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dc.contributor.authorSmith, Jacob Matthew
dc.date.accessioned2014-05-28T15:47:48Z
dc.date.available2014-05-28T15:47:48Z
dc.date.issued2014
dc.identifier.urihttp://hdl.handle.net/10713/4066
dc.descriptionUniversity of Maryland, Baltimore. Neuroscience. Ph.D. 2014en_US
dc.description.abstractI study the role of Met, the hepatocyte growth factor receptor, in the development of the cerebral cortex using a conditional mutant mouse line. This line expresses a kinase-dead Met in the Emx1 lineage of the cerebral cortex and hippocampus. Loss of Met signaling in the Emx1 lineage leads to a number of anatomical changes in adult, but not juvenile mice, including increased size of the frontal cortex and corpus callosum. Expansion of the cortex in these mice appears to be due to an increase in cortical surface area, rather than thickness. Histological examination of the cortex in Met mutants revealed that the cortex is actually thinner at the level of the cortical barrel fields. Subsequent analysis of layer morphology showed that this decrease was mostly due to a reduction in the thickness of layer II/III, with no change in deep layer morphology. Furthermore, some cells expressing Cux1 - a marker of superficial layers - were found in ectopically deep layers in Met mutants, suggesting a possible mechanism for the reduction of layer II/III. These findings have prompted an examination of cortical progenitor proliferation by bromodeoxyuridine birth-dating. Results from these studies indicate that Met plays a role in regulating proliferation in cortical progenitors, and that this role may be temporally restricted.en_US
dc.language.isoen_USen_US
dc.subjectHGFen_US
dc.subjectmeten_US
dc.subject.meshAutistic Disorderen_US
dc.subject.meshCerebral Cortexen_US
dc.subject.meshMiceen_US
dc.titleRole of the Autism-Associated Met Tyrosine Kinase Receptor in Cerebral Cortical Developmenten_US
dc.typedissertationen_US
dc.contributor.advisorPowell, Elizabeth M. (Elizabeth Mary)
refterms.dateFOA2019-02-19T17:39:11Z


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