Meeting Abstract

P2-77   -   Regulation of Neurogenesis by FGF Signaling and Neurogenin in the Invertebrate Chordate Ciona Kim, K*; Gibboney, S; Razy-Krajka, F; Lowe, EK; Wang, W; Stolfi, A; School of Biological Sciences, Georgia Institute of Technology, Atlanta, GA; School of Biological Sciences, Georgia Institute of Technology, Atlanta, GA; School of Biological Sciences, Georgia Institute of Technology, Atlanta, GA; School of Biological Sciences, Georgia Institute of Technology, Atlanta, GA; Department of Biology, New York University, New York, NY; School of Biological Sciences, Georgia Institute of Technology, Atlanta, GA quantae@gatech.edu

Ciona robusta is a good model organism for neurodevelopmental study. It has well-conserved chordate-specific genome and gene regulatory networks, and miniaturized but typically chordate CNS consisting of 177 neurons. In Ciona, bipolar tail neurons (BTNs) show noteworthy features of cell behaviors during their development, such as, delamination, migration, and polarized axon growth. Here, we ascertain the spatiotemporal upstream regulation which determines BTNs specification and differentiation. At the early stage, Fgf9/16/20 signaling from surrounding cells induces the expression of Neurog, the conserved proneural factor which is necessary and sufficient for BTN neurogenesis. However, at the later stages, Fgf8/17/18 signaling from tail tip cells represses the continuous expression of Neurog in the anterior BTN (aBTN) lineage. As a result, only the furthest cell from Fgf8/17/18 center continues Neurog expression and differentiate as aBTN. On the other hand, the posterior BTNs (pBTNs) lineage doesn’t seem to be affected by the diffusion of Fgf8/17/18. To reveal the gene expression related to BTN developmental process caused by Neurog, FACS/RNA seq and in situ hybridization were performed, as a result, several candidate genes were evaluated as key factors of neurogenesis in other animals including human beings.