regions that receive dopaminergic inputs. Together, these experiments demonstrate the nature
of signals that dopaminergic cells represent during learning, diverse roles dopamine plays in
various decision contexts, and finally how this neuromodulator influences neuronal computations
in other brain structures.

Speaker hosts:
Group leaders Sadegh Nabavi & Duda Kvitsiani, Dept. Molecular Biology and Genetics,
DANDRITE, Aarhus University

Joint DANDRITE & Kjeldgaard Lecture - 17 March 2016

Lecture on "Structural Biology of Human Membrane Proteins at the SGC"

By Liz Carpenter

Structural Genomics Consortium, Nuffield Department of Medicine, University of Oxford, United Kingdom

Where: Auditorium F (building 1534-125), Aarhus University
Ny Munkegade, 8000 Aarhus C
The lecture takes place Thursday 17 March 2016 13.15-14.00


Structural biology of membrane proteins is going through a revolution with the advent of new technologies,
which will allow us to solve structures of even the most challenging of targets. New structural
information will open up our understanding of the function of these proteins and their role in disease,
providing novel routes to therapies. Structural biology and biophysical methods are however still
dependant on the supply of high quality protein samples. At the SGC we have developed a pipeline for
producing human membrane proteins, growing crystals and solving structures. We have now solved
seven structures of human membrane proteins, from a range of families, using standard X-ray crystallography,
serial femtosecond crystallography and electron microscopy. These methods have allowed
us to begin to understand how the polymodal TREK-1 and TREK-2 K2P potassium channels are gated.
We have solved these structures in several conformations, including one using serial femtosecond crystallography,
which has allowed us to see a new conformation of the channel, in a membrane-like environment.
These structures, combined with simulations and electrophysiology data, revealed how these
channels can be gated by membrane stretch and inhibited by small molecule drugs.

Speaker host:
Poul Nissen, DANDRITE, Department of Molecular Biology and Genetics

Joint DANDRITE & Kjeldgaard Lecture - 22 October 2015

Lecture on "Controlling neuronal and non-neuronal components of networks in neurodegeneration"

By Francesco Roselli

Ulm University, Germany

Where: AIAS Aud. (building 1632-201), Aarhus University
Høegh-Guldbergs gade, 8000 Aarhus C
The lecture takes place Thursday 22 October 2015.
13.15- Lecture
14.00- coffee and cake and informal discussions with the guest
14.30- PhD session with the guest

All are welcome, and no sign up is needed.

An increasing number of neurodegenerative conditions are being linked to mutations in specific genes. This provides the unprecedented opportunity to model such conditions in experimental animals to untangle the pathogenic processes at work. Two salient features have been identified, that stand out both in human patients’ clinical course and in the animal models: despite being the mutant protein expressed in every neuron (and actually, in every cell of the body), only a precise population of neurons is overtly affected in so to produce telltale clinical syndromes; the pathogenic process unfolds over years or decades, during which multiple cell types participate to the cascade. Two sets of questions arise from these observations: what are the determinants of the selective (or relatively selective) vulnerability and how are they shaped in the course of the disease? Which events and which cell types are critical in the different stages of the disease, in order to have the full-blown phenotype appear?

A host of new technologies allow us to investigate these issues in unprecedented way in vivo. What makes some neurons so susceptible to specific mutations? Neurons are characterized by two classes of features: cell-autonomous biochemical processes and network-determined activity processes. While most of the research has focused on the former, the latter play a very large role in controlling neuronal biology (in fact, neuronal biology is geared toward producing neuronal activity). In motoneuron disease, in which lower motoneuron degenerate prominently and leave the patients (as well as the mice) paralyzed, we have demonstrated that modulating the activity of these neurons in vivo can rescue or worsen the appearance of disease markers and the degeneration of the neurons themselves. We have used a class of technologies collectively known as chemogenetics, based on receptors and ion channels engineered to recognize and be activated only by artificial agonists. Chemogenetics allow the control of neuronal activity (chemogenetic receptors must be expressed, usually by means of viral vectors) in vivo over periods of minutes to weeks without the need to implant optic fibers but by administering the cognate agonist. We have extended the use of these receptors beyond the control of neuronal activity to the control of synaptic plasticity-inducing signaling pathways and to the control of biological features of non-neuronal cells. Thus, we have achieved the manipulation of specific events in the pathogenic cascade with precise spatio (i.e., cellular identity and location)-temporal (i.e., in a specific phase of the pathogenic process) control. These approaches are revealing new features of the neurodegenerative process and are being applied outside this field for the control of neurons in neural circuits in vivo.

