Mentor: Michael Robinson, Ph.D.

FOXE3 is a transcription factor that plays a crucial role in the early development of the ocular lens. Mutations in FOXE3 across many species (Mouse, frog, human, zebrafish) result in devastating phenotypes such as primary aphakia (loss of the lens), Peters anomaly (attachment of lens to the cornea) and cataracts. However, how FOXE3 mechanically works and how these severe phenotypes arise from FOXE3 mutations remains a mystery. The proposed project will help elucidate how FOXE3 works in early development. I will conduct a temporal assessment of phenotypes resulting from the loss of FOXE3 by comparing eye development in wild-type and FOXE3 knock out (KO) mice at 3 different stages of embryonic development: embryonic day 12, 15 and postnatal day 0 (E12, E15 and P0). We will collect, fix, and embed tissue samples in paraffin. I will section these tissues for histological analyses including: hematoxylin and eosin (H&E) staining and immunohistochemistry (IHC) to identify relevant proteins that previous RNA-sequencing data suggest may be altered in the absence of FOXE3. These analyses will play a critical role in identifying target proteins that are under the regulation of FOXE3. By understanding how FOXE3 affects lens structure we will also better understand what exactly FOXE3 does during embryonic eye development. The protein data generated by this project should complement the existing transcriptomic data in a manuscript that we will submit next year. Lastly, this project may inspire other biomedically oriented undergraduate students to do research on topics directly relevant to human development and birth defects.

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