Michael Parsons, Ph.D.
Department of Surgery
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Johns Hopkins University
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733 N Broadway
Broadway Research Bldg 469
Baltimore, MD 21205
(410) 502-1853 (fax)
Our laboratory uses the zebrafish as a model system to study the endocrine pancreas, focusing on regulation of cellular differentiation and regeneration of the insulin producing beta cells. We are interested in pancreatic organogenesis at both the level of morphology and the molecular pathways that control differentiation. Much of our work is directed at how the Notch signaling pathway regulates the formation of the hormone producing cells, and in particular beta cells. As zebrafish embryos are opaque, we utilize transgenesis coupled to confocal microscopy to observe cellular behavior in real-time.
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In order to study beta cell regeneration, we have generated transgenic zebrafish that express a fusion protein in this cell type. This fusion protein simultaneously marks the beta cells with red fluorescence and confers susceptibility to a prodrug (metronidazole, Met). Addition of prodrug to the water leads to destruction of the beta cells. Following removal of the prodrug these cells regenerate providing a unique resource in which to study this regenerative process. We are using inducible genetic techniques to identify the progenitors of the new beta cells, and to establish their differentiation capability. Ascertaining the identity and behavior of these progenitors will be beneficial for driving therapeutic strategies to cure type I diabetes, as it will help define the cell types needed to be isolated from donors or grown in culture to use for transplantation.
In addition to identifying cell types responsible for beta cell regeneration, we intend to use our transgenic models in chemical screens to find compounds that increase beta cell production either during organogenesis or following ablation.
Ongoing studies in the lab include the following:
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- Elucidating the regulation of endocrine differentiation
- Characterizing beta cell regeneration in our model of beta cell ablation
- Identifying the progenitors which give rise to new beta cells
- Using genetic inducible systems to cell lineage trace these progenitors
- Carrying out chemical screens to find modifiers of both beta production and increased regeneration
- Davison J, et al. Transactivation from Gal4-VP16 transgenic insertions for tissue-specific cell labelling and ablation in zebrafish. Developmental Biology 304,811-824, 2007
- Pisharath H, et al. Targeted ablation of beta cells in the embryonic zebrafish pancreas using E.coli nitroreductase. Mechanisms of Development 124, 218-227, 2007
- Pollard S, et al. Redundant Roles for Laminin a1 and a4 in Notochord and Blood Vessel Formation. Developmental Biology 289, 64-76, 2006
- Coutinho P, et al. Differential Requirements for COPI Transport during Vertebrate Early Development. Developmental Cell 7, 547-558, 2004
- Feldman B, et al. Lefty antagonism of Squint is essential for normal gastrulation. Current Biology 12, 2129-2135, 2002
- Parsons M, et al. Zebrafish Mutants Identify an Essential Role for Laminins in Notochord Formation. Development 129, 3137-3146, 2002
- Parsons M, et al. Removal of dystroglycan causes severe muscular dystrophy in zebrafish embryos. Development 129, 3505-3512, 2002