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Institute of Cell Biology Seminar Series


Seminars are usually held on Mondays at 12.00 noon in Main Lecture Theatre, Michael Swann Building.

Everyone is welcome to attend.

Semester One: September - December 2014





8th Sept 2014

Dr Lindsay Hall

Norwich Medical School, University of East Anglia

Bill Earnshaw

15th Sept 2014

Dr Ulrike Gruneberg

Sir William Dunn School of Pathology, University of Oxford

Adele Marston/Julie Welburn

22nd Sept 2014

Dr Andrew Carter

MRC Laboratory of Molecular Biology

Julie Welburn

29th Sept 2014

Dr Yiliang Ding

Department of Cell and Developmental Biology, John Innes Centre

Naomi Nakayama

6th Oct 2014

Professor Matthias Peter

Institute of Biochemistry, ETH Zurich

Kevin Hardwick

13th Oct 2014

Dr Boris Lenhard

MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College, London 

Teuta Pilizota

20th Oct 2014

Dr Stephen Royle

Associate Professor in Biomedical Cell Biology, University of Warwick

Ken Sawin

27th Oct 2014

Professor Cyril Zipfel

The Sainsbury Laboratory, Norwich

Steven Spoel 

3rd Nov 2014

Dr Victoria Cowling

MRC Protein Phosphorylation Unit, College of Life Sciences, University of Dundee


David Tollervey

10th Nov 2014

Dr Christian Häring

Structural and Computational Biology Unit, EMBL, Heidelberg

Adele Marston

17th Nov 2014

Dr Rut Carballido Lopez

Micalis institute, L'Institut National de la Recherche Agronomique (INRA)

Meriem El Karoui

24th Nov 2014

To be confirmed


1st Dec 2014

Dr Sjors Scheres

MRC Laboratory of Molecular Biology

Laura Spagnolo

8th Dec 2014

To be confirmed


15th Dec 2014

No seminar





Other seminars

Date Event
8th Oct 2014
Michael Swann Building
Main Lecture Theatre

Rudolf Jaenisch, Massachusetts Institute of Technology

iPS technology, gene editing and disease research

Host: Adrian Bird

25th Jun 2014
Michael Swann Building
Main Lecture Theatre

Professor Caroline Dean - John Innes Centre, Norwich

Wellcome Trust PhD Programme in Cell Biology Symposium Lecture - Chromatin and antisense transcript dynamics underlying seasonal timing.

The study of adaptation in plants has led us into the dissection of conserved mechanisms that link antisense transcripts with chromatin dynamics. This work emerged from genetic and molecular analysis of flowering pathways that quantitatively modulate expression of the flowering repressor FLC in response to different environmental and developmental cues.

The antisense transcripts, collectively called COOLAIR, are alternatively spliced and polyadenylated, initiate in an R-loop covering the 3’ end of FLC and encompass the whole FLC sense transcription unit. The differentially processed forms of COOLAIR are associated with different FLC chromatin states via changes in recruitment of chromatin modifying complexes. The talk will describe our current understanding of these mechanisms.

Host: Wellcome Trust PhD Programme in Cell Biology

28th May 2014
Daniel Rutherford
G27 Lecture Theatre 1

Professor Sir Tom Blundell - Department of Biochemistry, University of Cambridge

WT PhD programme seminar - Genomes, Structural Biology and Drug Discovery: Combating Resistance in Cancer and Tuberculosis

Over the past fifty years our knowledge of the evolution of proteins in living cells has been mapped in terms of molecular architecture and amino acid sequence. We have begun to learn that many accepted mutations are selectively neutral but others appear to be selectively advantageous to the organism by optimising stability, activity and interactions at the molecular and cellular levels. More recently second generation methods of gene sequencing are allowing us to follow the evolution and emergence of resistance as tumours escape the restraints of tissue function and as pathogens such as Mycobacterium tuberculosis and HIV evade the immune response of the host.


To understand this is essential to the design of new medicines. I will discuss work in my laboratory funded by the Wellcome Trust on cancer and by the Gates Foundation on tuberculosis. The reality of evolution will take me to the Cambridge Science Park, to Astex the company I co-founded to work on cancer medicines, and to collaborations with India and Southern Africa on tuberculosis where many lives are impacted by HIV and TB.

