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Poster Full Abstracts - Pattern Formation
Poster board number is above title. The first author is the presenter
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regulators, D-cbl, which functions as an E3 ubiquitin ligase for EGFR, and Gap1, which promotes the inactivation of Ras. Through clonal analysis we show
that loss of D-cbl in follicle cells results in expansion of dorsal fates onto the ventral side of the follicular epithelium. Additionally, these clones display a
shortening of dorsal fates along the AP axis reminiscent of the sty phenotype. Through the same analysis we show that loss of Gap1 results in the expansion
of dorsal fates ventrally but fails to display any shortening of dorsal fates along the AP axis, possibly suggesting that the function of Gap1 is distinct from
that of D-cbl and Sty. We also looked at the regulation of a downstream transcription factor, Capicua, as a more direct readout of EGFR activity.
Interestingly, the pattern of EGFR-mediated changes in Capicua localization is expanded in D-cbl and Gap1 mutant clones along both the AP and DV axes.
This AP expansion is inconsistent with the observed decrease in dorsal fates in this dimension. This discrepancy is currently being explored.
697A
Pattern formation by graded and uniform signals: gene regulation by Dorsal and Zelda in the
Drosophila
embryo.
Bomyi Lim
1
, Jitendra S. Kanodia
1
,
Hsiao-Lan Liang
2
, Yoosik Kim
1
, Mei Zhan
3
, Hang Lu
3
, Christine A. Rushlow
2
, Stanislav Y. Shvartsman
1
. 1) Department of Chemical and Biological
Engineering and Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ 08544; 2) Center for Developmental Genetics,
Department of Biology, New York University, New York City, NY 10003; 3) School of Chemical and Biomolecular Engineering and Parker H. Petit
Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, GA 30332.
Graded distributions of maternal transcription factors in the early
Drosophila
embryo provide some of the best understood examples of morphogen
gradients. Recent studies revealed that multiple aspects of pattern formation by these gradients depend on uniformly expressed transcriptional activators,
such as Zelda. Removal of Zelda influences both the timing and the spatial expression patterns for most of the transcriptional targets of maternal
morphogens. We demonstrate that some of these patterning defects, which range from temporal delay to loss of expression, can be rationalized using a
mathematical model based on cooperative binding of graded and uniform factors. This model makes testable predictions and suggests an alternative
mechanism by which morphogen gradients can establish nested gene expression domains.
698B
Bonus is required maternally for dorsal-ventral pattern formation.
Stuart Newfeld, Janine Quijano, Estela Arciniega, Nancy Tran, Ashley Castillo,
Michael Stinchfield. Sch Life Sci, Arizona State Univ, Tempe, AZ. 85287-4501.
The discovery that a zygotic extracellular signaling system utilizing the secreted morphogens Dpp and Sog regulates dorsal-ventral axis formation across
species was a major advance in our understanding of developmental biology. Recent data from our lab suggests that a conserved maternal intracellular
system based on ubiquitination and deubiquitination of the Dpp signal transducer Medea is operating in parallel during this process. Experimental data
utilizing mutations in the Fat facets deubiquitinase revealed that these two systems are equally important since the zygotic system cannot function without
the maternal system. In an attempt to identify the Medea ubiquitin ligase that functions opposite to Fat Facets in dorsal-ventral patterning we analyzed two
candidates: Bonus and Highwire. Bonus is the most closely related fly protein to the family of vertebrate Tif1 proteins, of which Tif1gamma is the Smad4
(Medea homolog) ubiquitin ligase that operates opposite USP9X (Fat facets homolog) in Xenopus dorsal-ventral patterning. Bonus has not been previously
connected to Dpp signaling in flies but has been shown to function as a chromatin modifier. Highwire is a known antagonist of Medea activity at the larval
neuro-muscular junction but has not been shown to have any vital roles during embryonic development. Here we report that neither Highwire nor Bonus are
the sought after ubiquitin ligase for Medea. We found instead that Bonus is required maternally for dorsal-ventral patterning upstream of Dpp via
participation in the Dorsal signaling pathway.
699C
defective proventriculus
(
dve
), a new member of DV patterning in the eye.
Oorvashi Roy G. Puli
1
, Takeshi Yorimitsu
3
, Hideki Nakagoshi
3
, Amit
Singh
1,2,4
. 1) Department of Biology, University of Dayton, 300 College Park Drive, Dayton, OH; 2) Premedical Program, University of Dayton, 300 College
Park Drive, Dayton, OH; 3) School of Natural Science and Technology, Okayama University, 3-1-1 Tsushima-naka, Kita-ku, Okayama 700-8530, Japan; 4)
Center for Tissue Regeneration and Engineering at Dayton (TREND), University of Dayton, Dayton, OH.
Axial patterning is crucial to eye development. During eye development, Dorso-ventral (DV) axis determination is the first lineage restriction event. The
early eye primordium begins with the default ventral fate on which the dorsal eye fate is established by expression of a GATA-1 transcription factor,
pannier
(
pnr
). Loss-of-Function (LOF) of
pnr
results in dorsal eye enlargements and antennal duplications in adult flies. We found similar phenotypes in LOF of
defective proventriculus
(
dve
), which encodes a homeobox protein. We investigated if
dve
plays a role in axial patterning during early eye development. We
found that Gain-of-Function (GOF) of
dve
results in suppression of eye by downregulating Retinal Determination (RD) genes. We found that
dve
plays an
important role in dorsal eye fate selection during early eye development. In the eye imaginal disc, Dve expression is restricted to a small region anterior to
the Morphogenetic Furrow (MF) on the dorsal eye margin. This expression domain of Dve also overlaps with Wingless (Wg), which is expressed at the
lateral margins of the developing third instar eye discs. Interestingly, we found that
dve
is required to maintain a Wg morphogen gradient in the developing
Drosophila
eye field to promote DV patterning of the
Drosophila
eye. Here we present insights into the novel role of
dve
in dorsal eye fate selection in the
Drosophila
eye.
700A
Specification of Drosophila corpora cardiaca neuroendocrine cells by Daughterless homodimer.
Sangbin Park
1
, Seung K Kim
1,2
. 1) Developmental
Biology, Stanford University, Stanford, CA; 2) HHMI.
Many human diseases result from excessive or inadequate endocrine cell mass or function. Thus, there is intense interest in identifying evolutionarily-
conserved transcriptional codes for neuroendocrine cell development and expansion. Drosophila neuroendocrine cells comprising the corpora cardiaca are
essential for systemic glucose regulation and represent functional orthologues of vertebrate pancreatic α-cells. Our previous study identified a unique cell
signaling context in mesoderm where neuroendocrine precursor cells can be specified by two transcription factors; Tinman and Daughterless. Here, we show
that Daughterless homodimer alone can induce ectopic neuroendocrine cells in dorsal trunk mesoderm where cardiac mesoderm is specified, suggesting
Daughterless homodimer may convert cardiac precursors to neuroendocrine cells. We speculate the Daughterless homodimers compete with Twist to specify
neuroendocrine cell fate in dorsal trunk mesoderm where Tinman expression is high. Using gain and loss of function alleles of EGFR, we also show that the