Analysis of autophagy regulation: Discussion of recent research and new technologies

London
Thursday, 03 October 2013

This is a Euroscicon Small Conference,  an outline of the day can be found at 
www.euroscicon.com/EurosciconMeetingStructure.pdf

Analysis of autophagy regulation: Discussion of recent research and new technologies
Thursday, 03 October 2013 09:00 - 17:00

Cineworld: The O2
Peninsula Square
London
SE10 0DX
United Kingdom

Map and Directions
This meeting will present and discuss current research into autophagy regulation including new flow cytometric and imaging assays and approaches which  available to study this regulation. This event  has CPD accreditation.

This event is part of the 2013 Flow Cytometry Forum – www.FlowCytometry2013.com


Meeting Chair:  Dr. Gary Warnes, Blizard Institute, Barts & The London School of Medicine & Dentistry, Queen Mary University


Who Should Attend
Flow cytometry specialists
Biotech and Pharma Industry: CEOs, Chief Scientists, Group Heads, Senior and Junior Scientists, Research Managers
Academic and Research Institutes: Group and Lab Heads, Postdoctoral Scientists and Research Students

The Deadline for abstract submissions for oral presentation has now passed. Abstracts for poster presentation only can be submitted up to two weeks before the event. There will be a best poster prize.
You can download the instructions for authors at 
www.euroscicon.com/AbstractsForOralAndPosterPresentation.pdf 


9:00 – 9:45        Registration


9:45 – 10:00      Introduction by the Chair:  Dr. Gary Warnes, Blizard Institute, Barts & The London School of Medicine & Dentistry, Queen Mary University


10:00 – 10:30     Flow Cytometric Measurement of Cell Organelle Phagy

 Dr. Gary Warnes, Blizard Institute, Barts & The London School of Medicine & Dentistry, Queen Mary University     The mechanism of organelle autophagy is little understood. We employed a range of autophagy inducing agents to determine the relative preference for the type of organelle-phagy caused by rapamycin, chloroquine, nutrient and low serum starvation. Organelle autophagy of mitochondria and Endoplasmic Reticulum (ER), termed mitophagy and ER-phagy was determined flow cytometrically by the employment of organelle mass probes, MitoTracker Green (MTG) and ER Tracker Green (ERTG). Relative changes in linear scaled median fluorescence intensity (MFI), were compared to control cells to determine the degree and type of organelle-phagy induced by different inducers of autophagy. These flow cytometric organelle phagy assays can be used by researchers to study the autophagic process further in terms of cell function.

10:30 – 11:00     Autophagy and neurodegeneration

Professor David C Rubinsztein, Professor of Molecular Neurogenetics, Wellcome Trust Principal Research Fellow, Deputy Director, Cambridge Institute for Medical Research, Honorary Consultant, University of Cambridge, UK I will describe our recent studies that implicate the plasma membrane as a source for autophagosomes, before focussing on the roles of autophagy in neurodegeneration. We showed that the autophagy inducers reduced the levels of mutant huntingtin and related neurodegenerative disease-associated proteins. These compounds ameliorated the toxicity of these proteins in cells and in vivo. While autophagy induction is protective in models of various neurodegenerative diseases, certain other conditions, including lysosomal storage disorders, are associated with compromised autophagy. I will review these data and then describe how impaired autophagy compromises cellular processes, including the ubiquitin-proteasome system.

11:00 – 11:30     Speakers’ photo then mid-morning break and trade show/poster viewing


11:30  – 12:00    A role for Rab8 and autophagy in the regulation of synapse growth

Dr Sean T Sweeney, University of York, UK We have developed a model of Frontotemporal dementia (FTD) in Drosophila based on ESCRTIII dysfunction. In a screen for enhancers and suppressors of the FTD phenotype we identified Rab8. Mutations in Rab8 have overgrown neuromuscular synapses by a factor of 100%. Examination of Rab8 mutants revealed endosomal dysfunction and accumulation of autophagosomes. Within the dysfunctional endosome we have identified signaling events organizing the prolonged activation of TGF-beta and JNK/AP-1 signaling generating synapse overgrowth. Autophagic activity is also necessary for the generation of synaptic overgrowth observed. The novel events we describe are likely to be critical to neuronal atrophy in FTD.


12:00  – 12:30    Autophagy as a barrier to viral and non-viral gene delivery

Professor Tom Wileman, University of East Anglia, UK     There is great interest in the development of viral and non-viral gene therapy vectors to replace defective genes associated with specific illnesses. Our work shows that viruses and non-viral gene delivery vectors can activate autophagy resulting in delivery to  autophagosomes.   Autophagy provides a powerful means of killing intracellular viruses by delivering them to lysosomes for degradation, and  at the same time slows release of genes into cells.  Authophagy has therefore evolved as an efficient defence against viral infection, but becomes a major barrier to the development of gene therapy vectors.

