Suppression of macho-1-directed muscle fate by FGF and BMP is required for formation of posterior endoderm in ascidian embryos.
Specification of germ layers is a crucial event in early embryogenesis. In embryos of the ascidian, Halocynthia roretzi, endoderm cells originate from two distinct lineages in the vegetal hemisphere. Cell dissociation experiments suggest that cell interactions are required for posterior endoderm formation, which has hitherto been thought to be solely regulated by localized egg cytoplasmic factors. Without cell interaction, every descendant of posterior-vegetal blastomeres, including endoderm precursors, assumed muscle fate. Cell interactions are required for suppression of muscle fate and thereby promote endoderm differentiation in the posterior endoderm precursors. The cell interactions take place at the 16- to 32-cell stage. Inhibition of cell signaling by FGF receptor and MEK inhibitor also supported the requirement of cell interactions. Consistently, FGF was a potent signaling molecule, whose signaling is transduced by MEK-MAPK. By contrast, such cell interactions are not required for formation of the anterior endoderm. Our results suggest that another redundant signaling molecule is also involved in the posterior endoderm formation, which is likely to be mediated by BMP. Suppression of the function of macho-1, a muscle determinant in ascidian eggs, by antisense oligonucleotide was enough to allow autonomous endoderm specification. Therefore, the cell interactions induce endoderm formation by suppressing the function of macho-1, which is to promote muscle fate. These findings suggest the presence of novel mechanisms that suppress functions of inappropriately distributed maternal determinants via cell interactions after embryogenesis starts. Such cell interactions would restrict the regions where maternal determinants work, and play a key role in marking precise boundaries between precursor cells of different tissue types.
Kondoh
Keisuke
K
Department of Biological Sciences, Tokyo Institute of Technology, Nagatsuta, Yokohama 226-8501, Japan.
Kobayashi
Kenji
K
Nishida
Hiroki
H
D000818:Animals; D055415:Bone Morphogenetic Protein 4; D019485:Bone Morphogenetic Proteins / Q000378:metabolism*; D002352:Carrier Proteins / Q000378:metabolism / Q000502:physiology*; D002454:Cell Differentiation; D019070:Cell Lineage; D004527:Egg Proteins / Q000378:metabolism / Q000502:physiology*; D004707:Endoderm / Q000378:metabolism / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005346:Fibroblast Growth Factors / Q000378:metabolism*; D006133:Growth Substances / Q000378:metabolism; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D047908:Intracellular Signaling Peptides and Proteins; D020935:MAP Kinase Signaling System; D008954:Models, Biological; D009132:Muscles / Q000166:cytology / Q000196:embryology*; D016376:Oligonucleotides, Antisense / Q000494:pharmacology; D015398:Signal Transduction; D013997:Time Factors; D014561:Urochordata
D055415:Bone Morphogenetic Protein 4; D019485:Bone Morphogenetic Proteins; D002352:Carrier Proteins; D004527:Egg Proteins; D004791:Enzyme Inhibitors; D006133:Growth Substances; D047908:Intracellular Signaling Peptides and Proteins; D016376:Oligonucleotides, Antisense; C420970:macho-1 protein, Halocynthia roretzi; D005346:Fibroblast Growth Factors