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Abstracts - Society for Developmental Biology

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cranial neural crest cells, as they differentiate readily in culture to <strong>for</strong>m clusters of collagen I-positive cells. Other types of<br />

neural crest derivates (neurons, melanocytes) are not observed. These data support our hypothesis that the plastron of the<br />

turtle is <strong>for</strong>med by a late emerging population of neural crest cells that collect dorsally in the carapace, migrate ventrally to<br />

the plastron, and undergo intramembranous ossification.<br />

Program/Abstract # 216<br />

Raising the shield: the origin and loss of periodic patterning in the turtle shell<br />

Moustakas, Jacqueline, University of Helsinki, Helsinki, Finland; Cebra-Thomas, Judith (Millersville University,<br />

Millersville, United States); Mitchell, Katherine (Swarthmore College, Swarthmore, United States); Jernvall, Jukka<br />

(University of Helsinki, Helsinki, Finland); Gilbert, Scott F. (Swarthmore College, Swarthmore, United States)<br />

The developmental mechanisms responsible <strong>for</strong> the <strong>for</strong>mation of the turtle shell remain one of the great mysteries in<br />

evolutionary biology. The keratinous scutes of the turtle shell are novel epidermal structures, the patterns of which are<br />

diagnostic of different taxa. Looking at paracrine factors and their inhibitors, we show that scutes develop from placodal<br />

signaling centers that originate in a manner significantly distinct from those of other reptilian and avian ectodermal<br />

appendages. Inhibiting Shh and BMP signaling experimentally results in the loss of these signaling centers and scutes.<br />

Furthermore, we show that the scuteless soft-shelled turtle lacks these placodal signaling centers. We propose that these<br />

signaling centers represent a novel mechanism to develop ectodermal appendages and that the regulation of these centers<br />

have allowed <strong>for</strong> the diversification of turtle shell function.<br />

Program/Abstract # 217<br />

Determining the role of maternal IRF6 in extra-embryonic development<br />

Smith, Arianna; Klavanian, Jeannie; Siegersma, Kendra; Schutte, Brian, Michigan State University, East Lansing, United<br />

States<br />

Defects in trophectoderm differentiation and placental development are associated with a number of common pregnancy<br />

complications, including spontaneous abortion, preterm birth and preeclampsia. In mammals, the cell types that compose<br />

the placenta are derived from the trophectoderm. Interferon regulatory factor 6 (Irf6), a member of the interferon<br />

regulatory factor family of transcription factors, is maternally expressed in zebrafish and Xenopus. Genetic studies in<br />

zebrafish and Xenopus suggest a conserved role <strong>for</strong> maternal Irf6 in development of primary superficial epithelium (PSE).<br />

Inhibition of maternal Irf6 using a putative dominant negative Irf6-DNA binding domain results in embryonic lethality due<br />

to improper differentiation of the PSE. The PSE can be likened to the trophectoderm as they are both simple, monolayer<br />

epithelium that encompass the developing embryo. We hypothesize that maternal Irf6 is expressed in murine oocytes, and<br />

that it is necessary <strong>for</strong> proper differentiation of the trophectoderm in mice. To determine the presence of maternal Irf6 in<br />

oocytes, cross-sections of ovaries collected from wildtype female mice were immuno-stained with an antibody against Irf6.<br />

To determine the function of maternal Irf6 in trophectoderm differentiation, conditional gene knock-out was used.<br />

Specifically, a conditional Irf6 allele along with an oocyte-specific Cre recombinase was used to delete Irf6 in oocytes.<br />

Ovaries collected from females with oocyte-specific deletion of Irf6 were sectioned and stained with hematoxylin and<br />

eosin to assess morphological abnormalities in oocyte development. We observed that Irf6 was highly expressed in murine<br />

oocytes. Irf6 expression could be detected in the ooplasm of developing oocytes. Irf6 was also expressed in the granulosa<br />

cells surrounding the oocyte. Female mice with oocyte specific deletion of Irf6 are born at Mendelian ratios. Preliminary<br />

experiments show no morphological abnormalities in oocytes from mice with oocyte-specific deletion of Irf6 suggesting<br />

that maternal Irf6 is not required <strong>for</strong> oocyte development. The role of Irf6 of trophectoderm has yet to be determined. The<br />

expression data and conserved role <strong>for</strong> maternal Irf6 in zebrafish and Xenopus suggest that maternal Irf6 has a role in the<br />

differentiation of trophectoderm. The findings of this research will provide a novel role <strong>for</strong> Irf6 in development of extraembryonic<br />

tissue. This is research has clinical relevance because 30% of the population carries a DNA variant that alters<br />

IRF6 expression.<br />

Program/Abstract # 218<br />

Is TMED2 essential in the chorion <strong>for</strong> normal interaction between the allantois and the chorion in mice?<br />

Hou, Wenyang (Dominic), McGill University Human Genetics, Montreal, United States; Sarikaya, Didem (Cambridge,<br />

MA, United States)<br />

During vesicular transport between the endoplasmic reticulum and the Golgi, members of the transmembrane emp24<br />

domain (TMED) protein family <strong>for</strong>m hetero-oligomeric complexes that facilitate protein cargo transportation and<br />

secretion. In our laboratory, we are studying the function of one member of the TMED protein family, TMED2, in mouse<br />

placental labyrinth development. Formation of the mouse labyrinth layer requires proper interactions between two<br />

extraembryonic tissues, the allantois and the chorion; and is essential <strong>for</strong> nutrition, waste, as well as hormone exchange

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