Abstracts - Society for Developmental Biology

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guttifera fly. We will use the in situ hybridization technique to identify candidate regulators that govern the complex
yellow expression pattern.
Program/Abstract # 212
A potential patterning difference underlying the oviparous and viviparous development in the pea aphid
Bickel, Ryan, University of Nebraska, Lincoln, Lincoln, United States; Cleveland, Hillary; Barkas, Joanna; Belletier,
Nicollette; Davis, Gregory K., Bryn Mawr College Dept of Biology, Bryn Mawr, United States
The pea aphid, Acyrthosiphon pisum, exhibits several environmentally cued, discrete, alternate phenotypes (polyphenisms)
during its life cycle. In the case of the reproductive polyphenism, differences in day length determine whether mothers will
produce daughters that reproduce either sexually by laying fertilized eggs (oviparous sexual reproduction), or asexually by
allowing oocytes to complete embryogenesis within the mother without fertilization (viviparous parthenogenesis). Oocytes
and embryos that are produced asexually develop more rapidly, are yolk-free, and much smaller than oocytes and embryos
that are produced sexually. Perhaps most striking, the process of oocyte differentiation is truncated in the case of
asexual/viviparous development, potentially precluding interactions between the oocyte and surrounding follicle cells that
might take place during sexual/oviparous development. Given the important patterning roles that oocyte-follicle cell
interactions play in Drosophila, these overt differences suggest that there may be underlying differences in the molecular
mechanisms of pattern formation. Our preliminary work comparing the expression of homologs of torso-like and tailless,
as well as activated MAP kinase, suggests that there are important differences in the hemipteran version of the terminal
patterning system between viviparous and oviparous development. Establishing such differences in the expression of
patterning genes between these developmental modes is a first step toward understanding how a single genome manages to
direct patterning events in such different embryological contexts.
Program/Abstract # 214
Key regulator for developmental and evolutionary switch from Rohon-Beard cells to dorsal root ganglia
Yajima, Hiroshi, , Shimotsuke, Japan; Suzuki, Makoto (Okazaki, Japan); Ochi, Haruki (Ikoma, Japan); Ikeda, Keiko;
Sato, Shigeru (Shimotsuke, Japan); Ogino, Hajime (Ikoma, Japan); Ueno, Naoto (Okazaki, Japan); Kawakami, Kiyoshi
(Shimotsuke, Japan)
In the body of adult vertebrates, dorsal root ganglia (DRG) convey a variety of sensory modalities to the central nervous
system. However, during fish and amphibian development, intramedullary sensory neurons, Rohon-Beard (RB) cells, are
responsible for juvenile mechanosensation. As DRG start to process mechanosensory inputs, RB cells undergo cell death
by apoptosis. In Xenopus RB cells, the first expression of Six1 appears right before the onset of cell death, eliciting the
idea that Six1 mediates the developmental switch from RB cells to DRG. Indeed, forced expression of Six1 in early
Xenopus embryo resulted in precocious switching from RB cells to DRG, on the contrary, knockdown of Six1 prevented
the switching. Furthermore, genetic ablation of both Six1 and Six4 caused the emergence of RB-like cells in mice. These
results allow us to hypothesize that the precocious expression of Six1 in mouse sensory neuron development leads to the
disappearance of RB cells and investigate the molecular mechanism defining the onset of Six1 expression. Expression of
Six1 in mouse DRG was mediated by one of conserved Six1 enhancers. Xenopus orthologous enhancer activated
transcription when the endogenous Six1 expression is turned on in Xenopus RB cells. However, the mouse enhancer
activated transcription in RB cells earlier than the Xenopus element, indicating that the heterochronic shift of Six1
expression is caused by alteration of a single enhancer. Taken together, our findings suggest that the difference in the
architecture of primary sensory neurons is caused by the change of cis-regulatory element and that the precocious
expression of Six1 is a key process that facilitates the phylogenetic disappearance of RB cells in amniotes.
Program/Abstract # 215
Characterization of the bone-forming cells of the turtle plastron
Cebra-Thomas, Judith A.; Mangat, Gulnar; Branyan, Kayla; Shah, Sonal, Millersville University, Millersville, United
States; Gilbert, Scott (Swarthmore College, Swarthmore, United States)
Turtle plastron bones develop by intramembranous ossification, suggesting that they are derived, like the facial bones,
from neural crest cells. We have previously shown that a wave of cells expressing neural crest markers emerges from the
neural tube later than in comparably staged chick or mouse embryos, and appears to migrate ventrally to populate the
plastron dermis. This second, later wave of HNK1+ cells can also be observed migrating away from cultured neural tubes
from St.17 embryos. These late emerging neural crest cells also express PDGFRα, which is typically expressed by cranial
neural crest cells. We have examined the expression pattern of plastron mesenchyme cells by antibody staining and gene
expression analysis, and their potential for differentiation by in vitro culture. Plastron mesenchyme cells have a gene
expression pattern similar to cranial skeletogenic neural crest cells. They also appear to have functional similarities to