During embryogenesis, mesodermal signals induce the morphogenesis of endodermal organs. But what establishes the correct spatial relationship between the mesodermal signal-producing cells and the target endoderm? On p. 3209, Huang and colleagues report that, during zebrafish liver organogenesis, the expression of myosin phosphatase targeting subunit 1 (Mypt1, a protein that regulates myosin) in the lateral plate mesoderm (LPM) ensures that the liver primordium receives the mesodermal signals needed for its development by setting the relative positions of these two tissues. The authors identify a liverless mutant, sq181, that has an inactivating mutation in mypt1. Hepatoblasts form in this mutant but proliferate poorly and are lost by apoptosis. Other experiments indicate that the mutation alters the morphogenesis of the LPM, which leads to the mispositioning of bmp2a-expressing LPM cells relative to the liver primordium; this mispositioning of Bmp signals probably causes the sq181 phenotype. Thus, Mypt1 function (and myosin contractility) may establish the spatial interaction between mesoderm and endoderm that is essential for liver organogenesis in zebrafish.
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