Meeting Abstract
Notch signaling is vital for neural development in both vertebrate and insect models, but not much is known about this process in annelids. Here we use the model organism Capitella teleta, a marine annelid within Spiralia, to explore Notch function. We hypothesized that Notch signaling in annelids functions similarly to the known vertebrate model, where activated Notch blocks progression of neural stem cells towards cell cycle exit and differentiation. We used pharmacological treatments (DAPT, LY411575) to block Notch signaling and test this hypothesis. DAPT treatments caused a decrease in neural, foregut, and mesodermal tissues. In situ hybridization (ISH) of DAPT treated animals for Cte-ash1, a proneural homolog, showed an increase in expression throughout mesodermal and foregut tissue while ISH for Cte-syt1, a pan-neuronal marker, showed very little difference among treatments. These surprising results suggest that Notch signaling may not play a crucial role in annelid neural development, a finding that would be very different from vertebrates and insects. Preliminary ISH data for Cte-elav1, an earlier pan-neuronal marker, and Cte-ash1 after LY411575 treatment should further clarify the function of Notch signaling in this organism. We are also currently cloning the full length notch gene for future knockdown and misexpression experiments. Together, these methods will allow us to rigorously test and observe the function of Notch during annelid development.