Speaker hosts:
Anne von Philipsborn, DANDRITE and Department of Molecular Biology and Genetics

DANDRITE Lecture - 16 October 2015

Lecture on "Associating Neuromagnetic Oscillations with Perception and Awareness"

By Dr Sarang Dalal

Neuroelectromagnetic Oscillations Laboratory — NEMOlab
Dept. Psychology
University of Konstanz

Where: iNANO Auditorium (building 1593, room 013), Gustav Wieds Vej 14, 8000 Aarhus
The lecture takes place Friday 16 October 2015, 11.15-12.00.

All are welcome.

Neural activity faster than 50 Hz, often referred to as the “gamma” band, have gained attention in
recent years, due to their association with underlying spiking activity and better correlation with
fMRI results. Many consider these faster rhythms to be a more reliable marker of attention and perceptual
awareness. While this activity can be measured with intracranial EEG, it has been more
difficult to observe with MEG and EEG. However, time-frequency beamformer methods that I have
developed, together with advanced head modelling techniques, allow us to observe these
signals noninvasively with greater fidelity. They may also allow us to observe deeper brain activity,
such as from the hippocampus.
My new line of research is examining how the retina interacts with cerebral cortex. The retina is
known to substantially preprocess visual stimuli, and some even consider it to be an extension of
the brain due to the sophistication of its neural circuitry. The electrical activity of the retina, or the
electroretinogram (ERG), can be measured using special electrodes placed on or near the eye.
While the ERG is widely used as a clinical diagnostic technique in ophthalmology, it is nearly
unknown in human neuroscience research. Studies examining information transfer between
retina and cerebral cortex in humans remain especially rare.
Visual stimuli have been shown to induce occipital gamma band activity in visual cortex that is
measurable with MEG/EEG. However, they also evoke retinal "oscillatory potentials" in similar
frequency bands. We therefore hypothesized that a substantial portion of the visual cortical
gamma band response may follow directly from retinal responses.
Our present results suggest that visually induced gamma band activity may in fact arise as a
consequence of retinal processing, either in addition to or perhaps instead of local processing
within visual cortex. Furthermore, in addition to communicating sensory information to the brain,
the retina may receive measurable feedback or modulation from visual cortex. My ERC-funded
research project will further investigate the relationship between retinal and cortical oscillations.

Speaker hosts: Professor Poul Nissen, Dept. Molecular Biology and Genetics, and Keisuke Yonehara, Dept. Biomedicine, Group Leaders at DANDRITE, Aarhus University.

Keynote Lecture - 9 September 2015
at the Annual meeting for the Nordic Molecular Medicine Network

Lecture on "Extremity as the mother of metabolic invention:  The neurobiology of the naked mole-rat"

By Gary Lewin
Department of Neuroscience, Max Delbrück Center for Molecular Medicine
Berlin, Germany
Cluster of Excellence NeuroCure, Charité-Universitätsmedizin
Berlin, Germany

When: Wednesday 9th September 2015 from 18:15-19:00
Where: The Moesgaard Museum Auditorium


African mole-rats (Bathyergidae) are a family of subterranean rodents with very unusual physiological traits for mammals. The most famous African mole-rat is the naked mole-rat (Heterocephalus glaber), which is a mouse-sized rodent that shows several extraordinary phenotypic features like poikilothermy, extreme longevity (up to 32 years), and cancer resistance. We found that naked mole-rats are essentially insensitive to at least two substances that normally produce pain in rodents, the algogens capsaicin and acid [1]. Insensitivity to the stinging pain produced by contact with a weak acid (pH3.5) can at least partially be accounted by a novel variant in the naked mole-rat voltage gated sodium channel NaV1.7 that makes acid act like a local anesthetic on peripheral nerves [2]. We hypothesized that acid insensitivity may be related to the ability of naked mole-rats to thrive in the very low O2 and high CO2 environments that comes with living in very large underground eusocial groups. I will present new data using systems biology approaches combined with physiology that provides a molecular explanation for the unique lack of thermogenesis ability in this species as well as its extraordinarily low basal metabolic rate. These and other metabolic adaptations enable the naked mole-rat to survive extreme anoxia. Some of these adaptations involve changes in the way cells use oxidative metabolism and may be conserved with other species that are confronted with challenging hypoxic environments. The naked mole-rat, as well as closely related African mole-rat species, share a rodent genome that is, like the mouse, around 95% identical to the human genome. We believe that it is now feasible to identify differences in gene composition as well as expression that enable the naked mole-rat to deal with environmental stresses that are deadly for most other mammals.

