PhD Transfer Exam – Morley Willoughby (Bruce lab)

PhD Transfer Exam


Wednesday May 24th, 10:10 am – Ramsay Wright Building, Rm. 432


Morley Willoughby (Bruce lab)

Investigating the Role of the Small GTPase Rab25 during Zebrafish Epiboly”


The adult body plan of an organism is established during a process called gastrulation. Despite the diversity of organisms across the animal kingdom, gastrulation occurs through a limited number of dynamic, large scale cellular movements. Epiboly is a conserved morphogenetic movement that is defined as the thinning and expansion of a cellular sheet. Understanding the molecular mechanisms that control this process is critical to our understanding of developmental biology. The small GTPase Rab25 becomes upregulated at the onset of zebrafish epiboly.  Rab25 is a member of the Rab11 subfamily of GTPases, and is known to direct apical vesicle trafficking and transcytosis in polarized epithelial cells. Rab25 morpholino knockdown or knockout using CRISPR/Cas9 gene editing technology results in an epiboly delay during zebrafish morphogenesis. Remarkably, while rab25 expression becomes restricted to the enveloping epithelial layer (EVL), a single cell thick epithelium during epiboly, the underlying loosely packed deep cells exhibit a larger epiboly delay. I hypothesize that the small GTPase Rab25 functions in the EVL during zebrafish epiboly. I propose to use the CRISPR/Cas9 Gene Editing technology to create an endogenous Rab25 fusion protein in the zebrafish genome to examine the intracellular localization of Rab25 in live embryos. I will then characterize defects within the EVL of Rab25 mutant embryos to understand how aberrant vesicle trafficking is leading to the observed epiboly delay. It is anticipated that my project will help uncover the relatively unknown molecular mechanisms controlling epiboly.

Ramsay Wright is a wheelchair accessible building.


PhD Transfer Exam – Bradley Laflamme (Desveaux/Guttman labs)

PhD Transfer Exam


Tuesday May 23rd, 1:10 pm – Earth Sciences Centre, Rm. 3087


Bradley Laflamme (Desveaux/Guttman labs)


“Identifying new building blocks of type III effector-mediated virulence using the Arabidopsis-Pseudomonas syringae pathosystem”




Pseudomonas syringae is a Gram-negative bacterial pathogen which infects many plant species, including the model plant Arabidopsis. The virulence of this pathogen requires its type III secretion system, which is used to inject a collection of “effector” virulence proteins directly into host cells to evade immunity and improve pathogenesis. While each strain of P. syringae is virulent on only a small number of hosts, effectors isolated from phylogenetically diverse strains often still have virulence functions in non-hosts, reflective of the fact that they target conserved facets of immunity across plant species. However, the vast majority of diverse effector variants across all sequenced P. syringae isolates have no characterization in terms of how they contribute to virulence in any plant background. To address effector-mediated virulence as a broad phenomenon, our labs have begun developing a type III effector compendium (T3EC) which collects effector sequences from across diverse isolates as a resource for wet-lab experiments. Using several pathogenicity assays which characterize effector-mediated virulence in distinct ways, we plan to screen and annotate the T3EC for virulence activity in Arabidopsis. After identifying effectors which contribute to particular aspects of P. syringae virulence, we will then explore synergistic relationships between these effectors, with our final goal being to develop a novel pathogen of Arabidopsis with a profile of synergistic effectors not found in any naturally occurring strain. This project will elucidate how effectors involved in targeting distinct immune processes intersect and amplify one another to dismantle plant immunity in successful pathogens.


PhD Transfer Exam – Urfa Arain (Erclik lab)

PhD Transfer Exam


Thursday May 18th, 2:30 pm – Rm. DV 3138, University of Toronto at Mississauga


Urfa Arain (Erclik lab)

Mechanisms underlying neuronal migration in the Drosophila optic lobe


Our ability to see the world around us relies on the precise assembly of neurons into complex circuits in the visual centers of our brain. The Drosophila medulla, which comprises the largest structure of the optic lobe, is an excellent model to explore neural circuit assembly due to its precise organization of 40,000 neurons across 800 columns. These neurons can be subdivided into two major classes: uni-columnar and multi-columnar. Uni-columnar neurons are born throughout the entire medulla and have small dendritic arborizations that contact a single column. In contrast, multi-columnar neurons are fewer in number and have large arborizations that contact several columns. During development, the majority of multi-columnar neurons are born in a restricted region and express the transcription factor Vsx1. Subsequently, they migrate up to 60 microns from where they are born to cover the entire medulla. The goal of my research is to identify the mechanisms that underlie the migration of Vsx1-derived multi-columnar neurons during development. I have found that migration occurs as a two-step process that begins 20 hours after puparium formation (APF) and continues until 50 hours APF. Surprisingly, the cell bodies of multi-columnar neurons initially migrate with a ventral bias that persists for at least 10 hours of pupal brain development, after which they cover the entire dorsoventral axis of the medulla. Additionally, the axons of Vsx1-derived multi-columnar neurons target locally in the developing neuropil prior to migration, indicating that their movement is likely independent of axonal targeting. Remarkably, the steroid hormone Ecdysone plays a key role in the process; transgenic flies expressing a dominant-negative form of the Ecdysone receptor in Vsx1 neurons show a cluster of cell bodies that fail to migrate in the adult medulla. In this PhD, I propose to describe the development of an individual multi-columnar neuron using genetic and live-imaging techniques. I will also investigate the role played by Ecdysone in migration by generating mutant MARCM clones and following them developmentally. Lastly, I intend to explore whether heterotypic signals from adjacent cell types or homotypic signals within the same subtype affect the migration of multi-columnar neurons through attractive or repulsive cues. It is anticipated that the results of this project will inform our understanding of neuronal development, neural circuit assembly and neurodevelopmental disorders in which these processes are disrupted, such as autism.