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Abstract
The parathyroid glands are essential for regulating calcium homeostasis in the body. During mouse development, the parathyroid develops in the 3rd pharyngeal pouch along with the thymus. The messy separation of these two organs leaves behind ectopic parathyroid glands and cervical thymi. When few cervical thymi were found to have a history of expressing parathyroid hormone, parathyroid cell fate stability was shown to be unstable. It is unclear why parathyroid cell fate is unstable or how the fate switch occurs. One possible reason for parathyroid cell fate instability is low proliferation and/or long cell cycle as proliferation has been linked to cell stability. My research investigates parathyroid cell proliferation and cell cycle length throughout embryonic development. To address how the fate switch occurs, my data suggests that activation of the thymus program in parathyroid cells is sufficient to downregulate the parathyroid program.