Pelin Fahliogullari (Summer 2008)


Field of Research: Biology


Lab: Jason Dictenberg


School: Manhattan Hunter Science High School


Year: 10th/ 11th Grade





Research Abstract:


Studying the molecular causes of Autism


Synaptic plasticity is the connection between the axon and the dendrite of the inhibitory and excitatory synapses. We studied the proteins that are involved in synapse formation and how they are altered in Autism. Neuroligin1, 3, and 4 are located on the post-synaptic excitatory synapses, and NLG 2 is on the inhibitory. One hypothesis is that Fragile-X mental Retardation Protein (FMRP) is deleted in Fragile X syndrome, which disregulates levels of PSD-95 genes that are being translated, which alters the localization of neuroligins from inhibitory to excitatory or vise versa. MiRNAs may be involved in the deletion process of FMR1 gene that leads to this chain reaction. I concentrated on miRNAs that bind to FMR1 using sequence analysis tools on the web and took notes on their locations on the gene, their energy levels, conservation, and number of binding sites because this information is crucial in predicting their repression. We found that many miRNAs seemed to be involved with FMRP but only a few were conserved in most proteins altered in Autism, and even more few may actually be involved in its silencing, thus being an important part of the molecular biology of Autism.                                     

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