Figure 3.

Patterning of the PSM in T(s)∷Cre; R-NICD embryos. (A) In situ hybridization of wild-type (panels a,c,e,g,i,k,m) and T(s)∷Cre; R-NICD (panels b,d,f,h,j,l,n) embryos with the probes indicated on top demonstrates grossly normal subdivision of the PSM of T(s)∷Cre; R-NICD embryos. (B) Cyclic expression of Lfng (panels a–c,f–h) and Hes7 (panels k–m,p–r) in wild-type and static expression throughout the PSM in T(s)∷Cre; R-NICD embryos (panels d,e,i,j,n,o,s,t). (Panels e,j) Extended color development revealed low levels of Lfng transcription throughout the posterior PSM. Cyclic expression of Axin2 both in wild-type (panels u–w) and T(s)∷Cre; R-NICD (panels x–z) embryos. Cyclic expression of Spry2 in wild-type (panels za–zc) is disrupted in T(s)∷Cre; R-NICD (panels zd,ze) embryos. (C) Tail halves of T(s)∷Cre; R-NICD hybridized with Mesp2 (panels a′,b′,c′) and Lfng (panel a), Hes7 (panel b), and Spry2 (panel c), indicating that in the anterior PSM the Mesp2 expression domain overlaps with the high Lfng and Spry2 expression and with the decreasing Hes7 expression domain. The dotted lines depict the overlapping domains.