Neural crest cells generate numerous different cell types in vertebrate embryos, including the `sympatho-adrenal' precursors. These cells mature into sympathetic neurons (which control the `fight or flight' response) and adrenal chromaffin cells (which make adrenalin and noradrenalin). Now, Carmen Birchmeier and colleagues report that the insulinoma-associated 1(Insm1) gene, which encodes a zinc-finger transcription factor, is a central component of the transcriptional network that controls the differentiation of the sympatho-adrenal lineage (see ). The researchers show that the differentiation of sympatho-adrenal precursors is delayed and their proliferation reduced in Insm1 mutant mice. The expression of Mash1, Phox2 and other components of the transcriptional network that controls the differentiation of the sympatho-adrenal lineage is deregulated in Insm1 mutant mice, they report. In addition, Insm1 and Mash1 mutant mice have similar phenotypes. Other data indicate that Insm1 acts downstream of Mash1 and Phox2b genetically and that Insm1 represses Mash1. The researchers speculate, therefore, that Insm1 mediates certain aspects of Mash1 function during the differentiation of sympatho-adrenal precursors.
