Grant: Doctoral Award - Frederick Banting and Charles Best Canada Graduate Scholarships

The proper development and healthy functioning of the gastrointestinal tract and immune system in humans and other organisms depends on their association with symbiotic microorganisms. However, the molecular recognition mechanisms used to establish such relationships and differentiate symbiotic microbes from disease-causing pathogens are not well understood. Sponges are the most ancient group of extant animals that host vast and complex microbial communites. Therefore, sponge-microbial symbioses represent some of the oldest associations between animals and microorganisms, thus serving as useful model systems to explore symbiotic interactions. The first sponge-archaeal association described is the symbiosis between the sponge Axinella mexicana and its symbiont, Cenarchaeum symbiosum. The symbiont genome encodes for proteins potentially involved in mediating symbiosis, including five serpins, a protein family present in viruses and all domains of life implicated in a variety of functions including cell signaling and hormone transport. C. symbiosum serpins may be important in mediating this symbiosis by modulating the sponge immune response. The goal of this study is to identify the mechanisms underlying the A.mexicana-C. symbiosum relationship for cell signaling such that the symbiont does not elicit a host innate immune response without impairing the ability of the host to respond to pathogens and infections. Cultivation-independent approaches will be used to identify serpin targets and the host molecules involved in innate immune signaling. The results of this research will provide insight into evolutionarily-conserved pathways used in immune recognition with the possibility to discover novel, as yet-unknown mechanisms of cellular communication. Comparative analysis between sponge, insect and mammalian signaling pathways will shed light on how organisms, including humans, interact with and benefit from their microbial symbionts.