Leah and Jason to present at Student Seminar on Thursday (10.June) at noon in 2-501 BSB

Leah and Jason will be presenting Student Seminar this week in 2-501 BSB at noon. I have asked the speakers to provide a brief overview for their talks. Hope to see you there!

Background for Leah’s talk

Mutations in Interferon Regulatory Factor (IRF6, OMIM) cause two orofacial clefting syndromes, Van_der_Woude_syndrome (VWS, OMIM) and Popliteal pterygium syndrome (PPS, OMIM).  In addition to an oral defect, recent data show that VWS patients are more likely to have wound complications after corrective cleft surgery than patients with isolated cleft.  Thus we hypothesize that Irf6 is critical to wound closure.  To test this, we used keratinocytes from Irf6 null mice.  We created in vitro scratches and observed a significant delay in scratch closure.  To determine the cause of delay, we examined the cellular structure of Irf6-/- keratinocytes by staining for filamentous actin and found that these cells have more stress fibers.  In addition, we examined cellular adhesion by staining Irf6-/- keratinocytes for E-cadherin and vinculin. We found that these cells form junctions, but cell-cell contacts appear in an abnormal pattern, and there appear to be more focal adhesions.  Finally, we analyzed proliferation of Irf6-/- keratinocytes and found no deficiency.  Together, our data suggests Irf6-/- keratinocytes exhibit characteristics of less motile cells.  Thus, we speculate that the defect in Irf6-/- keratinocyte scratch closure is due to aberrant migration and/or adhesion, and that cellular proliferation is not inhibitory to closure.  Broadly, these data suggest that Irf6 is necessary for events critical to proper cutaneous wound healing.

Background for Jason’s talk

Leishmaniasis refers to a group of neglected tropical diseases caused by Leishmania species protozoa.  These parasites are delivered to mammals through the bite of a sand fly.  In the Wilson lab, my research interests include (1) developing sensitive qPCR assays for the detection and speciation of Leishmania in human samples and in sand flies collected from endemic sites, (2) determinants of gene expression in the parasite itself, and (3) genes associated with human susceptibility to leishmaniasis.

I will speak about a method and tools I have been developing to study regulatory sequences in the Leishmania genomes.  Leishmania express their genome in polycistronic transcripts, which are the processed into individual messages and regulated post-transcriptionally.  I am using the Leishmania genomes in a top-down bioinformatics approach to automatically identify, classify, and functionally annotate cis-regulatory sequences involved in post-transcriptional regulation.

I also will discuss our research in the genetics underlying host susceptibility and resistance to the visceral form of leishmaniasis.  Following up on a family-based genome-wide linkage scan of a population in Brazil, a fine mapping analysis was conducted.  We are analyzing this fine mapping data to better define regions of the human genome in linkage disequilibrium with susceptibility or resistance to visceral leishmaniasis.


Posted on June 7, 2010, in Student Seminar and tagged , , , , , , , . Bookmark the permalink. Leave a comment.

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