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Poster Full Abstracts - Neural Development
Poster board number is above title. The first author is the presenter
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peristaltic contraction of the body wall musculature. Immunostaining of the axons of the longitudinal segmental nerves identify focal swellings and
accumulations of transported components, reduced density of microtubules, and altered axonal morphology. Despite this neurological dysfunction, a small
percentage of stai mutants survive to the adult stage but exhibit severe movement defects, often dragging their hind limbs as they walk. In addition, viable
adult stai mutants have a significantly reduced lifespan. Unexpectedly, adult stai mutants also exhibit a progressive, age-dependent seizure phenotype
characteristic of the class of 'bang-sensitive' mutants that have altered neuronal excitability. We demonstrate directly that all observed phenotypes are due to
loss of stai function. First, mobilization of a mutagenic transposable element in one of the mutant stai alleles reverts all phenotypes to wildtype. Second,
genetic rescue of the phenotypes by introduction of an exogenous copy of a Drosophila stai transgene ameliorates all observed phenotypes. Interestingly, we
are also able to rescue the observed phenotypes in our Drosophila stai mutants with an exogenous copy of the human stathmin gene STMN1, indicating that
the Drosophila and human stathmin proteins are functional homologues. Collectively, our data identifies a novel, evolutionarily conserved role for stai in the
regulation of microtubule-based axonal transport.
685A
The T-box transcription factor
midline
collaborates with the insulin-regulated
dFOXO
transcription factor to regulate cell-fate specification in the
developing eye of
Drosophila melanogaster
.
Sudeshna Das
1
, Deepak Kumar
1
, Yan Zong
2
, Brandon Drescher
1
, Sarah Morgan
2
, Sandra Leal
1
. 1) Biological
Sciences, University Of Southern Mississippi, Hattiesburg, MS; 2) School of Polymers and High Performance Materials, University of Southern Mississippi,
Hattiesburg, MS.
The
Drosophila midline
(
mid
) gene encodes a highly conserved invertebrate ortholog of the mammalian Tbx20 transcription factor gene family and
regulates critical aspects of embryonic central nervous system (CNS) development. Embryos homozygous mutant for
mid
exhibit severe CNS defects due to
the misspecification of neuronal subtypes and axon guidance defects within the ventral nerve cord (VNC). To understand the molecular-genetic mechanisms
by which
mid
regulates neuronal specification and axon guidance, it is essential to decode the complex
mid
transcriptional networks that mediate these
functionally integrated processes. For this reason, we are using the
Drosophila
eye as a practical model system to combine a classical genetic modifier
screen with both RNA interference (RNAi) and the UAS-Gal4 expression system for the identification of
mid
-interacting genes. We then determine whether
mid
-interacting genes guide the differentiation of neurons within the embryonic CNS. We now report that specifically reducing
mid
expression in the larval
imaginal eye disc using RNAi results in significantly fewer interommatidial bristles within the adult eye. These results suggest that
mid
functions as a cell-
fate determinant during the pupal stage of disc morphogenesis, when specialized accessory cells are recruited to surround an R1-R8 photoreceptor neuron
cluster. Results from the genetic modifier screen also show that
mid
collaborates, either directly or indirectly, with the transcription factor
dFOXO
to
regulate interommatidial formation, placing
mid
downstream of insulin-stimulated signaling pathways that regulate cell growth, metabolism and survival.
We are currently examining whether
dFOXO
also interacts with
mid
to regulate distinct aspects of embryonic CNS development including cell fate
specification and axon guidance.
686B
The SUMO pathway promotes bHLH proneural factor activity via a direct effect on the Zn finger protein, Senseless.
Lynn M. Powell
1
, Yan Chang
Huang
2
, Angela Chen
2
, Andrew P. Jarman
1
. 1) Centre for Integrative Physiology, University of Edinburgh, George Square, Edinburgh, EH8 9XD, United
Kingdom; 2) Institute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan.
During development, proneural transcription factors of the bHLH family are required to commit cells to a neural fate. In
Drosophila
neurogenesis, a key
mechanism promoting sense organ precursor (SOP) selection is the synergy between proneural factors and their coactivator the Zn-finger transcription
factor, Senseless, in transcriptional activation of target genes. We present evidence that post-translational modification by SUMO enhances this synergy via
an effect on Senseless. Our data show that SUMO enhances the ability of Senseless to promote proneural activity in reporter gene assays in S2 cells and to
promote neurogenesis
in vivo
. Western blotting of cell lysates reveals that Senseless is a direct target for SUMO modification. Senseless interacts with Ubc9,
the SUMO-conjugating enzyme, in a yeast 2 hybrid assay, and Senseless and SUMO interact in a relocalisation assay in HeLa cells. Mutagenesis of a
predicted SUMOylation motif in Senseless reduces Senseless/proneural synergy both in cell culture and
in vivo
. We propose that SUMOylation of Senseless
promotes its synergy with proneural proteins during transcriptional activation, and hence regulates an important step in neurogenesis leading to the formation
and maturation of the SOPs.
687C
Tre1 GPCR signaling orients stem cell divisions in the
Drosophila
central nervous system.
Shigeki Yoshiura, Nao Ohta, Fumio Matsuzaki. RIKEN
CDB, Kobe, Hyogo, Japan.
During development, directional cell division is a major mechanism for establishing the orientation of tissue growth.
Drosophila
neuroblasts undergo
asymmetric divisions perpendicular to the overlying epithelium to produce descendant neurons on the opposite side, thereby orienting initial neural tissue
growth. However, the mechanism remains elusive. We provide genetic evidence that extrinsic GPCR signaling determines the orientation of cortical polarity
underlying asymmetric divisions of neuroblasts relative to the epithelium. The GPCR Tre1 activates the G protein oα subunit in neuroblasts by interacting
with the epithelium to recruit Pins, which regulates spindle orientation. Because Pins associates with the Par-complex via Inscuteable, Tre1 consequently
recruits the polarity complex to orthogonally orient the polarity axis to the epithelium. Given the universal role of the Par-complex in cellular polarization,
we propose that the GPCR-Pins system is a comprehensive mechanism controlling tissue polarity by orienting polarized stem cells and their divisions.
688A
Drosophila Neto is essential for clustering of glutamate receptors at neuromuscular junction.
Young-Jun Kim
1
, Hong Bao
2
, Liana Bonanno
1
, Bing
Zhang
2
, Mihaela Serpe
1
. 1) NICHD, NIH, Bethesda, MD; 2) Univ. of Oklahoma, Norman, OK.
Neurotransmitter receptor recruitment at postsynaptic specializations is key in synaptogenesis since this step confers functionality to the nascent synapse.
The Drosophila neuromuscular junction (NMJ) is a glutamatergic synapse, similar in composition and function to mammalian central synapses. Various
mechanisms regulating the extent of postsynaptic ionotropic glutamate receptors (iGluRs) clustering have been described, but none are known to be essential
for the initial localization and clustering of iGluRs at postsynaptic densities (PSDs). We identified and characterized the Drosophila neto (neuropilin and