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Date: | Mon, 7 Jan 2013 10:40:12 -0500 |
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Thesis Defense Announcement
To: The George Mason University Community
*Candidate: Farheen Shaikh
Program: Master of Science in Biology
*
*Date: Tuesday January 8, 2013
Time: 11:00 a.m.
Place: George Mason University,
Fairfax Campus
Krasnow Institute, Room 229
*
*Title: *"The Evolutionary Conserved LIM Homeobox Transcription Factor
CG4328 Is Required for Dendritic Morphogenesis and Tiling in Drosophila
Sensory Neurons"**
*Thesis Director*: Dr. Daniel N. Cox**
*Thesis Committee*: Dr. Geraldine M. Grant and Dr. Alan Christensen
*ABSTRACT *
Nail Patella Syndrome (NPS) is an autosomal dominant disorder,
characterized by nail malformations, patellar defects, glomerulopathy,
glaucoma, and a host of neurological disorders. Apart from the
aforementioned conditions, NPS is also responsible for affecting
multiple areas of the body. At the molecular level, NPS affects the
formation of certain proteins. Of particular importance is the product
of the human /Lmx1b /gene, which is a causative agent in the development
of this rare autosomal dominant disease. We have previously conducted a
large-scale /in vivo /RNAi screen to characterize the role of
transcription factors in mediating class-specific dendrite morphogenesis
using the /Drosophila /dendritic arborization (da) sensory neurons as a
model system. From this screen, we identified the gene /CG4328 /which
encodes a LIM homeodomain transcription factor that is the fly homolog
of the human /Lmx1b/. RNAi-mediated knockdown of /CG4328 /produced
significant defects in dendrite morphogenesis and dendritic tiling.
Based upon these preliminary observations, we performed systematic
loss-of-function and gain-of-function phenotypic analyses of /CG4328
/function in mediating da neuron dendrite development and tiling.
Quantitative analysis reveals that absolute levels of /CG4328/ are
required for proper dendritic morphogenesis. Altered levels of this
transcription factor lead to significant reductions in class specific
dendritic arbor complexity suggesting that /CG4328 /plays an essential
role in mediating dendritic homeostasis. Moreover, gene expression
analyses reveal a reduction in expression of genes /cut/, /cubitus
interruptus /(/ci/) and /elav/ when /CG4328/ levels are altered. The
results of these analyses indicate that this gene might be involved in
/hedgehog/ (/hh/) and/or /wingless/ (/wg/) signaling pathways. Further
analysis may provide novel insight into the mechanisms by which this
gene, and potentially its human homolog, function to generate the
neurological defects observed in patients with NPS as, to date, the
basis for these neurological abnormalities remain poorly understood.
A copy of the thesis will be available in the Johnson Center Library.
All are invited to attend.
*
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