Nd isotope variation between the Earth-Moon system and enstatite chondrites.

Reconstructing the building blocks that made Earth and the Moon is critical to constrain their formation and compositional evolution to the present. Neodymium (Nd) isotopes identify these building blocks by fingerprinting nucleosynthetic components. In addition, the 146Sm-142Nd and 147Sm-143Nd decay systems, with half-lives of 103 million years and 108 billion years, respectively, track potential differences in their samarium (Sm)/Nd ratios. The difference in Earth's present-day 142Nd/144Nd ratio compared with chondrites1,2, and in particular enstatite chondrites, is interpreted as nucleosynthetic isotope variation in the protoplanetary disk. This necessitates that chondrite parent bodies have the same Sm/Nd ratio as Earth's precursor materials2. Here we show that Earth and the Moon instead had a Sm/Nd ratio approximately 2.4 ± 0.5 per cent higher than the average for chondrites and that the initial 142Nd/144Nd ratio of Earth's precursor materials is more similar to that of enstatite chondrites than previously proposed1,2. The difference in the Sm/Nd ratio between Earth and chondrites probably reflects the mineralogical distribution owing to mixing processes within the inner protoplanetary disk. This observation simplifies lunar differentiation to a single stage from formation to solidification of a lunar magma ocean3. This also indicates that no Sm/Nd fractionation occurred between the materials that made Earth and the Moon in the Moon-forming giant impact.

TWIST1 interacts with ß/δ-catenins during neural tube development and regulates fate transition in cranial neural crest cells.

Cell fate determination is a necessary and tightly regulated process for producing different cell types and structures during development. Cranial neural crest cells (CNCCs) are unique to vertebrate embryos and emerge from the neural plate borders into multiple cell lineages that differentiate into bone, cartilage, neurons and glial cells. We have previously reported that Irf6 genetically interacts with Twist1 during CNCC-derived tissue formation. Here, we have investigated the mechanistic role of Twist1 and Irf6 at early stages of craniofacial development. Our data indicate that TWIST1 is expressed in endocytic vesicles at the apical surface and interacts with ß/δ-catenins during neural tube closure, and Irf6 is involved in defining neural fold borders by restricting AP2α expression. Twist1 suppresses Irf6 and other epithelial genes in CNCCs during the epithelial-to-mesenchymal transition (EMT) process and cell migration. Conversely, a loss of Twist1 leads to a sustained expression of epithelial and cell adhesion markers in migratory CNCCs. Disruption of TWIST1 phosphorylation in vivo leads to epidermal blebbing, edema, neural tube defects and CNCC-derived structural abnormalities. Altogether, this study describes a previously uncharacterized function of mammalian Twist1 and Irf6 in the neural tube and CNCCs, and provides new target genes for Twist1 that are involved in cytoskeletal remodeling.