12: 30 – 13:30   Lunch and trade show/poster viewing


13:30– 14:20     Question and Answer Session


14:20 – 15:00    Oral Presentations:


   

14:20 – 14:30  17 BETA-ESTADIOL AND PROGESTERONE ENHANCE EXPRESSION OF AUTOPHAGIC GENES IN BOVINE MAMMARY EPITHELIAL CELLS.
M. Gajewska, K. Zielniok, A. Majewska, T. Motyl    
Department of Physiological Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences (SGGW), Nowoursynowska 159, 02-672 Warsaw, Poland, e-mail: malgorzata_gajewska@sggw.pl

14:30 – 14:40    INDUCTION OF AUTOPHAGY IN CHRONIC MYELOID LEUKAEMIA FOLLOWING TREATMENT WITH TYROSINE KINASE INHIBITORS MAY CONTRIBUTE TO DISEASE PERSISTENCE
A. Mukhopadhyay, G.V. Helgason, M. Karvela, E. Allan, R. Mitchell, T.L.Holyoake
Paul O'Gorman Leukaemia Research Centre, College of Medical, Veterinary & Life Sciences, Institute of Cancer Sciences, University of Glasgow

14:40 – 14:50    THE CORE AUTOPHAGY PROTEIN ATG4B IS CRITICAL TO THE SURVIVAL OF LEUKEMIC STEM/PROGENITOR CELLS AND PREDICTS CLINICAL OUTCOMES OF CML PATIENTS TREATED WITH IMATINIB THERAPY
Katharina Rothe1,2, Kevin B.L. Lin1, Hanyang Lin1,3, Amy Leung4, Hui Mi Wang1, Mehrnoush Malekesmaeili1, Ryan Brinkman1, Donna Forrest3,5, Sharon Gorski4, Xiaoyan Jiang1,2,3
1Terry Fox Laboratory, BC Cancer Agency; 2Department of Medical Genetics, University of British Columbia; 3Department of Medicine, University of British Columbia; 4Genome Sciences Centre, BC Cancer Agency; 5Leukemia/BMT program of BC, BC Cancer Agency, Vancouver, BC, Canada

  

14:50 – 15:00    DYNAMIC ASSOCIATION OF THE ULK1 COMPLEX WITH OMEGASOMES DURING AUTOPHAGY INDUCTION
E. Karanasios, E. Stapleton, M. Manifava, T. Kaizuka, N. Mizushima, S. A. Walker and N. T. Ktistakis
Signalling Programme, The Babraham Institute, Babraham Research Campus, Cambridge, CB22 3AT, UK 
     

15:00 – 15:30    Afternoon Tea


15:30– 16:00     Molecular mechanisms of mammalian autophagy

Dr Sharon A. Tooze, London Research Institute, UK Autophagy, a highly conserved cell survival pathway essential for cell health and homeostasis, is a membrane-mediated lysosomal degradation process that can be acutely induced. Induction by amino-acid starvation has been fundamental in the identification of the 36 autophagy-related (Atg) genes first in yeast, and more recently in mammals. Formation of autophagosomes requires the concerted effort of at least 18 Atg proteins, initiated by the activity of the ULK complex and the PI3-kinase complex including Beclin 1. I will discuss our recent findings about key protein-protein interactions and membrane contributions from a variety of subcellular compartments that drives autophagosome formation.

16:00 – 16:30     Autophagy in host-pathogen interaction

Dr Agnes Foeglein, MRC Laboratory of Molecular Biology, Cambridge, UK Cells deploy autophagy to protect their cytosol against infection. For efficient delivery to autophagy invading pathogens are specifically recognized by NDP52 and other cargo receptors. I will discuss the interplay between autophagy and pathogens with special emphasis on how cells restrict the proliferation of bacteria in their cytosol, how professional cytosol-dwelling bacteria avoid such attack, and how viruses even appropriate autophagy.


16:30 – 17:00     Chairman’s summing up

   


Keywords:  autophagy, Flow Cytometric & Image Analysis, LC3-II, organelle phagy, Necrobiology, Apoptosis, Flow cytometry, apoptosis, Image Stream, T cells, Immunosenescence, Wnt, colorectal cancer, GMP-compliant, cytotoxicity Humira, ADCC, CDC, Cell death, proliferation dyes, cell imaging, cell morphology, Flow cytometry, benchtop, quantitative imaging, 10-12 colour flow cytometry, synapse, neuromuscular, autophagy, Frontotemporal Dementia, endosome,ULK1/2, WIPI2, autophagosome, viruses, liposomes and lipoplex, gene delivery, cell-autonomous immunity, Salmonella, NDP52, Galectin-8, autophagy; neurodegeneration; treatment


Registration Website: www.regonline.co.uk/autophagy2013


 

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