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THE MECHANISMS BY WHICH APOPTOTIC NEURONS ARE CLEARED IN DEVELOPING DORSAL ROOT GANGLIA

During development of the nervous system, about half of the neurons generated undergo apoptosis. How these neurons are cleared in the peripheral nervous system was largely unknown. Our lab discovered that clearance in the dorsal root ganglia of mouse embryos was achieved by amateur phagocytes, cells that have other important roles besides phagocytosis. Specifically, the resident glia, satellite glial cell precursors are responsible for engulfing neurons in developing dorsal root ganglia. In addition, we identified the novel receptor Jedi-1, and the purported engulfment receptor MEGF10, as two receptors expressed in the glia that are involved in engulfing apoptotic neurons. Although nothing was known about the signaling mechanisms of Jedi-1 or MEGF10, my dissertation work revealed that both receptors contain two intracellular Immune receptor Tyrosine-based Activation Motifs that are phosphorylated by Src Family Kinases and interact with the non-receptor tyrosine kinase Syk. This interaction was necessary for either receptor to promote phagocytosis. Here, I describe these interactions as well as the importance of apoptotic cell clearance, including possible links to autoimmune disorders.

Identiferoai:union.ndltd.org:VANDERBILT/oai:VANDERBILTETD:etd-09242012-105452
Date01 October 2012
CreatorsScheib, Jami Lynn
ContributorsDonna Webb, Bruce Carter, Graham Carpenter, William Valentine
PublisherVANDERBILT
Source SetsVanderbilt University Theses
LanguageEnglish
Detected LanguageEnglish
Typetext
Formatapplication/pdf
Sourcehttp://etd.library.vanderbilt.edu/available/etd-09242012-105452/
Rightsunrestricted, I hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to Vanderbilt University or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report.

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