MSc Exit Seminar – Chun Hua Wei- Tuesday, August 7, 2018

MSc Exit Seminar

Tuesday, August 7, 2018 at 1:10 pm SW -403, University of Toronto at Scarborough

Chun Hua Wei (Hasenkampf Lab)

The role of HOP2 in Homologous Recombination in Arabidopsis thaliana


The purpose of this study was to investigate the role of HOP2 protein in non-meiotic cells in Arabidopsis. HOP2 is already known to be important to meiotic chromosome pairing and homologous recombination, yet the role of HOP2 outside of meiosis is far from being fully elucidated. My study focused on the mitotic chromosome events with and without the application of radiation. In the absence of radiation, no fragments and chromatin bridges were found in hop2-1 plants, but they did seem to experience a modest chromosome separation delay. When irradiated, both genotypes had significant decreases of mitotic indices and increases of bridges. The decreases in mitotic indices were comparable for the two genotypes, suggesting they accomplish repair at similar rates. Irradiated hop2-1 had significantly more mis-repaired breaks, as determined by the bridges. My findings suggest that HOP2 is also important for the fidelity of the exchange process in non-meiotic HR repair.

PhD Exit Seminar – Samantha Mahabir -Tuesday, August 7, 2018

PhD Exit Seminar

Tuesday, August 7, 2018 at 12:10pm, DV 3130 – University of Toronto at Mississauga

Samantha Mahabir (Gerlai Lab)

The effect of embryonic alcohol exposure on brain function and behavior in zebrafish strains”


The biological mechanisms that underlie fetal alcohol spectrum disorder (FASD) are complex and poorly understood. This thesis aims to investigate potential underlying mechanisms of FASD by using zebrafish as a model organism. The research question asked is how does embryonic alcohol exposure alter brain function and behavior in different zebrafish strains? My first experiment explored the influence of environmental factors salinity and olfactory cues on zebrafish behavior. This was conducted to reduce experimental error variation and create more sensitive behavioral paradigms. My second experiment focused on characterizing the development of shoaling behavior and correlated neurochemicals in the absence of embryonic alcohol in order to establish baseline behavior. Next, I examined the effect of embryonic alcohol exposure on neurochemicals dopamine, serotonin and their metabolites and found embryonic alcohol exposure to disrupt the dopaminergic and serotonergic systems in the developing fish; as well I discovered these effects to be strain- dependent. I found that the specific development time point, concentration and short duration of alcohol exposure used in my experiments do not alter amino acid neurotransmitters glutamate, glycine, aspartate, taurine and GABA. Lastly, I have investigated apoptosis and have adapted the labeling TUNEL assay, for zebrafish. I found that mild alcohol exposure during development results in an increase in apoptosis and that these early responses result in long-lasting changes in neuronal markers and number of cells in specific brain areas. I included results on different zebrafish strains in some of my studies. Strain differences will facilitate the discovery of molecular mechanisms underlying changes in alcohol-related genes and will also allow researchers to choose the more appropriate strain for drug or mutation screening all of which will facilitate a better understanding of FASD.


PhD Exit Seminar -Nihar Bhattacharya-Tuesday, August 7, 2018

PhD Exit Seminar

Tuesday, August 7, 2018 at 9:30am, Ramsay Wright Building, Room 432

Nihar Bhattacharya (Chang Lab)



Vertebrate dim light vision is mediated by the rod visual pigment, rhodopsin, a member of the G protein-coupled receptor (GPCR) superfamily of proteins. In the dark, rhodopsin is covalently bound to a vitamin A-derived 11-cis chromophore, which acts as an inverse agonist to stabilize the inactive state of rhodopsin. When exposed to light of a maximal wavelength (λmax), the 11-cis retinal chromophore isomerizes to an all-trans conformation, initiating a series of structural shifts to the light-activated state of rhodopsin. This results in a signalling cascade within the rod photoreceptor cell and, ultimately, the perception of light. The goal of this thesis is to investigate natural variation in rhodopsin function in the context of evolutionary adaptation, chromophore usage, and disease mutations. Following a general introduction, in Chapter II, I characterize the visual system of the diurnal colubrid snake Pituophis melanoleucus using immunohistochemistry of retinal sections and spectroscopy of purified visual pigments expressed in vitro, revealing an unusual rhodopsin with cone opsin properties found in cone-like rod photoreceptors. In Chapter III, I investigate the effects of the rare vertebrate chromophore, 11-cis 3,4 dehydroretinal (A2), on the spectral and non-spectral properties of rhodopsin. In Chapters IV and V, I study the effects of pathogenic mutations in rhodopsin that cause the retinal degenerative disease retinitis pigmentosa (RP). In Chapter IV of my thesis, I identify the phenotype of RP mutations found in the extracellular loop 2 of rhodopsin and assess the effects of functional rescue using two different approaches. Finally, in Chapter V, I characterize three novel RP mutations to investigate the relationship between the in vitro and clinical disease phenotypes. The investigations in this thesis expand our understanding of snake retinal evolution, the role of the chromophore in rhodopsin function, and the effect of pathogenic mutations on rhodopsin structure and function. This thesis combines data from non-model organisms, non-mammalian chromophores, and non-wildtype pathogenic mutations to significantly increase our understanding of the scope of rhodopsin functionality.