1) Park el al PlosBiol 2008 e13. doi: 10.1371/journal.pbio.0060013. 2) Smith et al Science 2011 334(6062):1557-60. doi: 10.1126/science.1213760.

EMBL Group Leader Lecture - 9 September 2015
at the Annual meeting for the Nordic Molecular Medicine Network

Lecture on "Structural basis and mechanism of the selective autophagy receptor p62/SQSTM1"

By Carsten Sachse
Group Leader
Structural and Computational Biology Unit
European Molecular Biology Laboratory (EMBL)
Heidelberg, Germany

When: Wednesday 9th September 2015 from 15:00-15:30
Where: The Moesgaard Auditorium

The multifunctional signaling adaptor and selective autophagy receptor p62/SQSTM1 is commonly found in dense light-microscopic loci of eukaryotic cells. Recently, Ciuffa et al. demonstrated that p62 is able to form organized polymers of helical symmetry once purified and reconstituted in the test tube [1]. In selective autophagy, p62 acts both as a substrate and as a receptor to bridge LC3 attached to the autophagosomal membrane with ubiquitinated cargo destined for degradation in the lysosome [2]. In signaling, p62 acts as an adaptor protein by interacting with protein kinases (atypical protein kinase C, MEKK3, MEK5, ERK1 and RIP) and ubiquitin ligases such as TRAF6 and the KEAP1-Cul3 complex [3]. In the talk, I will present a cryo-EM structural analysis of p62. Together with structures of assemblies from the PB1 domain we show that p62 is organized in flexible polymers with the PB1 domain constituting a helical scaffold. We determined the ~10 Å resolution structures of a series of PB1 constructs and found that isolated PB1 domains have the ability to form flexible helical filaments (Figure 1). Using biochemical assays, we demonstrated that the p62 filamentous assemblies interact with their biologically relevant binding partners LC3 and ubiquitin. These studies provide first structural insights into how p62 assemblies recognize ubiquitylated cargo while at the same time they can act as a scaffold for the nascent autophagosome.

1) Ciuffa, R. et al. Cell Rep. 2015; 11:748-758. 2) Johansen, T. et al. Autophagy. 2011; 7:279-296. 3) Moscat, J. et al. Trends. Biochem. Sci. 2012; 37:230-236.

EMBL Group Leader Lecture - 8 September 2015
at the Annual meeting for the Nordic Molecular Medicine Network

Lecture on "Systems biology of human cell division using light microscopy"

By Jan Ellenberg

Head of Unit and Senior Scientist
Cell Biology and Biophysics Unit
European Molecular Biology Laboratory (EMBL)
Heidelberg, Germany

When: Tuesday 8th September 2015 from 17:00-17:30
Where: The AIAS Auditorium, Aarhus University

Human cells contain over 20 000 different genes and essential functions of life, such as cell division, require several hundreds of these to be expressed. Using systematic gene silencing by RNA interference and subsequent phenotyping by high throughput microscopy we have defined close to 600 proteins that are needed for a human cell to divide normally. These proteins have to be precisely orchestrated in space and time to drive the faithful segregation of the genome and the cleavage of one cell into two. Understanding how this dynamic network of mitotic proteins drives one of the most dramatic morphological and functional changes cells can undergo, will require to map their interactions in space and time. To address this challenge, we have established an integrated systems biology workflow, consisting of genome editing, imaging and computational modeling to map the mitotic network in live dividing human cells. After homozygous genome editing to tag all endogenous copies of a given mitotic protein fluorescently, we image its absolute abundance and subcellular distribution by calibrated 4D imaging relative to spatio-termporal landmarks of cell division. Computational image analysis and modeling then allows us to align the dynamic cell morphology in space and time to obtain a standard mitotic cell into which we can integrate the data of all proteins imaged. Using image parameterization and machine learning, we can measure the dynamic subcellular localization of mitotic proteins as well as fluxes between subcellular compartments and structures. This allows us to predict protein clusters, the chronological order of their formation and disassembly and the abundance of their subunits. To validate the predicted network behavior, we then perform high-throughput fluorescence cross correlation spectroscopy (HT-FCCS) of fluorescently tagged pairs of binding partners during division. Our integrated computational and experimental method is generic and makes many dynamic cellular processes amenable to dynamic protein network analysis.

