Alissa and Janine to present st Student Seminar Thursday (18.Feb) at noon in 2-501 BSB

Alissa and Janine 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 Alissa’s talk

THE ROLE OF A NOVEL CDC42 EFFECTOR PROTEIN IN XENOPUS DEVELOPMENT AND NEUROGENESIS

Many cellular functions, such as axis determination and cell movement, are dependent on the asymmetrical distribution of proteins and RNAs.  In Xenopus laevis, several maternal mRNAs essential for normal development are localized to the oocyte vegetal cortex, and our lab has used microarrays to identify numerous additional localized RNAs.  In this work we characterize one of these cortex-enriched transcripts, cep4l.  CEP4L belongs to a family of Cdc42 effector proteins (CEPs) that bind Cdc42 and related small GTPases, which can regulate the actin cytoskeleton.  Using in situ hybridization we found that cep4l is expressed in the oocyte vegetal cortex and throughout embryonic development.  The embryonic expression pattern includes migratory cell populations during gastrulation and neurulation, and neural regions in older embryos.  To begin to ascertain the function of cep4l in development we misexpressed cep4l RNA in embryos.  We found that this overexpression causes convergent extension defects, cell disaggregation, and induces ectopic neural and neuronal marker expression, indicating a potential role in neurogenesis.  Structure-function analyses using deletion mutant constructs show a role for the CRIB domain, a conserved GTPase binding domain.  We also present loss of function data showing a role for cep4l in normal axial and nervous system development.  Although the roles of small GTPases in cell migration and adhesion are well-characterized, our results suggest novel roles for these proteins and their effectors in neurogenesis and early development.

Background for Janine’s talk

DYT1 (OMIM) is the most common form of inherited dystonia (OMIM), a disabling neurologically based movement disorder.  This incurable disease is caused by the deletion of a glutamic acid residue in the protein torsinA (torA(ΔE)).  Because this mutation is found in nearly all DYT1 patients and that torA(ΔE) is believed to act in a dominant negative manner over torA(WT), allele-specific silencing of torA(ΔE) may be a potential therapeutic strategy for DYT1.  My research involves developing a viral mediated RNAi therapy and test both its safety and effectiveness in DYT1 murine models.  Optimization of therapeutic vectors and plans for ongoing and future experiments will be discussed.

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Posted on February 15, 2010, in Student Seminar and tagged , , , , , , , . Bookmark the permalink. Leave a comment.

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