Meeting Abstract
P1.147 Saturday, Jan. 4 15:30 FGF-independent Mek signaling is required for proper specification of embryonic ectodermal neurons in the sea anemone Nematostella vectensis STEINWORTH, BM*; LAYDEN, MJ; CHOCK, T; ROTTINGER, E; MARTINDALE, MQ; Whitney Laboratory for Marine Bioscience; Whitney Laboratory for Marine Bioscience; Whitney Laboratory for Marine Bioscience; Université de Nice Sophia; Whitney Laboratory for Marine Bioscience bsteinworth@gmail.com
To gain insight into mechanisms regulating neurogenesis in Nematostella, we treated embryos with Mek inhibitor U0126 and assayed expression of NvashA. NvashA is expressed in a salt and pepper pattern in wild type animals and promotes neurogenesis by activating expression of neural genes. Treatment with U0126 inhibits expression of NvashA and its previously identified targets. Because our previous studies suggested NvashA regulated development of a subset of the early nervous system, we wondered if U0126 regulated additional neural or salt and pepper genes during embryogenesis. We used a custom genome-wide microarray to identify transcription factors downregulated by U0126. In situ hybridization on wild-type animals identified transcription factors with a salt and pepper expression pattern. We tested whether array-identified genes functioned downstream of NvashA by activating or decreasing NvashA function and assaying for changes in gene expression. Data suggest only Nvgfi-like and Nvtailless-like are downstream of NvashA, suggesting the remaining genes may regulate NvashA-independent neurogenesis. Lastly, we asked if Mek promotes neurogenesis through NvashA by a linear pathway. We reasoned that if the pathway were linear, overexpression of NvashA in U0126-treated animals would rescue expression of NvashA neural target genes. Surprisingly, we were unable to rescue NvashA target genes in U0126-treated animals. These data suggest Mek plays at least two roles in embryonic neurogenesis in Nematostella: first, to promote expression of the neurogenic gene NvashA, and second, to confer competence for cells to positively respond to NvashA expression.
