Stephanie H Nowotarski

Stephanie H Nowotarski, B.S.

(Ph.D. in progress)
  • Position:
    Graduate student

    Biology

    University of North Carolina at Chapel Hill (Chapel Hill, NC)

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  • Advisor:

    Mark Peifer

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  • Degrees:
     
    Ph.D. (in progress), Biology , University of North Carolina at Chapel Hill (Chapel Hill, NC)
     
    B.S., Genetic Engineering, Cedar Crest College (Allentown, PA)
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  • Past Advisors:
     
    Cristen Rosch (as Undergraduate Student)
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  • Research:
    Determining Enabled's role in regulating the actin cytoskeleton in Drosophila development

    How fully assembled organisms arise from one cell is a fascinating process. In order for a single cell to give rise to a human, or a fly- it must divide and subsequent cells must be able to differentiate, communicate and coordinate cell adhesion to indivdual cells shape change to produce morphogenetic movements. This coordination of cell adhesion and the actin cytoskeleton is not only important in morphogenesis, but oogenesis, wound healing and homeostasis of adult tissue. Adherens junctions mediate cell adhesion and provide a link to the actin cytoskeleton. Enabled (Ena), an actin regulator in Drosophila and has 3 mammalian homologs. Ena localizes to adherens junctions, promotes the formation of long unbranched actin and may function in actin bundling. Previous work has shown that while Ena is not required for cell adhesion, it does play a role in a subset of morphogenetic processes such as germband extension and head involution. Work in cell culture and the bacterium Listeria has shown that the EVH2 domain is sufficient for motility and anticapping function. Also the EVH1 domain is required for localization to sites of active actin turnover, while a proline rich region is known to bind profilin and Abelson Kinase ( a known negative regulator of Ena). This data suggests that different Ena domains are responsible for different morphogenetic processes in Drosophila and that a protein structure function is required for dissecting Ena's biological role in normal development. I am currently assembling transgenes in different domains of Ena to identify which processes are rescued in a maternal and zygotic background in order to understand how each biological process works based on the subset of Ena mutants that affect it.

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  • Other Experience:

    2008-2009 Cell and Molecular Biology Training Grant (NIH)

Life Sciences
Communities:

Stephanie Nowotarski's Genealogy

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Stephanie Nowotarski's Publications (2)



Stephanie Nowotarski's Posters and Presentations (2)

  • Roles of Ena/VASP and Capping Protein in Drosophila Development (poster)

    S. Nowotarski1, R. Banerjee1, J. Gates3, M. Peifer1,2

    ASCB 2009; 12/2009
  • Ena's Role in Regulating the Actin Cytoskeleton in Drosophila Development (poster)

    Stephanie H Nowotarski, Julie Gates PhD, Mark Peifer PhD

    49th Annual Drosophila Research Conference; 04/2008

One Figure

One Figure for Stephanie H Nowotarski

Loss of Capping Protein from Drosophila somatic follicle cells leads to elevated F-actin. GFP negative cells are cpa clones.



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