Fig. 7

Local signals regulate MPC versus PWPC fate. (A-B′) Heat shock induction of msgn1 at the start of gastrulation (shield stage) results in the absence of notochord and the ectopic expansion of somites across the midline at 24hpf. (C-D′) Heat shock induction of msgn1 after gastrulation (bud stage) causes the notochord to end abruptly, followed posteriorly by the expansion of somites at the midline at 24hpf. The arrowhead indicates the transition from notochord to somite at the midline. (E-J′) In embryos heat shocked at bud stage, myoD expression at 24hpf is present in posterior regions of the embryo (E,G) and, when viewed dorsally, can be seen extending across the midline (E′,G′). Fluorescent in situ hybridization of myoD expression reveals (by digital transverse section) the absence of notochord and presence of muscle across the midline (F,H, asterisk marks the position of the spinal cord). Expression of col2a1 indicates that the notochord is truncated (I-J′). (K,L) Ectopic msgn1 expression at bud stage cell-autonomously converts some MPCs to a somitic fate, as seen in transplanted cells. Control donor cells only contribute to floor plate, notochord and hypochord (K); somite contribution was observed in 1/16 embryos. By contrast, HS:msgn1 donor cells transition from notochord contribution to somite contribution (L, white arrow; notochord to somite switch was observed in 12/16 embryos) without affecting floor plate contribution. Green, red and blue arrowheads indicate notochord, hypochord and floor plate, respectively. (M-N′′) A serial transplantation scheme (M) was used to target MPCs to the PWPCs. MPCs (green) from the 12-somite stage tailbud are able to contribute to skeletal muscle tissue when analyzed at 24hpf (N-N′′).