Abstracts - Society for Developmental Biology
Abstracts - Society for Developmental Biology
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