DANDRITE Lecture - 31 August 2015

Lecture on "Structural studies of ryanodine receptor gating by cryoelectron microscopy"

By Oliver B. Clarke

The Hendrickson laboratory, Dept. of Biochemistry and Molecular Biophysics
Columbia University, New York

When: Monday 31 August 2015 from 9:15-10:00.
Where: The Physiology Aud., Dept. Biomedicine, Aarhus University, building 1162-013, Ole Worms Allé 3, 8000 Aarhus.

All are welcome, and no sign up is needed.

Speaker hosts:
Poul Nissen, DANDRITE and Dept. Molecular Biology and Genetics, Aarhus University


Structures of the type 1 ryanodine receptor (RyR1) have revealed the architecture of the closed channel, but the structural basis for RyR1 activation has not previously been described. Here we present cryo-EM reconstructions of RyR1 in multiple defined functional states, including activated states, allowing us to provide a detailed description of the conformational changes, both in the transmembrane region and elsewhere, that are associated with calcium binding and channel activation.

DANDRITE Lecture - Keynote Speaker at the DANDRITE retreat - 20 May 2015

Lecture on "Canine neurological and neuropsychiatric conditions"

Hannes Lohi
Professor at University of Helsinki, Finland
Link to group website

When: The lecture takes place Wednesday 20 May 2015 at 13:00 - 13:45
Where: Sandbjerg Manor, Aarhus University Conference Facility, Sandbjergvej 102, 6400 Sønderborg

Speaker hosts:
Poul Nissen, DANDRITE and Department of Molecular Biology and Genetics, Aarhus university

Joint DANDRITE & Kjeldgaard Lecture - 7 May 2015

Lecture on "Reprogramming the Genetic Code"

By Jason Chin

Centre for Chemical and Synthetic Biology
MRC Laboratory of Molecular Biology
Protein & Nucleic Acid Chemistry Division
Cambridge, UK

When: The lecture takes place Thursday 7 May 2015 at 12:15 - 13:00 (note: free sandwiches before the lecture from 11:45-12:15 outside the auditorium)
Where: The AIAS auditorium (bulding 1632, room 201), Aarhus University, Høegh-Guldbergs gade, 8000 Aarhus.

All are welcome, and no sign up is needed.

Speaker hosts:
Daniel Otzen, Department of Molecular Biology and Genetics and The Interdisciplinary Nanoscience Center
Mads Fuglsang, DANDRITE and Department of Biomedicine


The information for synthesizing the molecules that allow organisms to survive and replicate is encoded in genomic DNA. In the cell, DNA is copied to messenger RNA, and triplet codons (64) in the messenger RNA are decoded - in the process of translation - to synthesize polymers of the natural 20 amino acids. This process (DNA RNA protein) describes the central dogma of molecular biology and is conserved in terrestrial life. We are interested in rewriting the central dogma to create organisms that synthesize proteins containing unnatural amino acids and polymers composed of monomer building blocks beyond the 20 natural amino acids. I will discuss our invention and synthetic evolution of new 'orthogonal' translational components (including ribosomes and aminoacyl-tRNA synthetases) to address the major challenges in re-writing the central dogma of biology. I will discuss the application of the approaches we have developed for incorporating unnatural amino acids into proteins and investigating and synthetically controlling diverse biological processes, with a particular emphasis on understanding the role of post-translational modifications.

Joint DANDRITE & iNANO Lecture - 17 April 2015

Lecture on "Behind the Scenes of Scientific Publishing"

By Anne Færch Nielsen

PhD, Editor
The EMBO Journal

When: Friday 17 April 2015 from 10:15-11:00.
Where: The iNANO Aud., Aarhus University, building 1593, Gustav Wieds Vej 14, 8000 Aarhus.

All are welcome, and no sign up is needed.

Speaker hosts:
Poul Nissen, DANDRITE and Dept. Molecular Biology and Genetics, Aarhus University


Publishing research papers is a cornerstone of working in life sciences, but do you know what actually happens to your manuscript once it is submitted to a scientific journal?

