The course of pathogenic bacterial infection is dependent on the interactions between the
host immune response and the bacterial virulence mechanisms. Our lab previously
discovered that the Survival of Motor Neuron (SMN) protein complex undergoes a change in
subcellular localization during infection with invasive Shigella bacteria, forming novel cytoplasmic aggregates called "U bodies". Similar results were obtained with other intracellular bacterial pathogens suggesting that these U bodies are a fundamental entity in microbial pathogenesis. Notably, the SMN complex normally plays a key role in the assembly of the spliceosomal U snRNA. We have shown during infection that there are changes in U snRNA maturation and splicing patterns. Importantly, we have found that U bodies are downstream of a stress pathway involving the stress-inducible ATF3 protein. Altogether, intracellular bacterial infection induces novel cellular stress pathways that disrupt
normal SMN complex function and leads to changes in U snRNA associated functions.
| Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:OTU.1807/29944 |
| Date | 13 September 2011 |
| Creators | Ling, Arthur |
| Contributors | Girardin, Stephen |
| Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
| Language | en_ca |
| Detected Language | English |
| Type | Thesis |
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