Dr. Ronald Podesta
Signalling Mechanisms of Human Blood Flukes & Trypanosomes
Office: BGS 3070
Office phone: 519 661-2111 x 81203
Fax: 519 661-3935
Our research on the tropical disease caused by Schistosome blood flukes stems from our results indicating that the parasites are capable of avoiding being killed by the host's immune system by rapidly renewing their surface membranes. This process is accelerated in response to signals emanating from the host's immune response (serotonin and the 3rd component of the host's complement). We have identified surface membrane receptors, second messenger systems, protein kinases/phosphatases, and phosphorylation cascades associated with the signalling systems. We continue to clone schistosome genes encoding various components of the signalling pathways for the purpose of developing vaccines. We are expressing schistosome genes in mammalian/insect cell lines and Vaccinia viruses. This work also involves evaluation of the protective immune responses.
Unlike most eucaryotic systems, regulation of gene expression in these parasites occurs predominantly at the post-transcriptional level. We suggest that this was an adaptation to the requirement for rapid protein synthesis in response to new environments encountered during parasite life cycles. We also demonstrated that the immune system of the host was capable of inhibiting the post-transcriptional mechanisms responsible for the regulation of gene expression in these parasites. This work involves determining quantitative shifts of mRNA species among mRNPs and polysomal/nonpolysomal RNA using our cDNA probes and the trans-splicing machinery in schistosomes.
We are also undertaking studies on the surface signalling mechanisms in Trypanosoma brucei (agents of African sleeping sickness) that are modelled on similar studies conducted on schistosomes. The purpose of our experiments is to determine the signalling pathways accompanying the trypanosomes switch from one antigenic type to another.
This page was last updated on
January 30, 2008
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