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. 2020 Jun 23;8:477. doi: 10.3389/fcell.2020.00477

FIGURE 4.

FIGURE 4

Models of FGF-dependent regulation of BTN specification and differentiation. (a) Early U0126 treatment confirms role of Fgf9/16/20 (FGF9) in specifying BTN lineage founder cells (from Stolfi et al., 2015). (b) Perturbing late FGF signaling, either via late U0126 treatment (Stolfi et al., 2015), or dnFGFR overexpression or Fgf8/17/18 knockout using CRISPR results in supernumerary aBTNs, through loss of repression of Neurog in posterior cells of the aBTN lineage. (c) Ectopic FGF/ERK activation via CA-Mras overexpression suppresses maintenance of Neurog expression and abolished aBTN fate. (d) Summary of our model encompassing the distinct roles of early and late FGF signals, and the distinct aBTN lineage-specific requirement for Fgf8/17/18 to restrict differentiation.