Abstract
Author SummaryBilateral animals that are externally symmetric in appearance often have internal organs that are asymmetric with respect to the left and right sides of their bodies. Two signals, Nodal and BMP, have been shown to establish this asymmetry during vertebrate embryogenesis. We investigate here whether the same mechanisms that establish left-right patterning in vertebrates are conserved in invertebrate animals, specifically in the California purple sea urchin. This sea urchin passes through various stages in its lifecycle before developing to adulthood, including a feeding larva stage in which the tissue that goes on to form the adult, the so-called adult rudiment, forms on the left side. Previous studies have shown that right-sided Nodal signaling in sea urchins prevents the formation of the adult rudiment. In this study, we show that BMP signaling is activated on the left side and is required for the development of this left-sided structure. We also demonstrate that Nodal signaling blocks BMP activity and induces apoptosis of the tissue that forms the adult rudiment on the right side. We propose that the roles of Nodal and BMP signals in establishing left-right asymmetry are evolutionarily conserved.
Highlights
One of the most fascinating features of bilaterian development is the consistent left-right (LR) asymmetry of their internal organs
Results pSmad1/5/8 Was Detected on the Left Side of the Larva To study the role of Bone morphogenic protein (BMP) signaling in LR asymmetry in sea urchins, we first examined the expression patterns of genes related to the BMP signaling pathway
It is known that both small micromeres (Smm) and the veg2 mesoderm contribute to the coelomic pouch (CP), past studies were unable to clearly identify genes that are expressed in either lineage
Summary
One of the most fascinating features of bilaterian development is the consistent left-right (LR) asymmetry of their internal organs. It has been suggested that the mechanisms of initial symmetry breaking are not conserved across different vertebrate classes [2]. A leftward fluid flow generated by the posteriorly tilted nodal cilia initiates left-sided gene expression in the mouse embryo [3]. Detailed symmetry-breaking mechanisms vary among different vertebrate species, the common outcome is the expression of nodal, which encodes a transforming growth factor b (TGFb) ligand, in the left lateral plate mesoderm (LPM) [5]. The Nodal pathway regulates LR asymmetry in vertebrates and controls the formation of the left-sided adult rudiment in sea urchins [6] and body chirality in snails [7]
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