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Poster Full Abstracts - Neural Development
Poster board number is above title. The first author is the presenter
308
Biology, Univ North Carolina, Chapel Hill, Chapel Hill, NC; 2) Dept. of Biochemistry and Biophysics, Univ North Carolina, Chapel Hill, Chapel Hill, NC.
The generation of cellular diversity in the central nervous system (CNS) is a critical process in the development of complex metazoans. The CNS midline
of
Drosophila
is a segmentally repeated cluster of ~20 interneurons, motoneurons, and glia. With well-defined lineages and a common origin from the
mesectoderm, these cells provide an isolated system that facilitates studying the establishment of this diversity. Using fluorescence-activated cell sorting
(FACS), we have purified embryonic CNS-midline cells at two developmental time-points and performed RNA-seq to study gene expression. A comparison
with information on our lab’s publicly available database of midline expressed genes, MidExDB, revealed a 100% correlation between the RNA-seq data
and the 77 genes previously examined via confocal microscopy. Additional validation of the data using fluorescent in situ hybridization also indicates an
accurate representation of gene expression. Data analyses have led to the discovery that 8 neuropeptide precursor genes and 12 neuropeptide receptor genes
produce expression in subsets of CNS-midline cells, including the glia. The characterization of this gene expression has provided an increased understanding
of both the segmental variation and cellular diversity that exists in these cells. One example of this is
Myoinhibiting peptide precursor
(
Mip
) which only
shows CNS midline expression in a single cell of segments S1 and S3. As an initial step in characterizing the transcriptional programs involved in setting up
this diversity, we find
short neuropeptide F precursor
(
sNPF
) expression in ventral unpaired median interneuron 5 (iVUM5) to be downstream of the
transcription factor Castor. Future work will involve identifying additional factors responsible for the regulation of these neural function genes, as well as
analyzing RNA-seq data collected from isolated ventral unpaired median motoneurons (mVUM), a subset of the CNS-midline cells.
661A
Genome-wide expression profiling identifies genes regulated by JAK/STAT in the
Drosophila
optic lobe.
Hong Luo, Hongbin Wang. School of Life
Sciences, Tsinghua University, Beijing, China.
The JAK/STAT pathway is evolutionarily conserved from invertebrates to vertebrates, and plays important roles in animal development and human
disease. Although the signaling pathway has been well established, we know relatively little about what are the relevant target genes that mediate the effects
of JAK/STAT activation. Here, we have used DNA microarrays to identify JAK/STAT targets in the
Drosophila
larval brain and identified 45 genes that are
positively regulated by JAK/STAT; many of these genes contain clustered STAT92E binding sites in short conserved genomic sequences suggesting that
they may be direct target genes. More than two thirds of the genes identified encode proteins that have orthologs in humans. Analyses of
Nop56
, which
encodes a conserved protein involved in ribosome biogenesis and cell growth, reveal an essential role of
Nop56
in optic lobe development, as loss of
Nop56
activity prevented neuroepithelial growth and expansion. RNAi knockdown of
Nop56
in clones of cells caused premature differentiation of neuroepithelial
cells into neuroblast-like cells. Interestingly,
Nop56
knockdown in the lamina precursor cells accelerated lamina neurogenesis while ectopic expression of
Nop56
inhibited lamina neuron differentiation. Thus, Nop56 promotes neuroepithelial cell growth and division and suppresses their differentiation into both
medulla neuroblasts and lamina progenitor cells. These results provide a novel insight into the control of lamina neurogenesis in the
Drosophila
brain.
662B
Identification of novel maternal neurogenic genes that are potential components of Notch signaling in
Drosophila
.
Kenjiroo Matsumoto
1
, Naoki
Aoyama
1
, Takahiro Seto
1
, Ryo Hatori
1
, Akira Ishio
1
, Takahiro Maeda
1
, Tamiko Itou
1
, Syusuke Shimaoka
1
, Hironao Iida
1
, Takuma Gushiken
1
, Yuu Atsumi
1
,
Tomoko Yamakawa
1
, Takeshi Sasamura
1
, Kenji Matsuno
1,2
. 1) Dept. Biol. Sci./Tec., Tokyo Univ of Science; 2) Res. Inst. Sci./Tec., Tokyo Univ of Science.
Notch signaling regulates many cell-fate specifications through local cell-cell interaction in
Drosophila
development. Notch signaling is involved in
“lateral inhibition” that prevent proneural cells that neighbor a neuroblast from choosing the neuroblast-fate during neuroblast segregation. Thus, in the
absence of Notch signaling, proneural cells, differentiate into neuroblast at the expense of epidermoblasts. Therefore, the disruption of Notch signaling
results in the hyperplasia of neuronal cells in
Drosophila
embryos, which is referred to as the “neurogenic phenotype”. Because most of the genes that
encode Notch-signaling components are essential for lateral inhibition, these genes were first identified by the neurogenic phenotype resulting from their
disruption. Although mutants that show neurogenic phenotype in their homozygotes have been studied extensively in
Drosophila
, we probably failed to
identify many mutants that potentially lead to neurogenic phenotype, because maternal supply of their gene functions can suppress this phenotype. To
address this problem, we screened for mutants that showed neurogenic phenotype in their homozygous embryos lacking their maternal contribution. This
phenotype is designated as “maternal neurogenic phenotype”, and genes whose mutants show maternal neurogenic phenotype are called maternal neurogenic
genes. We screened the left arm of the second chromosome, which covers about 20% of the
Drosophila
genomes. We identified 5 mutants that showed
maternal neurogenic phenotype. Currently, we are mapping the genetic loci of these mutants. The summary of this screen and molecular genetics analyses of
these maternal neurogenic genes will be presented. Our analyses of these maternal neurogenic genes will contribute to the understanding the molecular
mechanism of Notch signaling.
663C
The Role of Dscam in Dendrite Development of an identified Drosophila Motoneuron.
Katie M Hutchinson, Carsten Duch. Arizona State University,
Interdisciplinary Graduate Program in Neuroscience, Tempe, AZ 85287-4501.
Correct dendritic architecture development requires precise control over various dendritic arborization characterstics in order to ensure that dendrites cover
a specific input territory non-redundantly. We have previously analyzed the complex dendritic tree of an identified adult Drosophila flight motoneuron,
MN5, by means of quantitative geometric dendritic arbor reconstruction. The complex MN5 dendritic trees develop during pupal life, comprise more than
4000 dendritic branches which add to 6500 microns of total dendritic length, and cover a well-defined input territory according to specific rules. First, self
dendrites avoid each other. Further, different sub-trees cover different non-interdigitating areas of the input space (intra-neuronal tiling), which is predicted
to have consequences for the flight motor network and computation of synaptic input. This study aims to unravel the developmental mechanisms underlying
intra-neuronal tiling of complex dendritic fields in the CNS. We hypothesize a combination of activity dependent competition for synaptic partners and
dendritic self-avoidance. Based on findings in sensory dendritic arborization neurons that do not receive input synapses, we propose that Down syndrome
cell adhesion molecule (Dscam) underlies dendritic self-avoidance in central neurons. In fact, targeted expression of UAS-Dscam-RNAi in MN5 causes
increased fine dendrite branching and self-dendrite contacts. Inclusion of extra DICER (UAS-DICER) in MN5 causes a range of phenotypes. The most
severe is a loss of all mature dendrites with only intermingled filopodia. To circumvent unspecific network or RNAi effects we created mutant MN5 in an
otherwise wildtype background by employing the MARCM technique. Preliminary MARCM and RNAi data suggest dual functions for Dscam in adult