Cell fates in sea urchin embryos are remarkably labile. For example,mesodermal lineages can activate the transcriptional gene regulatory network(GRN) that drives skeletogenesis if the micromere precursors of the primary mesenchyme cells (PMCs, the cells that form the embryonic skeleton) are removed. To determine the molecular basis of this plasticity, Ettensohn and colleagues have examined the conversion of non-skeletogenic mesoderm (NSM) to a PMC fate during gastrulation and reveal that most, but not all, of the upstream transcription factors in the skeletogenic GRN are recapitulated by transfating cells (see ). They show that the transcription factor alx1, a key component of the skeletogenic GRN, is expressed in transfating NSMs, that alx1 expression in transfating NSMs and in PMCs requires MAPK signalling, and that alx1 expression in micromeres normally suppresses NSMs from transfating. However, the transcription factor pmar1 (which activates the skeletogenic GRN in PMCs) is not needed in transfating NSMs. Thus, the skeletogenic GRN is activated by distinct mechanisms during normal and regulative development.