In this talk, Anne Færch Nielsen – scientific editor for The EMBO journal – will take you behind the scenes of scientific publishing at EMBO and explain how editors make decisions, find referees and work with authors to improve the revised manuscript. She will also discuss some of the challenges faced by the current publishing landscape, talk about the efforts EMBO is making to prevent errors and fraud from entering the literature, and offer you direct advice on manuscript writing and submission.

Short biography
Anne Færch Nielsen obtained her PhD in molecular biology from Aarhus University in Denmark in 2008 and worked as a postdoc in Javier Martinez' lab at IMBA in Vienna for three years before leaving the lab in early 2012 to become a scientific editor for The EMBO Journal in Heidelberg.

Brian Clark Biotech Lecture - 26 March 2015

Lecture on "Open Access Research Tools (Proteins, Structures, Probes and Assays) for Pre-Clinical Target Validation"

By Michael Sundstrøm
Scientic Director of European Initiatives, SGC
Department of Medicine
Karolinska University Hospital and Karolinska Institutet

When: Tuesday 26 March 2015 at 15.15
Where: Conferenceroom in the Science Park, building 3130-303, Aarhus University, Gustav Wieds Vej 10C, 8000 Aarhus

Speaker host: Poul Nissen, DANDRITE


Although the annual number of new drug approvals is trending upwards, the number of ‘rst-in-class’ therapies has remained relatively constant — often fewer than 10 per year. For such new medicines for ‘pioneer targets’, attrition in Phase II proof-of-concept clinical studies remains the biggest hurdle1, in large part because the target–disease associations derived from the currently dominant cell-line or animal preclinical models of disease often do not translate into clinical ecacy.

It is increasingly appreciated that the use of disease models based on human samples is critical both to increase our understanding of pathophysiology and to reduce clinical attrition. However, securing regular access to well-annotated samples from patients is challenging to organize and raises ethical issues. Here, we propose that these issues can most easily be addressed by creating an open-source partnership.

Joint DANDRITE & MEMBRANES Lecture - 29 January 2015

Lecture on "Structural basis for Ca2+-activation in TMEM16 chloride channels and lipid scramblases"

By Raimund Dutzler
Department of Biochemistry
University of Zurich

When: Thursday 29 January 2015 at 12.15 - 13.00
Where: Aud. 6, building 1170, 3rd floor, Dept. Biomedicine, Aarhus University, Ole Worms Allé 3, 8000 Aarhus

Speaker host: Poul Nissen, DANDRITE

The TMEM16 proteins (or Anoctamins) feature a remarkable functional diversity. They contain the long sought-after Ca2+-activated chloride channels but also lipid scramblases. We have determined the crystal structure of nhTMEM16, a fungal family member that operates as a Ca2+-activated lipid scramblase. Each subunit of the homodimeric protein contains ten transmembrane helices and a hydrophilic membrane-traversing cavity that is exposed to the lipid bilayer as a potential site of catalysis. This cavity harbors a conserved Ca2+-binding site located within the hydrophobic core of the membrane. Mutations of residues involved in Ca2+ coordination affect both, lipid scrambling in nhTMEM16 and gating in the Cl--channel TMEM16A. The nhTMEM16 structure thus reveals the general architecture of the family and its mode of Ca2+-activation. It also provides insight into potential scrambling mechanisms and serves as a framework to unravel the conduction of ions in certain TMEM16 proteins.

Joint DANDRITE & NeuroCampus Lecture - 5 November 2014

Seminar on "Identifying the dynamics of Lewy body formation in Lewy body diseases"

By Glenda Halliday
Neuroscience Research Australia and School of Medical Science, Faculty of Medicine, University of New South Wales, Sydney, Australia

When: Wednesday 5 November 2014 at 15:00-16:00
Where: Palle Juul-Jensen/DNC Auditorium, bldg. 10, Nørrebrogade 44, 8000 Aarhus C
Aarhus University Hospital

Speaker host: Prof. Poul Henning Jensen, DANDRITE.

