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Gregory T. REEVES

Department of Chemical Engineering
Lewis-Sigler Institute for Integrative Genomics
Princeton University
Princeton, NJ 08544
Phone: 609-258-7254
gtreeves@princeton.edu

EDUCATION:

2002-present: Ph.D. candidate in Chemical Engineering

1997-2002 University of Florida, Gainesville, FL

B.S. Chemical Engineering

B.S. Mathematics


PROFESSIONAL EXPERIENCE:

Ph.D Thesis Project (Jun 2003 - present):
Mathematical modeling of pattern formation and quantitative experiments during Drosophila development
Advisor: Dr. Stanislav Y. Shvartsman (Department of Chemical Engineering and Lewis-Sigler Institute of Integrative Genomics, Princeton University)

Undergraduate Research Study (Jan 2000 - Aug 2002):
Non-linear dynamics of continuous-culture microbial growth
Advisor: Dr. Atul Narang (Department of Chemical Engineering, University of Florida)


RESEARCH INTERESTS:

The morphogen gradient patterning model can be applied to tissue patterning many times in development of all animal species. However, despite the prevalence of morphogen gradients in developmental pattern formation, direct in vivo measurements of morphogen concentration profiles are difficult. On the other hand, the general mechanism of gradient formation – localized production, diffusion, and degradation of the chemical signal – is well understood, and formulation of mechanistic models of pattern formation in developing tissues is feasible. Using such models, in conjunction with indirect experimental measurements, we can predict morphogen profiles that we cannot measure directly. I focus on the EGFR-mediated patterning of the Drosophila embryonic ventral ectoderm as a model system. In embryonic St. 9, the ventral ectoderm (VE) is exposed to a morphogen-like gradient in the EGFR ligand Spitz. In response, a negative feedback loop modulates the distribution of Spitz through the inhibitor Argos. Argos, a secreted molecule, and the only known secreted inhibitor of receptor tyrosine kinases, acts by sequestering the EGFR ligand Spitz. I have analyzed a mechanistic model of patterning in the VE, showing that Argos need not be long-ranged in order to account for known genetic data. In our models, Argos action over both long and short length scales can effectively inhibit Spitz-mediated EGFR signaling. Thus, the spatial range of Argos does not have to be tightly regulated or may depend on the developmental context. To determine the spatial range of Argos action, as well as other related parameters such as the spatial range of Spitz and the Argos/Spitz binding strength, I am using the model of EGFR patterning of the VE coupled with quantitative experimental measurements. In particular, I am monitoring the behavior of marker genes in various genetic backgrounds. Fitting the model to such data tightly constrains the model parameters, and predictions regarding the shape of the morphogen and inhibitor profiles can be made. I am currently proposing further experiments to verify this modeling approach. Overall, I hope to show that such approaches, which use quantitative modeling to help answer experimentally inaccessible questions, are feasible and powerful in developmental biology research.

HONORS AND AWARDS:


SELECTED PUBLICATIONS

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