Two of the three major gastropod clades with feeding larvae are sister groups and larval morphogenesis for members of these clades, the Caenogastropoda and Heterobranchia, has been well studied. The third clade, the Neritimorpha, has an unstable phylogenetic position and little is known about development of their planktotrophic larvae. Information about larval morphology of neritimorphs and resolution of their controversial phylogenetic placement is critically important for understanding evolution of larval feeding within the Gastropoda. We describe larval morphogenesis to metamorphic competence for laboratory-reared larvae of Nerita melanotragus (Smith, 1884) (Neritimorpha: Neritidae). Preliminary observations suggest that prehatch larvae are capable of delayed hatching, possibly by entering a diapause state. Our description of larval morphogenesis, as based on tissue sections for light and transmission electron microscopy, scanning electron microscopy, three-dimensional-reconstructions of sectioned tissue, and labeling of muscles with fluorphore-tagged phalloidin, revealed four features that are unprecedented among both feeding and nonfeeding gastropod larvae. Larvae of N. melanotragus have muscles on the left and right side that both meet current criteria of a larval retractor muscle; shell-anchored muscles with oblique striations that project inside the visceral nerve loop to insert mainly on the velar lobes. They also have left and right digestive glands of similar size and a left and right hypobranchial gland. A larval "heart" is absent, but water circulation through the mantle cavity may be facilitated by large circular orifices, lined by patches of motile cilia, leading in and out of the mantle cavity. Comparison of larval traits among all three groups of gastropods with feeding larvae indicates that larvae of N. melanotragus have many unique characteristics, but they show more similarities to caenogastropod than to heterobranch larvae. These results are a significant step toward the goal of identifying primitive versus derived larval traits among feeding gastropod larvae.
Background/purpose: The goal of this study was to determine the role of the collagen binding receptor integrin α1β1 in regulating osmotically induced [Ca2+]i transients in chondrocytes. Methods: The [Ca2+]i transient response of chondrocytes to osmotic stress was measured using real-time confocal microscopy. Chondrocytes from wildtype and integrin α1-null mice were imaged ex vivo (in the cartilage of intact murine femora) and in vitro (isolated from the matrix, attached to glass coverslips). Immunocytochemistry was performed to detect the presence of the osmosensor, transient receptor potential vanilloid-4 (TRPV4), and the agonist GSK1016790A (GSK101) was used to test for its functionality on chondrocytes from wildtype and integrin α1-null mice. Results/interpretation: Deletion of the integrin α1 subunit inhibited the ability of chondrocytes to respond to a hypo-osmotic stress with [Ca2+]i transients ex vivo and in vitro. The percentage of chondrocytes responding ex vivo was smaller than in vitro and of the cells that responded, more single [Ca2+]i transients were observed ex vivo compared to in vitro. Immunocytochemistry confirmed the presence of TRPV4 on wildtype and integrin α1-null chondrocytes, however application of GSK101 revealed that TRPV4 could be activated on wildtype but not integrin α1-null chondrocytes. Integrin α1β1 is a key participant in chondrocyte transduction of a hypo-osmotic stress. Furthermore, the mechanism by which integrin α1β1 influences osmotransduction is independent of matrix binding, but likely dependent on the chondrocyte osmosensor TRPV4.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.