Lewy bodies are intraneuronal cytoplasmic inclusions with core fibrils made from aggregations of alpha-synuclein. The dynamics of how these inclusions form within individual neurons, infiltrate the brain, and interact with other age-related pathologies have been identified.
Results: Within individual neurons, Lewy bodies form from a build up of punctate membrane aggregates of phosphorylated alpha-synuclein that coalesce into loosely packed filaments that undergo ubiquitination and “mature” by compaction. A slow pace of relatively restricted regional Lewy body involvement occurs in Parkinson’s disease, while the most rapid and spatially expansive molecular involvement occurs in patients with dementia. Lewy pathology has been shown to be transmitted between vulnerable neurons in humans.
Conclusions: While Lewy bodies are the same in different neurodegenerative diseases, assessment of different pathological cohorts shows that the timing and tempo of their cellular progression relates to their clinical phenotype and involve different molecular interactions.

Biography: Glenda Halliday, BScHons, PhD
Prof. Halliday received her degrees at the University of New South Wales and postdoctoral training at the Centre for Neuroscience, Flinders University of South Australia prior to returning to Sydney as an Australian Research Council Queen Elizabeth II Fellow. She has been a Research Fellow of the National Health and Medical Research Council of Australia (NHMRC) since then and is one of the senior scientists at Neuroscience Research Australia (joined in 1993). She is currently Professor of Neuroscience at the University of New South Wales and Director of the Sydney Brain Bank, as well as a NHMRC Senior Principal Research Fellow working on the pathogenesis of frontotemporal and motor neurodegenerative syndromes, including parkinsonian disorders. Prof. Halliday has published over 300 research articles and was elected president of the Australian Neuroscience Society for 2006-2007. She serves on a number of international editorial and advisory boards.

Joint DANDRITE & iSEQ Lecture - 3 October 2014

Seminar on "Genomic surveillance elucidates Ebola virus origin and transmission during the 2014 outbreak"

By Kristian Andersen
Harvard University, Broad Institute of MIT and Harvard

When: Friday 3 October 2014 at 11:00-12:00 (followed by sandwich lunch in the ground area - please sign up, see below)
Where: The Large Anatomy Auditorium (building 1232, room 115), Aarhus University, Wilhelm Meyers Allé, 8000 Aarhus C

This is a joint seminar with the Centre for Integrative Sequencing (iSEQ), Aarhus University.

Speaker host: Prof. Poul Nissen, DANDRITE.
If you wish to meet with speaker Kristian Andersen during his visit, please contact the host or the speaker directly.

In its largest outbreak, Ebola virus disease is spreading through Guinea, Liberia, Sierra Leone, Nigeria, and Senegal with thousands of people infected.
Our group sequenced 99 Ebola virus genomes from 78 patients in Sierra Leone to high depth of coverage. We found that the virus rapidly accumulates mutations inter- and intra-host, and we characterized patterns of viral transmission over the initial weeks of the epidemic. The West African variant likely diverged from central African lineages around 2004, crossed from Guinea to Sierra Leone in May 2014, and has exhibited sustained human-to-human transmission subsequently, with no evidence of additional zoonotic sources. Because many of the mutations alter protein sequences and other biologically meaningful targets, continued sequence-based monitoring as the outbreak progresses is critical to understand the impact of viral evolution on diagnostics, vaccines, and therapies.


Joint DANDRITE & Kjeldgaard Lecture - 25 September 2014

Seminar on "Molecular machines governing exocytosis of synaptic vesicles"

By Reinhard Jahn
Department of Neurobiology, Max-Planck-Institute for Biophysical Chemistry, Germany

When: Thursday 25 Sept. 2014 at 11:30-13:00 (Sandwiches outside the iNANO Aud. from 11.30, lecture start at 12.00)
Where: iNANO Auditorium (building 1593-012), Interdisciplinary Nanoscience Center (iNANO), Aarhus University, Gustav Wieds Vej 14, 8000 Aarhus C

This is a joint seminar with the Department of Molecular Biology and Genetics, Aarhus University.

Speaker host is Associate professor Ernst-Martin Füchtbauer, Dept. Molecular Biology and Genetics, Aarhus University.


Neurotransmitter release from presynaptic nerve endings is mediated by Ca2+ -dependent exocytosis of synaptic vesicles. During the past years the molecular steps mediating exocytotic membrane fusion have been unraveled although a lot of open question remain. Fusion is carried out by the SNARE proteins synaptobrevin/VAMP, syntaxin 1, and SNAP-25. Upon membrane contact, the vesicular SNARE synaptobrevin forms complexes with the plasma membrane-resident SNAREs SNAP-25 and syntaxin 1. Complex formation proceeds from the N-terminal end towards the C-terminal membrane anchors, thus pulling the membranes together and initiating fusion (“zipper” hypothesis of SNARE function). The steps of SNARE assembly are controlled both by members of conserved protein families such as the SM- and CATCHR-proteins, and they are tightly controlled by specialist proteins responsible for calcium regulation such as the calcium sensor synaptotagmin and complexins.

