WNT/β-catenin signaling plays a crucial role in myoblast fusion through regulation of nephrin expression during development.

Skeletal muscle development is controlled by a series of multiple orchestrated regulatory pathways. WNT/β-catenin is one of the most important pathways for myogenesis; however, it remains unclear how this signaling pathway regulates myogenesis in a temporal- and spatial-specific manner. Here, we show that WNT/β-catenin signaling is crucial for myoblast fusion through regulation of the nephrin () gene in the -expressing myoblast population.

The role of acetyltransferases for the temporal-specific accessibility of β-catenin to the myogenic gene locus.

Molecules involved in WNT/β-catenin signaling show spatiotemporal-specific expression and play vital roles in muscle development. Our previous study showed that WNT/β-catenin signaling promotes myoblast proliferation and differentiation through the regulation of the cyclin A2 (Ccna2)/cell division cycle 25C (Cdc25c) and Fermitin family homolog 2 (Fermt2) genes, respectively. However, it remains unclear how β-catenin targets different genes from stage to stage during myogenesis.

Bioengineering a 3D integumentary organ system from iPS cells using an in vivo transplantation model.

The integumentary organ system is a complex system that plays important roles in waterproofing, cushioning, protecting deeper tissues, excreting waste, and thermoregulation. We developed a novel in vivo transplantation model designated as a clustering-dependent embryoid body transplantation method and generated a bioengineered three-dimensional (3D) integumentary organ system, including appendage organs such as hair follicles and sebaceous glands, from induced pluripotent stem cells. This bioengineered 3D integumentary organ system was fully functional following transplantation into nude mice and could be properly connected to surrounding host tissues, such as the epidermis, arrector pili muscles, and nerve fibers, without tumorigenesis.

Antagonistic interplay between necdin and Bmi1 controls proliferation of neural precursor cells in the embryonic mouse neocortex.

Neural precursor cells (NPCs) in the neocortex exhibit a high proliferation capacity during early embryonic development and give rise to cortical projection neurons after maturation. Necdin, a mammal-specific MAGE (melanoma antigen) family protein that possesses anti-mitotic and pro-survival activities, is expressed abundantly in postmitotic neurons and moderately in tissue-specific stem cells or progenitors. Necdin interacts with E2F transcription factors and suppresses E2F1-dependent transcriptional activation of the cyclin-dependent kinase Cdk1 gene.

Necdin controls proliferation and apoptosis of embryonic neural stem cells in an oxygen tension-dependent manner.

Neural stem cells (NSCs) reside in vivo in hypoxic environments, and NSC proliferation is enhanced in vitro under hypoxic conditions. Various adaptive responses to hypoxia are mediated by hypoxia-inducible factors (HIFs), a family of basic helix-loop-helix Per-Arnt-Sim (PAS) transcription factors. Necdin, a MAGE (melanoma antigen) family protein, is expressed abundantly in postmitotic neurons and possesses potent antimitotic and antiapoptotic activities.

Analysis of SDF-1/CXCR4 signaling in primordial germ cell migration and survival or differentiation in Xenopus laevis.

Directional migration of primordial germ cells (PGCs) toward future gonads is a common feature in many animals. In zebrafish, mouse and chicken, SDF-1/CXCR4 chemokine signaling has been shown to have an important role in PGC migration. In Xenopus, SDF-1 is expressed in several regions in embryos including dorsal mesoderm, the target region that PGCs migrate to.