Host: JP Arulanandam

21st May 2014
Daniel Rutherford
G27 Lecture Theatre 1

Dr Julie Ahringer - Wellcome Trust/Cancer Research UK Gurdon Institute, University of Cambridge

WT PhD programme seminar - Exploring chromatin and the landscape of transcription initiation in C. elegans

Chromatin is the substrate upon which DNA is regulated for events such as transcription, replication, and DNA repair. More recently, regulation at the level of chromatin has also been shown to impact mRNA post-transcriptional events.  Hundreds of chromatin-associated proteins are known, and many have activities such as modification or binding to histone tails, or nucleosome movement, and these are thought to alter local and/or higher order chromatin structure.  However how most chromatin proteins regulate chromatin structure and function is poorly understood.  We use the model organism C. elegans to address these questions as it has many features that make it especially well-suited for such studies.  The genome is small (30X smaller than human) and well-annotated, and there is a rich resource of chromatin mutants and RNAi knockdowns that make functional analysis of any gene straightforward.  Importantly, C. elegans has a complement of chromatin factors very similar to that of humans.


I will discuss our work on transcription initiation and elongation at promoters and enhancers, genome organizational principles inferred through chromatin state mapping and the role of CpG dinucleotides in chromatin accessibility and relationship with HOT regions in C. elegans and humans.

Host: Adrian Bird

7th May 2014
Daniel Rutherford
G27 Lecture Theatre 1

Professor Witold Filipowicz - Friedrich Miescher Institute for Biomedical Research, Switzerland

WT PhD programme seminar - Mechanisms and regulation of miRNA repression and metabolism in mammalian cells

MiRNAs are ~20-nt-long regulatory RNAs expressed in eukaryotes. They regulate gene expression post-transcriptionally, by imperfectly base-pairing to 3’UTRs of mRNAs which results in translational repression and mRNA deadenylation and degradation. Most mammalian genes are predicted to be subject to miRNA regulation.


We will discuss current knowledge about the mechanism of miRNA-mediated repression, focusing on a role of GW182 proteins and the multi-subunit CCR4-NOT complex in translational repression and mRNA deadenylation. Our recent work revealed that CCR4-NOT complex mediates recruitment of the DEAD-box ATPase DDX6 to mRNA and that the interaction with CCR4-NOT activates ATPase activity   of DDX6 which appears to be required for the miRNA-mediated repression of translation. Recent work also revealed that biogenesis and turnover of miRNAs, and the miRNA-mediated repression itself, are highly regulated processes, involving a plethora of different protein factors. For example, miRNAs in retinal and hippocampal neurons turn over much faster than in non-neuronal cells and the miRNA turnover in neurons appears to be a subject of complex activity-dependent regulation. Some other examples of post-transcriptional control of miRNAs will also be discussed.

Host: David Tollervey

17th Feb 2014
Daniel Rutherford
G27 Lecture Theatre 1

Professor Peter Becker - Ludwig Maximilians Universität, München, Germany

WT PhD programme seminar - Get the numbers right or die: how male fruit flies get away with just one X chromosome

Eukaryotic genomes are highly evolved systems of gene expression that are challenged by sex chromosome aneuploidies, In humans and fruit flies the females bear a diploid genome with two X chromosome, but the male genome only contains a single X. This reduced dose is compensated for by an elaborate regulatory 'dosage compensation' process, which increases most of the transcription on the X in the two-fold range. The dosage compensation machinery comprises five protein subunits, amongst which three are enzymes, and a long, non-coding RNA. How does this machinery identify the X chromosome so stringently? How can transcription levels be tuned in such a fine range? Which role does the non-coding RNA play in answering these questions will reveal fundamental principles of gene regulation that are harnessed for the task of genome balancing.

Host: Irina Stancheva

10th Feb 2014
Daniel Rutherford
G27 Lecture Theatre 1

Dr Chris Smith - University of Cambridge

WT PhD programme seminar - Understanding the roles of alternative pre-mRNA splicing in shaping smooth muscle cell transcriptomes

Alternative pre-mRNA splicing is a key molecular mechanism that allows diversification of expressed proteomes far beyond the limitations suggested by a simple "gene-count" of a genome. Many examples of functionally important alternative splicing events have been described, while diseases arising from disruption of alternative splicing show that not only is RNA splicing an essential step in gene expression, but that appropriate regulation of alternative splicing programmes is essential for healthy development. Analyses of alternative splicing have employed both molecular dissection of individual alternative splicing events, as well as global profiling and computational analyses of co-regulated programmes of alternative splicing. I will describe the use of both types of approach by my lab in the analysis of alternative splicing in smooth muscle cells.


