Jeffrey Savas, PhD, a recent NYU GPP graduate is presenting a Thesis Seminar in conjunction with the Proteomics Interest Group.  He invites you to attend this special presentation.   Jeffrey defended on March 13, 2009 at New York University.  Please come and support graduate student research at the NIH. 

Proteomics Interest Group Student Thesis Seminar Announcement

Date: June 8, 2009

Time: 11 am - 12 pm

Location: Building 50, NIH Campus, 1st Floor Auditorium

"Huntington’s disease protein contributes to RNA-mediated gene silencing through association with Argonaute and P bodies/Neuronal granules"

Huntington’s disease (HD) is a dominant autosomal neurodegenerative disorder caused by an expansion of polyglutamines in the Huntingtin (Htt)protein, whose cellular function remains controversial. To gain insight into Htt function, we purified epitope-tagged Htt and identified Argonaute as associated proteins. Colocalization studies demonstrated Htt and Ago2 to be present in P bodies, and depletion of Htt showed compromised RNA-mediated gene silencing. Two sets of HD mouse model cells expressing mutant Htt showed fewer P bodies and reduced reporter gene silencing activity compared with wild-type counterparts. We went on to show that Htt is present in a subset of dendritic RNA granules and interacts/colocalizes with several known dendritic mRNAs. Further, we have shown Htt traffics in live neurons and can cotraffic with Staufen. We believe Htt functions in several pathways linked to post-transcriptional gene silencing and may bridge the miRNA pathway with cytoplasmic polyadenylation through interaction with Argonaute and Symplekin. These data suggest that the previously reported transcriptional deregulation in HD may be attributed in part to mutant Htt’s role in post-transcriptional processes.
 
This Event Will NOT Be Videocast