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Abstracts - Society for Developmental Biology

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understood. Here, we have established the genetic interactions between prdm1a, ap2a/c, and foxd3, key regulators of<br />

neural plate border and neural crest specification in zebrafish embryos. We have shown that prdm1a acts downstream of<br />

Wnt and Notch signaling and <strong>for</strong>ms regulatory feedback loops with foxd3 and tfap2a/c, where perturbation of any of these<br />

members of the gene cascade influences expression of the others as well as normal development of the neural crest.<br />

Through rescue experiments and chromatin-immuno precipitation (ChIP), we have determined that Prdm1a directly binds<br />

to and regulates a putative enhancer <strong>for</strong> foxd3, an established neural crest specifier, and that foxd3 is a functional direct<br />

target of Prdm1a regulation. Based on these and previous data, we predict that Prdm1a is transcriptional activating foxd3 at<br />

the neural plateborder. Additional data using dominant-activator and dominant-repressor versions of Prdm1a suggest that<br />

Prdm1a functions both as a transcriptional activator and transcriptional repressor during development. By comparing<br />

RNA-seq and ChIP-seq data, we will elucidate the nature of Prdm1a regulation of neural crest specification genes at the<br />

transcriptional level. Through this work, we have demonstrated that prdm1a is an important regulator in the gene network<br />

that is required <strong>for</strong> proper neural crest <strong>for</strong>mation.<br />

Program/Abstract # 253<br />

A characterization of regulatory linkages in a genetic network <strong>for</strong> a derived fruit fly trait.<br />

Butts, John C.; McNamee, Connor, University of Dayton, Dayton, United States; Rebeiz, Mark (University of Pittsburgh,<br />

Pittsburgh, United States); Williams, Thomas (University of Dayton, Dayton, United States)<br />

Phenotypes are the culmination of spatial and temporal patterns of gene expression of genes comprising a genetic network.<br />

These patterns are controlled by cis-regulatory elements (CREs) and genes are connected into networks when a CRE<br />

regulating its expression possesses binding sites <strong>for</strong> network transcription factor proteins - so called regulatory linkages.<br />

Gains and losses of linkages are a suspected common route of CRE and network evolution; though, their emergence<br />

remains poorly understood as few case have revealed the be<strong>for</strong>e and after states in sufficient detail. The male-specific<br />

abdominal pigmentation of Drosophila melanogaster evolved from a monomorphic ancestral state, a key modification to<br />

the pigmentation network being the evolution of sexually dimorphic expression of the Bab transcription factor proteins.<br />

These proteins turn off expression of the yellow and tan genes that are required <strong>for</strong> pigmentation. The research presented<br />

here addresses two questions. First, does Bab <strong>for</strong>m direct regulatory linkages with CREs that control the male-specific<br />

expression of the Drosophila melanogaster yellow and tan genes? Second, when historically were these CREs and the<br />

irregulatory linkages gained? To answer these questions we are: systematically mutating CRE sequences to find motifs<br />

needed to integrate the repressive effects of Bab, and evaluating the regulatory activities of sequences related to the<br />

Drosophila melanogaster CREs. Future studies will explore whether this divergence included the gain of Bab binding sites<br />

in dimorphic species or whether these binding sites were ancestral and conserved during trait evolution.<br />

Program/Abstract # 254<br />

Inspecting the regulatory architecture of a toolkit gene locus governing trait development and evolution<br />

Camino, Eric; Francis, Kaitlyn; Velky, Jordan; Williams, Thomas, University of Dayton, Dayton, United States<br />

Complex spatial and temporal patterns of gene expression are crucial to animal development and changes in expression<br />

patterns are a common mode of evolutionary innovation. Thus, understanding development requires answering: (1) what<br />

are the DNA elements, so called CREs, controlling expression, (2) how the DNA sequences of CREs encode gene<br />

regulatory capabilities, (3) whether and how CREs work together to make complex expression patterns, and (4) how CRE<br />

sequences identify their gene target(s) of regulation in a 3-dimensional nucleus? These answers will aid studies to reveal<br />

the mechanisms of gene expression, and thus animal, evolution. A model to address these questionsis the bab locus of fruit<br />

flies. This locus contains the duplicate bab1 and bab2 genes that shape a derived pattern of pigmentation in the species<br />

Drosophila melanogaster. The relevant bab expression pattern is controlled by two CREs which we found to interact in a<br />

non-additive, or synergistic, way to yield this pattern. Ongoing studies seek to trace: when and how CRE synergism<br />

evolved, which CRE sequences encode their synergistic activity, how these CREs interact with the bab gene promoters,<br />

and whether synergistic regulation extends to additional gene loci. Ultimately, this work aims to connect how animal <strong>for</strong>m<br />

is programmed into 1-dimensional DNA sequence and how this program evolves.<br />

Program/Abstract # 255<br />

Fbxo16 mediated protein degradation regulates neurogenesis in Xenopus laevis<br />

Saritas-Yildirim, Banu; Casey, Elena Silva, Georgetown University, Washington, DC, United States<br />

The development of the central nervous system is a dynamic process during which protein levels are regulated temporally<br />

and spatially by synthesis and degradation. While much is known about the regulation of gene expression during<br />

development, little is known about the control of protein degradation. Studies of cell cycle regulation show that a major<br />

mechanism of protein degradation is through F-box ubiquitin ligases, which function in the recognition and recruitment of

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