CSB Seminar: Dr. Dalia Barsyte, Principal Investigator, Structural Genomics Consortium
Departmental Seminar
Host: Prof. David Lovejoy <david.lovejoy@utoronto.ca>
Abstract:
Epigenetic regulators are broad protein families that enzymatically modify histones/proteins or bind to the modified histones/substrates. These methyl-, acetyl-transferases, bromodomain proteins or demethylases play a role in gene transcription, chromatin condensation, cell division, DNA repair, telomere maintenance and retroviral silencing. To study the function of the epigenetic regulators, we generated specific small molecule inhibitors that allow chemical modulation of the system without perturbing the protein complexes. Such chemical targeting enabled the investigation into the function of G9a and GLP in ES cell specific retroviral silencing, SUV420 enzyme role in homologous DNA repair and PRMT5 enzyme driven methylation of protein substrates involved in splicing and cellular signaling. PRMT5 methyltransferase is essential for leukemia stem cell survival and interaction with the stroma cells that facilitates the expression of the stem cell markers. Inhibition of PRMT5 down-regulates the stem cell markers and leukemia cell survival. The protective role of the stroma-leukemia cell interaction and the niche-based micro-environment modulation by epigenetic regulators is being investigated.
Video Conferencing at UTM (DV 3131) & UTSc (MW229)
CSB Seminar: Prof. James Dowling, Staff Physician, Hospital for Sick Children, Senior Scientist, Genetics and Genome Biology, Department of Molecular Genetics, University of Toronto
Departmental Seminar
Senior Scientist: Genetics and Genome Biology
Department of Molecular Genetics, University of Toronto
“Swimming toward therapy: zebrafish and the quest for drug discovery in rare genetic diseases”
Host: Prof. Vince Tropepe <v.tropepe@utoronto.ca>
Abstract:
There are over 7000 rare diseases, and they affect more than 1 million Canadians. Advances in genomics have led to an unprecedented understanding of the genetic basis of rare disease, though despite this nearly half of all patients with genetic disorders do not yet have an identified gene mutation. More importantly, there estimated to be less than 500 therapies for these 7000 diseases, with the vast majority of conditions without any meaningful treatments. My research program has set out to tackle these barriers. We have used the zebrafish model system as our main solution. In this seminar, I will discuss our use of zebrafish for rare disease gene discovery and therapy identification. I will present specific examples of our successes, and discuss where we have encountered challenges. Most of our work has centered on understanding and treating human muscle diseases, though the discussion will be framed around how these studies are potentially broadly applicable to most/all rare diseases.
CSB Seminar: Prof. Will Wood, Wellcome Trust Senior Research Fellow, School of Cellular and Molecular Medicine, Faculty of Biomedical Sciences, University of Bristol, on sabbatical at Memorial Sloan Kettering Cancer Centre, New York
Departmental Seminar
School of Cellular and Molecular Medicine
Faculty of Biomedical Sciences,
University of Bristol
"Detecting Death and Damage in vivo; Understanding Macrophage migration in Drosophila"
A critical early wound response is the recruitment of inflammatory cells drawn by danger cues released by the damaged tissue. Hydrogen peroxide has been identified as the earliest wound attractant in Drosophila and Zebrafish and more recently we have shown using fly embryos that laser wounding triggers an instantaneous calcium flash in the epithelium which in turn activates the NADPH oxidase DUOX to generate Hydrogen Peroxide. As a consequence of hydrogen peroxide production, macrophages (hemocytes) within the fly embryo rapidly migrate toward the wound site powered by the formation of dynamic actin-rich lamellipodia. We are using live imaging to understand the mechanism by which inflammatory cells are able to detect hydrogen peroxide and generate the dynamic actin-rich structures necessary for their migration. We are particularly interested in how immune cells are able to integrate competing cues such as wound induced damage signals and ‘eat me’ cues from apoptotic corpses and how previous exposure to one cue is able to influence the cell’s ability to respond to subsequent signals.
CSB Seminar: Graduate student presentations - Virlana Shchuka (Mitchell lab), TBA
Departmental Seminar
CSB Seminar: Prof. Federica Brandizzi
Departmental Seminar
CSB Seminar: Professor Nick Kaplinsky, Swarthmore College
Departmental Seminar
Host: Prof. Peter McCourt <peter.mccourt@utoronto.ca>
Video Conferencing at UTM (DV3138) & UTSc (MW229)
CSB Seminar: Dr. Andrew Catalano, Smart-Biology.com, Toronto, Ontario
Departmental Seminar
Hosts: Prof. Tony Harris <tony.harris@utoronto.ca>
Prof. Sergey Plotnikov <sergey.plotnikov@utoronto.ca>
Prof. Maurice Ringuette <maurice.ringuette@utoronto.ca>
Video Conferencing at UTM (DV3138) & UTSc (MW229)
CSB Seminar: Prof. Antje Heese, University of Missouri
Departmental Seminar
University of Missouri
Host: Prof. Keiko Yoshioka <keiko.yoshioka@utoronto.ca>
Video Conferencing at UTM (DV3138) & UTSc (MW229)
CSB Seminar: Prof. Frieder Schöck, Department of Biology, McGill University
Departmental Seminar
"Organizing the actomyosin cytoskeleton in muscle and nonmuscle cells"
Host: Prof. Ulrich Tepass <u.tepass@utoronto.ca>
Abstract:
Cells can build highly complex intracellular structures from small protein subunits. My scientific interests lie in the cell biological mechanisms by which cells assemble a contractile actomyosin cytoskeleton and connect it to surrounding tissues. One aspect of our research focuses on how myofibrils and in particular Z-discs assemble in the fruit fly Drosophila melanogaster. Z-discs border the sarcomere, the smallest contractile unit of muscles, and anchor the barbed ends of antiparallel actin filaments. Here we analyze how actin filaments are organized by filamin and Zasp52 at Z-discs. We also investigate the giant scaffold protein obscurin, which in muscles aligns thick filaments at the M-line of sarcomeres. We want to know if obscurin is involved in formation of myosin II bipolar filament stacks in nonmuscle cells, as well as the general function of obscurin in nonmuscle cells.
Video Conferencing at UTM (DV3138) & UTSc (MW229)