Fig. 6. A model to explain the phenotypes obtained when FGF signaling is progressively reduced in mes/r1. Schematic diagrams illustrate dorsal views of mes/r1 in embryos of the genotypes indicated at the somite stages denoted. The intensity of the blue color in the triangle to the left of a diagram illustrates the level of FGF signaling. (A) The regions in which cells are dying or have already died are indicated by red stippling. (B) The regions that contain the progenitors (p) of the superior colliculus (SC), inferior colliculus (IC), cerebellar vermis (CbV) and cerebellar hemispheres (CbH) are indicated. The phenotypes observed in mutants that attain progressively lower levels of FGF signaling are illustrated. In mes/r1-S2GOF embryos, the anterior mes has been lost, and the surviving posterior cells are specified to an anterior (SC) fate. Consequently the IC does not develop. In mes/r1-S2GOF;F8 embryos, the effects on the mes are similar and, in addition, the vermis fails to develop because roof plate (RP) expansion in r1 results in a loss of CbV progenitors. (C) In the wild-type embryo, FGF signaling induces/maintains the expression of Grem1, which functions to inhibit BMP signaling and expression of the BMP effector MSX1. This pathway maintains the normal balance of vermis and roof plate development. In the mes/r1-S2GOF;F8 embryo, the reduction in the level of FGF signaling results in a severe reduction in Grem1 expression. In the absence of this antagonist, the level of BMP signaling and therefore MSX1 expression increases and an expanded roof plate develops where the vermis progenitors normally reside.