scholarly journals Exploratory cell dynamics: a sense of touch for cells?

2018 ◽  
Vol 399 (8) ◽  
pp. 809-819 ◽  
Author(s):  
Perihan Nalbant ◽  
Leif Dehmelt
Keyword(s):  
Mechanical Properties ◽  
Cell Fate ◽  
Cell Behavior ◽  
Directional Migration ◽  
Cell Dynamics ◽  
Cell Fate Decisions ◽  
External Cues ◽  
Dynamic Cell ◽  
Sense Of Touch ◽  
Efficient Mechanisms

Abstract Cells need to process multifaceted external cues to steer their dynamic behavior. To efficiently perform this task, cells implement several exploratory mechanisms to actively sample their environment. In particular, cells can use exploratory actin-based cell protrusions and contractions to engage and squeeze the environment and to actively probe its chemical and mechanical properties. Multiple excitable signal networks were identified that can generate local activity pulses to control these exploratory processes. Such excitable signal networks offer particularly efficient mechanisms to process chemical or mechanical signals to steer dynamic cell behavior, such as directional migration, tissue morphogenesis and cell fate decisions.

scholarly journals A somatic proteoglycan controls Notch-directed germ cell fate

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Sandeep Gopal ◽  
Aqilah Amran ◽  
Andre Elton ◽  
Leelee Ng ◽  
Roger Pocock
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Germ Cell ◽  
Cell Fate ◽  
Notch Receptor ◽  
Cell Behavior ◽  
Cell Fate Decisions ◽  
Calcium Dependent ◽  
Notch Receptors ◽  
Germline Proliferation

AbstractCommunication between the soma and germline optimizes germ cell fate programs. Notch receptors are key determinants of germ cell fate but how somatic signals direct Notch-dependent germ cell behavior is undefined. Here we demonstrate that SDN-1 (syndecan-1), a somatic transmembrane proteoglycan, controls expression of the GLP-1 (germline proliferation-1) Notch receptor in the Caenorhabditis elegans germline. We find that SDN-1 control of a somatic TRP calcium channel governs calcium-dependent binding of an AP-2 transcription factor (APTF-2) to the glp-1 promoter. Hence, SDN-1 signaling promotes GLP-1 expression and mitotic germ cell fate. Together, these data reveal SDN-1 as a putative communication nexus between the germline and its somatic environment to control germ cell fate decisions.

scholarly journals Drosophila as a Model for Developmental Biology: Stem Cell-Fate Decisions in the Developing Nervous System

2018 ◽  
Vol 6 (4) ◽  
pp. 25 ◽  
Author(s):  
Katherine Harding ◽  
Kristin White
Keyword(s):  
Stem Cells ◽  
Nervous System ◽  
Stem Cell ◽  
Neural Stem Cells ◽  
Cell Fate ◽  
Cell Behavior ◽  
Stem Cell Fate ◽  
Cell Fate Decisions ◽  
Unique System ◽  
Developing Nervous System

Stem cells face a diversity of choices throughout their lives. At specific times, they may decide to initiate cell division, terminal differentiation, or apoptosis, or they may enter a quiescent non-proliferative state. Neural stem cells in the Drosophila central nervous system do all of these, at stereotypical times and anatomical positions during development. Distinct populations of neural stem cells offer a unique system to investigate the regulation of a particular stem cell behavior, while comparisons between populations can lead us to a broader understanding of stem cell identity. Drosophila is a well-described and genetically tractable model for studying fundamental stem cell behavior and the mechanisms that underlie cell-fate decisions. This review will focus on recent advances in our understanding of the factors that contribute to distinct stem cell-fate decisions within the context of the Drosophila nervous system.

scholarly journals UPMaBoSS: a novel framework for dynamic cell population modeling

2020 ◽  
Author(s):  
Gautier Stoll ◽  
Aurélien Naldi ◽  
Vincent Noël ◽  
Eric Viara ◽  
Emmanuel Barillot ◽  
...  
Keyword(s):  
Population Dynamics ◽  
Cell Fate ◽  
Cellular Networks ◽  
Cell Population ◽  
Cell Fate Decisions ◽  
Dynamic Cell ◽  
Drug Treatments ◽  
A Cell ◽  
The Impact

AbstractOne of the aims of mathematical modeling is to understand and simulate the effects of biological perturbations and suggest ways to intervene and reestablish proper cell functioning. However, it remains a challenge, especially when considering the dynamics at the level of a cell population, with cells dying, dividing and interacting. Here, we introduce a novel framework for the dynamical modelling of cell populations packaged into a dedicated tool, UPMaBoSS. We rely on the preexisting tool MaBoSS, which enables probabilistic simulations of cellular networks, and add a novel layer to account for cell interactions and population dynamics. We illustrate our methodology by means of a case study dealing with TNF-induced cell death. Interestingly, the simulation of cell population dynamics with UPMaBoSS reveals a mechanism of resistance triggered by TNF treatment. This appoach can be applied to diverse models of cellular networks, for example to study the impact of ligand release or drug treatments on cell fate decisions, such as commitment to proliferation, differentiation, apoptosis, etc. Relatively easy to encode, UPMaBoSS simulations require only moderate computational power and execution time.To ease the reproduction of simulations, we provide several Jupyter notebooks that can be accessed within a new release of the CoLoMoTo Docker image, which contains all required software and the example models.

scholarly journals Quantitative assessment of cell fate decision between autophagy and apoptosis

2017 ◽  
Author(s):  
Bing Liu ◽  
Zoltán N. Oltvai ◽  
Hulya Bayir ◽  
Gary A. Silverman ◽  
Stephen C. Pak ◽  
...  
Keyword(s):  
Cell Fate ◽  
Cellular Damage ◽  
G Protein Signaling ◽  
Protein Signaling ◽  
Cell Fate Decision ◽  
Cell Fate Decisions ◽  
Dynamic Cell ◽  
Stress Signals ◽  
Fate Decision ◽  
Amp Activated Protein Kinase

AbstractAutophagy and apoptosis regulate cell survival and death, and are implicated in the pathogenesis of many diseases. The same type of stress signals can induce either process, but it is unclear how cells ‘assess’ cellular damage and make a ‘life’ or ‘death’ decision by activating autophagy or apoptosis. A computational model of coupled apoptosis and autophagy is built here to study the systems-level dynamics of the underlying signaling network. The model explains the differential dynamics of autophagy and apoptosis in response to various experimental stress signals. Autophagic response dominates at low-to-moderate stress; whereas the response shifts from autophagy (graded activation) to apoptosis (switch-like activation) with increasing intensity of stress. The model reveals that this dynamic cell fate decision is conferred by a core regulatory network involving cytoplasmic Ca2+ as a rheostat that fine-tunes autophagic and apoptotic responses. A G-protein signaling-mediated feedback loop maintains cytoplasmic Ca2+ level, which in turn governs autophagic response through an AMP-activated protein kinase (AMPK)-mediated feedforward loop. The model identified Ca2+/calmodulin-dependent kinase kinase β (CaMKKβ) as a determinant of the opposite roles of cytoplasmic Ca2+ in autophagy regulation. The results also demonstrated that the model could contribute to the development of pharmacological strategies modulate cell fate decisions.

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