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Embryos Assist Each Other’s Morphogenesis: calcium and ATP signaling mechanisms in collective resistance to teratogens

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Xenopus laevis

PROVIDER: GSE245782 | GEO | 2023/12/02

REPOSITORIES: GEO

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Embryos Assist Each Other’s Morphogenesis: calcium and ATP signaling mechanisms in collective resistance to teratogens (Stage 25)

Project description:We investigated whether normal embryonic developmental cues are only at the level of cells within the embryo or whether they exist in interactions between embryos. To explore this, we subjected groups of embryos with disruptors of normal development while varying group size. RNA-seq analysis revealed a small set of transcripts specific for teratogen response in large groups but not small ones.

2023-12-02 | GSE245780 | GEO

Embryos Assist Each Other’s Morphogenesis: calcium and ATP signaling mechanisms in collective resistance to teratogens (Stage 35)

2023-12-02 | GSE245781 | GEO

Embryos assist morphogenesis of others through calcium and ATP signaling mechanisms in collective teratogen resistance.

Project description:Information for organismal patterning can come from a variety of sources. We investigate the possibility that instructive influences for normal embryonic development are provided not only at the level of cells within the embryo, but also via interactions between embryos. To explore this, we challenge groups of embryos with disruptors of normal development while varying group size. Here, we show that Xenopus laevis embryos are much more sensitive to a diverse set of chemical and molecular-biological perturbations when allowed to develop alone or in small groups, than in large groups. Keeping per-embryo exposure constant, we find that increasing the number of exposed embryos in a cohort increases the rate of survival while incidence of defects decreases. This inter-embryo assistance effect is mediated by short-range diffusible signals and involves the P2 ATP receptor. Our data and computational model emphasize that morphogenesis is a collective phenomenon not only at the level of cells, but also of whole bodies, and that cohort size is a crucial variable in studies of ecotoxicology, teratogenesis, and developmental plasticity.

| S-EPMC10794468 | biostudies-literature

Embryos Assist Each Other’s Morphogenesis: calcium and ATP signaling mechanisms in collective resistance to teratogens

Project description:Embryos Assist Each Other’s Morphogenesis: calcium and ATP signaling mechanisms in collective resistance to teratogens

| PRJNA1029966 | ENA

Embryos Assist Each Other’s Morphogenesis: calcium and ATP signaling mechanisms in collective resistance to teratogens (Stage 35)

Project description:Embryos Assist Each Other’s Morphogenesis: calcium and ATP signaling mechanisms in collective resistance to teratogens (Stage 35)

| PRJNA1029976 | ENA

Embryos Assist Each Other’s Morphogenesis: calcium and ATP signaling mechanisms in collective resistance to teratogens (Stage 25)

Project description:Embryos Assist Each Other’s Morphogenesis: calcium and ATP signaling mechanisms in collective resistance to teratogens (Stage 25)

| PRJNA1029975 | ENA

Mechanics regulates ATP-stimulated collective calcium response in fibroblast cells.

Project description:Cells constantly sense their chemical and mechanical environments. We study the effect of mechanics on the ATP-induced collective calcium response of fibroblast cells in experiments that mimic various tissue environments. We find that closely packed two-dimensional cell cultures on a soft polyacrylamide gel (Young's modulus E = 690 Pa) contain more cells exhibiting calcium oscillations than cultures on a rigid substrate (E = 36 000 Pa). Calcium responses of cells on soft substrates show a slower decay of calcium level relative to those on rigid substrates. Actin enhancement and disruption experiments for the cell cultures allow us to conclude that actin filaments determine the collective Ca(2+) oscillatory behaviour in the culture. Inhibition of gap junctions results in a decrease of the oscillation period and reduced correlation of calcium responses, which suggests additional complexity of signalling upon cell-cell contact. Moreover, the frequency of calcium oscillations is independent of the rigidity of the substrate but depends on ATP concentration. We compare our results with those from similar experiments on individual cells. Overall, our observations show that collective chemical signalling in cell cultures via calcium depends critically on the mechanical environment.

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Pathological mechanisms of connexin26-related hearing loss: Potassium recycling, ATP-calcium signaling, or energy supply?

Project description:Hereditary deafness is one of the most common human birth defects. GJB2 gene mutation is the most genetic etiology. Gap junction protein 26 (connexin26, Cx26) encoded by the GJB2 gene, which is responsible for intercellular substance transfer and signal communication, plays a critical role in hearing acquisition and maintenance. The auditory character of different Connexin26 transgenic mice models can be classified into two types: profound congenital deafness and late-onset progressive hearing loss. Recent studies demonstrated that there are pathological changes including endocochlear potential reduction, active cochlear amplification impairment, cochlear developmental disorders, and so on, in connexin26 deficiency mice. Here, this review summarizes three main hypotheses to explain pathological mechanisms of connexin26-related hearing loss: potassium recycling disruption, adenosine-triphosphate-calcium signaling propagation disruption, and energy supply dysfunction. Elucidating pathological mechanisms underlying connexin26-related hearing loss can help develop new protective and therapeutic strategies for this common deafness. It is worthy of further study on the detailed cellular and molecular upstream mechanisms to modify connexin (channel) function.

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ECM Signaling Regulates Collective Cellular Dynamics to Control Pancreas Branching Morphogenesis.

Project description:During pancreas development, epithelial buds undergo branching morphogenesis to form an exocrine and endocrine gland. Proper morphogenesis is necessary for correct lineage allocation of pancreatic progenitors; however, the cellular events underlying pancreas morphogenesis are unknown. Here, we employed time-lapse microscopy and fluorescent labeling of cells to analyze cell behaviors associated with pancreas morphogenesis. We observed that outer bud cells adjacent to the basement membrane are pleomorphic and rearrange frequently; additionally, they largely remain in the outer cell compartment even after mitosis. These cell behaviors and pancreas branching depend on cell contacts with the basement membrane, which induce actomyosin cytoskeleton remodeling via integrin-mediated activation of FAK/Src signaling. We show that integrin signaling reduces E-cadherin-mediated cell-cell adhesion in outer cells and provide genetic evidence that this regulation is necessary for initiation of branching. Our study suggests that regulation of cell motility and adhesion by local niche cues initiates pancreas branching morphogenesis.

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Cellular Architecture Regulates Collective Calcium Signaling and Cell Contractility.

Project description:A key feature of multicellular systems is the ability of cells to function collectively in response to external stimuli. However, the mechanisms of intercellular cell signaling and their functional implications in diverse vascular structures are poorly understood. Using a combination of computational modeling and plasma lithography micropatterning, we investigate the roles of structural arrangement of endothelial cells in collective calcium signaling and cell contractility. Under histamine stimulation, endothelial cells in self-assembled and microengineered networks, but not individual cells and monolayers, exhibit calcium oscillations. Micropatterning, pharmacological inhibition, and computational modeling reveal that the calcium oscillation depends on the number of neighboring cells coupled via gap junctional intercellular communication, providing a mechanistic basis of the architecture-dependent calcium signaling. Furthermore, the calcium oscillation attenuates the histamine-induced cytoskeletal reorganization and cell contraction, resulting in differential cell responses in an architecture-dependent manner. Taken together, our results suggest that endothelial cells can sense and respond to chemical stimuli according to the vascular architecture via collective calcium signaling.

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