CHD7 and CHD8 are chromatin remodeling proteins that regulate gene expression. Alterations in gene expression are needed for synaptic plasticity and long-term memory. Mutations in these chromatin remodeling genes occur in Autism Spectrum Disorders and CHARGE Syndrome. The Drosophila homolog of CHD7 and CHD8 is Kismet (Kis). We found that kis mutant synapses have increased BMP signaling, increased levels of cell adhesion molecules, and decreased endocytosis. These pathways/proteins are vital for synapses to efficiently communicate and remodel. We sought to better characterize the kis mutant phenotypes. Collectively, these data lend support to the model where Kis may lead to an increase in DNlgs which, results in an increase in pMad. In this study, we found that Kis is important for proper localization of Syt1 and may play a role in wnt signaling. An increase in DNlgs and BMP signaling could collectively causing synaptic dysfunction in kis mutants, through altering glutamate subunit localization and levels. These data will help us better understand the importance of chromatin remodeling for synaptic structure and function and the molecular changes correlated with neurodevelopmental disorders.
|Commitee:||Fowler, Thomas, Williams, Jason|
|School:||Southern Illinois University at Edwardsville|
|School Location:||United States -- Illinois|
|Source:||MAI 81/12(E), Masters Abstracts International|
|Subjects:||Neurosciences, Cellular biology|
|Keywords:||BMP signaling, Cell adhesion molecules, Chromatin remodeling, Drosophila, Endocytosis, Kismet|
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