RRM
2010 Rustbelt RNA Meeting
RRM
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Talk abstracts
Abstract:
More than 80% of the population is infected by herpes simplex virus 1 (HSV-1). It is known for causing cold sores and infects mucous membranes, moreover, it can cause severe infections to newborns and immunosuppressed individuals. HSV-1 is an enveloped virus. It has a double stranded DNA genome that codes for more than 80 genes, thus necessitating effective genetic regulation. Viral genes are expressed in a temporal cascade of immediate-early, early and late kinetics. One of the modes of regulation utilized by HSV-1 is alternative polyadenylation: a post-transcriptional event that allows one gene to use two different polyadenylation signals. This process generates transcripts that differ in their 3’ untranslated region (3’UTR), which can affect translation efficiency among other things. One of the HSV-1 genes whose expression is regulated by alternative polyadenylation is UL24. Short UL24 transcripts arise from use of the UL24 polyadenylation signal and are expressed with early kinetics. Long, polycistronic UL24 transcripts arise from use of the UL26 polyadenylation signal, and these transcripts exhibit late kinetics. We hypothesized that the switch from short to long UL24 transcripts is due to changes in levels of polyadenylation factors over the course of infection. To test this hypothesis, we prepared lysates from Vero and HeLa cells at early and late times following infection. Levels of various cellular polyadenylation factors were assessed by Western blotting. We are also using an RNA affinity approach to isolate proteins that interact with the 3’UTRs of the long and short UL24 transcripts. The results from this project will contribute to a better understanding of post-trancriptional regulation during HSV-1 infection.
Keywords: gene regulation, RNA binding proteins, viral gene expression
