The oviduct is an important organ in reproduction where fertilization occurs, and through which the fertilized eggs are carried to the uterus in mammals. This organ is highly polarized, where the epithelium forms longitudinal folds along the ovary-uterus axis, and the epithelial multicilia beat towards the uterus to transport the ovulated ova. Here, we analyzed the postnatal development of mouse oviduct and report that multilevel polarities of the oviduct are regulated by a planar cell polarity (PCP) gene, Celsr1. In the epithelium, Celsr1 is concentrated in the specific cellular boundaries perpendicular to the ovary-uterus axis from postnatal day 2. We found a new feature of cellular polarity in the oviduct -the apical surface of epithelial cells is elongated along the ovary-uterus axis. In Celsr1-deficient mice, the ciliary motion is not orchestrated along the ovary-uterus axis and the transport ability of beating cilia is impaired. Epithelial cells show less elongation and randomized orientation, and epithelial folds show randomized directionality and ectopic branches in the mutant. Our mosaic analysis suggests that the geometry of epithelial cells is primarily regulated by Celsr1 and as a consequence the epithelial folds are aligned. Taken together, we reveal the characteristics of the multilevel polarity formation processes in the mouse oviduct epithelium and suggest a novel function of the PCP pathway for proper tissue morphogenesis.
The surface oxidized layer of a TiN barrier metal thin film grown on a Pt electrode was used as a resistive switching material. The fabricated memory cell shows bipolar resistive switching on a nanosecond order. A TiO2 anatase layer of about 2.5nm thick on TiN thin film was characterized by high-resolution scanning transmission electron microscopy. The results suggested that the high-speed resistive change was derived from the Mott transition in the TiO2 anatase nanolayer, and the obtained results could relate to the formation of filament paths previously reported in binary transition metal oxide thin films exhibiting resistive switching.
Early in the development of the central nervous system, progenitor cells undergo a shape change, called apical constriction, that triggers the neural plate to form a tubular structure. How apical constriction in the neural plate is controlled and how it contributes to tissue morphogenesis are not fully understood. In this study, we show that intracellular calcium ions (Ca 2+ ) are required for Xenopus neural tube formation and that there are two types of Ca 2+ -concentration changes, a single-cell and a multicellular wave-like fluctuation, in the developing neural plate. Quantitative imaging analyses revealed that transient increases in Ca 2+ concentration induced cortical F-actin remodeling, apical constriction and accelerations of the closing movement of the neural plate. We also show that extracellular ATP and N-cadherin (cdh2) participate in the Ca 2+ -induced apical constriction. Furthermore, our mathematical model suggests that the effect of Ca 2+ fluctuations on tissue morphogenesis is independent of fluctuation frequency and that fluctuations affecting individual cells are more efficient than those at the multicellular level. We propose that distinct Ca 2+ signaling patterns differentially modulate apical constriction for efficient epithelial folding and that this mechanism has a broad range of physiological outcomes.
Epithelia exhibit various three-dimensional morphologies linked to organ function in animals. However, the mechanisms of three-dimensional morphogenesis remain elusive. The luminal epithelium of the mouse oviduct forms well-aligned straight folds along the longitudinal direction of the tubes. Disruption of the Celsr1 gene, a planar cell polarity-related gene, causes ectopically branched folds. Here, we evaluated the mechanical contributions of the epithelium to the fold pattern formation. In the mutant oviduct, the epithelium was more intricate along the longitudinal direction than in the wild-type, suggesting a higher ratio of the longitudinal length of the epithelial layer to that of the surrounding smooth muscle (SM) layer (L-Epi/SM ratio). Our mathematical modeling and computational simulations suggested that the L-Epi/SM ratio could explain the differences in fold branching between the two genotypes. Longitudinal epithelial tensions were increased in well-aligned folds compared with those in disorganized folds both in the simulations and in experimental estimations. Artificially increasing the epithelial tensions suppressed the branching in simulations, suggesting that the epithelial tensions can regulate fold patterning. The epithelial tensions could be explained by the combination of line tensions along the epithelial cell-cell boundaries with the polarized cell arrays observed in vivo. These results suggest that the fold pattern is associated with the polarized cell array through the longitudinal epithelial tension. Further simulations indicated that the L-Epi/SM ratio could contribute to fold pattern diversity, suggesting that the L-Epi/SM ratio is a critical parameter in the fold patterning in tubular organs.
Mammalian embryos develop in coordination with extraembryonic tissues, which support embryonic development by implanting embryos into the uterus, supplying nutrition, providing a confined niche, and also providing patterning signals to embryos. Here, we show that in mouse embryos, the expansion of the amniotic cavity (AC), which is formed between embryonic and extraembryonic tissues, provides the mechanical forces required for a type of morphogenetic movement of the notochord known as convergent extension (CE) in which the cells converge to the midline and the tissue elongates along the antero-posterior (AP) axis. The notochord is stretched along the AP axis, and the expansion of the AC is required for CE. Both mathematical modeling and physical simulation showed that a rectangular morphology of the early notochord caused the application of anisotropic force along the AP axis to the notochord through the isotropic expansion of the AC. AC expansion acts upstream of planar cell polarity (PCP) signaling, which regulates CE movement. Our results highlight the importance of extraembryonic tissues as a source of the forces that control the morphogenesis of embryos.
Erythrocyte sedimentation rate and high-sensitivity C-reactive protein concentration were higher in patients with knee osteoarthritis and were related to clinical features. In knee osteoarthritis, high-sensitivity C-reactive protein concentration may increase in early-stage KL-II.
Organs and tissues in multi-cellular organisms exhibit various morphologies. Tubular organs have multi-scale morphological features which are closely related to their functions. Here we discuss morphogenesis and the mechanical functions of the vertebrate oviduct in the female reproductive tract, also known as the fallopian tube. The oviduct functions to convey eggs from the ovary to the uterus. In the luminal side of the oviduct, the epithelium forms multiple folds (or ridges) well-aligned along the longitudinal direction of the tube. In the epithelial cells, cilia are formed orienting toward the downstream of the oviduct. The cilia and the folds are supposed to be involved in egg transportation. Planar cell polarity (PCP) is developed in the epithelium, and the disruption of the Celsr1 gene, a PCP related-gene, causes randomization of both cilia and fold orientations, discontinuity of the tube, inefficient egg transportation, and infertility. In this review article, we briefly introduce various biophysical and biomechanical issues in the oviduct, including physical mechanisms of formation of PCP and organized cilia orientation, epithelial cell shape regulation, fold pattern formation generated by mechanical buckling, tubulogenesis, and egg transportation regulated by fluid flow. We also mention about possible roles of the oviducts in egg shape formation and embryogenesis, sinuous patterns of tubes, and fold and tube patterns observed in other tubular organs such as the gut, airways, etc.
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