I 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.