In our own work, we have focused on understanding the mechanisms of SNARE assembly and SNARE-induced fusion using structural and biochemical approaches and in-vitro fusion reactions with native and artificial membranes. Our recent results lend strong support to the zipper hypothesis, showing that during SNARE complex formation the helical bundle extends into the membrane and that only few SNARE complexes may suffice for effective fusion of bilayers. Furthermore, we have studied intermediate states of the SNARE-dependent fusion pathway involving techniques such as cryo-electron microscopy, resulting in novel insights into the structure of fusion intermediates.

In addition, we have investigated the interactions of the calcium sensor synaptotagmin 1 with SNAREs and with membranes. Our results lend support to the view that the interactions with membranes that are primarily of electrostatic nature are indeed crucial for synaptotagmins function in regulating exocytosis. Currently we believe that the calcium-dependent formation of a cross-link between the vesicle and the plasma membrane may play a central role in activating the SNARE proteins.

Joint DANDRITE & iNANO Lecture - 19 September 2014

Seminar on "EM-analyses of Nanomachines in Action"

By Arne Möller
Team Leader at DANDRITE and Assistant professor at the Interdisciplinary Nanoscience Center (iNANO).

This joint seminar with the Interdisciplinary Nanoscience Center (iNANO) is the first seminar in the DANDRITE seminar series.

When: Friday 19 Sept. 2014 at 10:15-11:00
Where: iNANO Auditorium (building 1593-012), Interdisciplinary Nanoscience Center (iNANO), Aarhus University, Gustav Wieds Vej 14, 8000 Aarhus C


Over the past decade Transmission Electron Microscopy of biological samples has seen significant improvements by means of resolution, reliability and throughput. Advances in EM-design, powerful computers and software and most importantly a new generation of EM cameras have recently led to results that are on par with those solved by X-ray crystallography.

In my presentation I will talk about our ongoing efforts to install a facility for streamlined EM data acquisition and processing at Aarhus University. The goal of this joint venture between iNANO and DANDRITE is to make EM accessible to a wider range of researches. With two state of the art TEMs, including a highest end Titan Krios, the current setup at Aarhus University is ideally suited for such an endeavor.

As EM only uses minute sample amounts and does not rely on crystallization this method is amenable to a large array of biological problems. Furthermore the “direct view” by EM is often priceless for sample optimization and also allows to immediately observe the dynamic processes that constitute the function of macromolecules.
In the second part of my talk I will discuss examples from my own research in which we utilized EM to analyze proteins undergoing many conformational states, with a special focus on ABC transporter and AAA enzymes.

Joint DANDRITE & iNANO Lecture - 25 April 2013

Lecture on "Biophysical Studies of Virus Maturation: Insights into Elegantly Programmed Nano-machines"

By John Johnson
The Scripps Research Institute

Where: The iNANO auditorium (1593-012), Gustav Wieds Vej 14, 8000 Aarhus C
When: 25 April 2013 at 13:15-14:00

Biophysical Studies of Virus Maturation: Insights into Elegantly Programmed Nano-machines
Virus particles with quasi-equivalent surface lattices (i.e. identical gene products in different quaternary structure environments) often assemble as a fragile, spherical shell in which the subunits are properly positioned on the appropriate surface lattice with differences in the environments minimized. Quasi-equivalent subunit contacts then differentiate during particle maturation, creating a robust, faceted particle with subunits in dramatically different local environments. Nudaurelia Capensis w Virus (NwV) is a eukaryotic, quasi-equivalent virus, with a T=4 surface lattice, where this process is dramatic (a change in particle size of 100Å during maturation) and is novel in that maturation can be investigated in vitro. Here we use X-ray crystallography,  biochemistry, Small Angle X-ray Scattering, and electron cryo-microscopy and image reconstruction (CryoEM), to characterize maturation intermediates, an associated auto-catalytic cleavage, the kinetics of morphological change and to demonstrate that regions of NwV subunit folding are maturation-dependent and occur at rates determined by their quasi-equivalent position in the capsid.

Host: Professor Poul Nissen, DANDRITE & PUMPkin

Coffee, tea and cake will be served from 13:00