​Plants rely on innate immunity to perceive and respond to pathogenic microbes. Developmental age can also affect a plant’s ability to defend itself from pathogens. Although plants do not possess moving immune cells, they possess the ability to alert systemic tissues to ongoing localized infections. In the Cameron lab we are interested in understanding systemic and developmental resistance in plants with the long-term goal of enhancing disease resistance in crop plants. Systemic Acquired Resistance (SAR) allows a plant to perceive an initial infection in one leaf and transmit a signal to inform systemic leaves about the pathogen threat. We use Arabidopsis, cucumber and tobacco to understand how SAR long-distance signals move from initially infected leaves to distant healthy leaves. We are investigating how DIR1, a lipid transfer protein (LTP) moves to distant leaves during SAR. We also study developmentally regulated Age-Related Resistance in Arabidopsis. Young plants are highly susceptible to the bacterial pathogen, Pseudomonas syringae, but when mature, Arabidopsis displays ARR and responds with a super immune response to these same pathogens. Our studies indicate that during ARR, mature  plants defend themselves by limiting  bacterial growth and biofilm formation. Although both SAR and ARR pathways allow plants to respond in a resistant manner to normally virulent pathogens, our evidence to date indicates that the mechanisms responsible are unique to each pathway.

​Transcriptional-regulatory networks establish the gene expression programs responsible for normal growth and disease states.  They are composed of interactions between transcription factors and their target genes by direct binding to the promoter.  The complete mapping of these networks in model systems by identifying the binding specificities and target genes of each transcription factor remains an important goal to achieve a comprehensive understanding of cellular and organismal systems.  The transcriptional-regulatory network of the fission yeast Schizosaccharomyces pombe consists of approximately 100 sequence-specific DNA-binding transcription factors regulating about 5000 genes in the genome.  Despite being an extensively-studied model organism, its transcriptional-regulatory network remains substantially incomplete.  We have carried out systematic genetics combined with functional genomic approaches such as transcriptomics, genome-wide chromatin immunoprecipitation and synthetic genetic array analysis to functionally characterize S. pombe transcription factors and identify their target genes.  These studies have elucidated a novel transcriptional-regulatory network that governs flocculation, implicated new transcription factors and metabolism genes in cell cycle regulation and estimated the functional redundancy of transcription factor gene pairs in S. pombe.

Dr. Gary Armstrong is Assistant Professor in the Department of Neurology and Neurosurgery at the Montreal Neurological Institute, McGill University. Prior to joining the MNI he was a Post-Doctoral Research Fellow at the Research Centre of the Centre Hospitalier de l’Université de Montréal in the Department of Neurosciences in the laboratory of Pierre Drapeau. His Ph.D. and M.Sc. were completed at Queen’s University in the Department of Biology under the guidance of Dr. Mel Robertson, where he investigated neuronal circuit dysfunction arising during hyperthermia and hypoxia, and the protective mechanisms that preserve neural function during exposure to extreme stress. His current research interests lie in gaining a better understanding of the physiological and molecular mechanisms which culminate in neuronal dysfunction resulting from mutations in genes associated with amyotrophic lateral sclerosis (ALS). Studying this disease requires a model system which can facilitate detailed manipulations of the genes and proteins involved and a nervous system accessible to electrophysiological investigations of neuronal and synaptic activity. The zebrafish larva offers the rare opportunity to combine cutting edge genetic techniques (such as the use of the CRISPR/Cas9 mutagenic system) with in vivo neurophysiological (patch-clamp) recordings of identified neurons, allowing for thorough investigations into the physiological nature of defects arising as a result of mutant protein expression.