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Schizophrenia is a devastating brain disorder that affects a surprising 1% of the world's population. Despite this prevalence, little is known about the molecular aspects of this disorder making it both difficult to diagnose and treat. Several studies have identified the CHL1 gene (Close Homolog of L1), sometimes referred to as CALL, as a risk gene for schizophrenia. CHL1, a neural cell adhesion molecule, has major roles in cell migration, and the development of dendritic and axonal projections. Therefore any deficiency in CHL1 may result in brain defects similar to those identified in schizophrenic populations. Moreover, in genetically engineered mice, studies have shown that deficiency of the CHL1 gene results in altered emotional reactivity (such as altered fear responses) and motor coordination, reduced sensorimotor gating and impaired working memory and spatial-temporal integration, similar characteristics to those seen in patients with schizophrenia.

The focus of this study is to assess the research literature available for CHL1 as well as investigate a single point mutation in the CHL1 sequence altering a leucine residue to a phenylalanine in the signal peptide of the protein (Leu17Phe) in order to produce a functional deficit of the CHL1 gene. This missense polymorphism has been identified as a risk factor for schizophrenia in Asian populations. Through this mutagenesis, we are able to study CHL1 protein recruitment to the cell membrane in order to understand CHL1's role in schizophrenia at a molecular level.

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Biology Commons



Faculty Mentor

Mona C. Buhusi

Departmental Honors Advisor

Kimberly A. Sullivan

Capstone Committee Member

Dennis L. Welker