Host: Steve West

20th Jan 2014
Daniel Rutherford Building
G27 Lecture Theatre 1

Dr Hervé le Hir - CNRS, Paris

WT PhD programme seminar - The Exon Junction Complex, a multifaceted RNP complex dissected by different approaches from single-molecule to RNA-seq

To function properly, eukaryotic messenger RNAs (mRNAs) must contain a complete open reading frame to serve as an adequate template for protein synthesis, but also all the information that specifies their export from the nucleus, subcellular localization, translation, and stability. Much of this information is carried by the proteins composing mRNA-protein (mRNP) particles. My group is studying the multiprotein exon junction complex (EJC) deposited onto nuclear mRNAs by the splicing machinery. The EJC is composed of a dozen proteins and accompanies mRNAs to the cytoplasm to communicate with various machineries involved in export, translation, degradation, and subcellular localization. The EJC is also involved in the quality control process of nonsense-mediated mRNA decay (NMD) that eliminates aberrant mRNAs. In order to dissect EJC structure and the mechanisms by which it achieves its multiple functions, we are combining various approaches including biochemistry, structural and molecular biology, transcriptomics as well as single-molecule biophysics (magnetic tweezers). One peculiar aspect of the EJC is that it contains two RNA helicases, the DEAD-box eIF4AIII serving as an RNA clamp and Upf1 essential for NMD. Therefore, the EJC is a perfect model to understand how these ATP-dependent molecular motors are regulated by their binding partners.

Host: Atlanta Cook

16th Jan 2014
Darwin Building

Maria Christophorou, Gurdon Institute, University of Cambridge

Molecular mechanisms and cellular functions controlled by citrullination

Host: David Tollervey/Robin Allshire

13th Jan 2014
Daniel Rutherford
G27 Lecture Theatre 1

Dr Aurelie Bertin - Institut Curie, Paris

WT PhD programme seminar - Septins: ultrastructural plasticity of cytoskeletal multi-tasking proteins.

Septins are cytoskeletal filaments bound to the inner cell membrane. They are ubiquitous in eukaryotes and are essential for cell division. During cytokinesis, the last step of cell division, septins are arranged circumferentially around constriction sites. Septins are involved in building diffusion barriers for transmembrane proteins or proteins anchored to the membrane. By complementary electron microscopy and cryo-electron microscopy methods we have carried out a global study from the molecule to the cell. Using single particle image analysis and cryo-tomography, we have shown that the ultrastructural organization of septins is highly variable both in vitro and in situ. First, we have determined by single particle image analysis that the budding yeast septin complex, assemble into a linear, symetric and octameric oligomer. This minimal complex can then assemble into a nonpolar paired filament in low salt conditions [1]. To mimic the septin-membrane interaction, we have used biomimetic assays. Hence, we have shown that PI(4,5)P2 interacts specifically with septins and organizes septins in a novel manner [2]. Conversely, septins are able to deform vesicles into plaque-like structures.  Besides, we have described the organization of septin filaments in situ for the first time within budding yeast dividing cells, by electron cryo-tomography [3]. Besides we have  recently shown that septins from higher eukaryotes are able to bundle and curve actin filaments.

1. Bertin, A., et al., Saccharomyces cerevisiae septins: supramolecular organization of heterooligomers and the mechanism of filament assembly. Proc Natl Acad Sci U S A, 2008. 105(24): P. 8274-9.
2. Bertin, A., et al., Phosphatidylinositol-4,5-bisphosphate promotes budding yeast septin filament assembly and organization. J Mol Biol, 2010. 404(4): P. 711-31.
3. Bertin, A., et al., Three-dimensional ultrastructure of the septin filament network in Saccharomyces cerevisiae. Mol Biol Cell, 2012. 23(3): P. 423-32.

Host: Julie Welburn

26th Jun 2013
Michael Swann Building
Main Lecture Theatre

Professor Adrian Bird

Wellcome Trust PhD Programme in Cell Biology Symposium Lecture - Epigenetics and Rett syndrome

Autism is genetically complex, but several conditions within the autistic spectrum have simple causes. Because of their known origin, single gene disorders of this kind are more straightforward to understand and may hold lessons that apply broadly. An example is Rett syndrome, a profound autism spectrum disorder, which almost exclusively results from mutations in the MECP2 gene. Normally this gene makes a protein that binds to sites on DNA that are chemically altered by DNA methylation. In fact the MECP2 protein appears to interpret this “epigenetic” mark to affect gene expression. Why should loss of this function affect the brain? Are the resulting defects reversible? What are the prospects for therapy for this and perhaps related conditions? Professor Bird will draw upon the latest research that addresses these questions.

Host: Wellcome Trust PhD Programme in Cell Biology