MSc Exit Seminar – Syed Saad Husainie -Friday, January 12th, 2018

MSc Exit Seminar

Friday, January 12th, 2018 at 10:10am Ramsay Wright Building, Room 432

Syed Saad Husainie (Godt Lab)

Analysis of the Function of Protein Kinase C δ in Regulating Collective Cell Migration during Drosophila Oogenesis through Live Imaging

Abstract:

Border cell cluster (BCC) migration during Drosophila oogenesis has provided an excellent model to study collective cell migration. We have previously demonstrated that the serine/threonine kinase Protein Kinase C δ (PKCδ) is a regulator of BCC motility and protrusion morphology. My project aimed at examining the effects of altered PKCδ expression on BCC motility through live imaging, focusing mainly on BCC migration behaviour and protrusion dynamics. Although known for its pro-apoptotic role, I found no evidence of cell death in BCCs with increased or decreased PKCδ expression. Live imaging revealed that BCCs require normal levels of PKCδ expression to migrate at a normal speed. Increasing PKCδ expression levels in BCCs delayed detachment from the epithelium and significantly slowed down migration. Decreased PKCδ expression caused BCCs to migrate slower and less linearly during the early phase of migration. In addition, PKCδ-deficient BCCs showed defects in cellular protrusion dynamics, including frequent bifurcations and multiple cycles of extension and partial retraction. In summary, my analysis contributed to a better understanding of the function of PKCδ in regulating migration and protrusion dynamics during collective cell migration.

MSc Exit Seminar – Wednesday, December 13, 2017 – Gordana Scepanovic

MSc Exit Seminar

Wednesday, December 13th, 9:10am –University of Toronto at Mississauga – CC-2150

Gordana Scepanovic (Stewart lab)

Analysis of Drosophila Nervous System Development Following a Brief Exposure to Ethanol”

Abstract

Improper neuronal mapping predisposes many of the neurodevelopmental deficits that arise in patients of Fetal Alcohol Spectrum Disorders (FASD). Here I used Drosophila embryos as a model to investigate the neuronal defects that arise after exposure to ethanol. Drosophila is an excellent model for studying the mechanisms underlying FASD due to their vulnerability to the toxic effects of alcohol and the ease of manipulating their development. Using this model, I was able to provide detailed morphological analyses of the effects of a brief ethanol exposure on Drosophila neural development. I also examined the mechanisms that may regulate the FASD phenotype, specifically the serum response factor (SRF) signaling pathway. SRF signaling regulates numerous functions in the nervous system, including neuronal growth and migration. Through SRF manipulation in Drosophila, I was able to show that SRF is necessary for proper Drosophila axonogenesis, and that it may contribute to the FASD phenotype.

MSc Exit Seminar- Alexa Chioran – Tuesday, November 14, 2017

MSc Exit Seminar

Tuesday November 14th, 2:30 pm – Earth Sciences Centre, Rm. 3087

Alexa Chioran (Ringuette lab)

“SPARC promotes proper nucleation and assembly of collagen IV from Drosophila melanogaster embryonic haemocytes”

Abstract

Basement membranes (BMs) are a hallmark feature of all multicellular organisms in which they support essential developmental events. Collagen IV is the major structural component of the BM, however, its spatiotemporal assembly into stereotypic lattice networks is poorly understood. SPARC (Secreted Protein Acidic and Rich in Cysteine), a collagen IV-binding glycoprotein, is enriched in the BMs of Drosophila embryos and larvae. Fat body cells of Drosophila larvae and egg chamber follicular epithelial cells of the adult deficient in SPARC expression exhibit a fibrotic-like accumulation of collagen IV and other BM components in the pericellular space, resulting in larval lethality. Thus, SPARC is hypothesized to be an extracellular chaperone-like protein, whereby its association with collagen IV prevents aberrant collagen IV polymerization. In this study, I utilized molecular markers distinguishing secretory pathway compartments to demonstrate that SPARC and collagen IV co-localize primarily in the trans-Golgi network prior to secretion. Moreover, knockdown of SPARC expression in cultured embryonic haemocytes supports a role for SPARC in preventing premature nucleation of collagen IV molecules in embryonic haemocytes adherent to a laminin matrix. In order to gain further mechanistic insight on the functional relationship between SPARC and collagen IV, CRISPR gene editing technology was used to generate a sparc-null mutant. This genetic tool will be used in future experiments to unmask the structural domains of SPARC responsible for collagen IV assembly, maturation, and BM homeostasis.