scholarly journals Cell tip growth underlies injury response of marine macroalgae

2021 ◽  
Author(s):  
Maki Shirae-Kurabayashi ◽  
Tomoya Edzuka ◽  
Masahiro Suzuki ◽  
Gohta Goshima
Keyword(s):  
Cell Biology ◽  
Cellular Response ◽  
Tip Growth ◽  
Nuclear Translocation ◽  
Nuclear Division ◽  
Live Cell ◽  
Marine Macroalgae ◽  
Regeneration Ability ◽  
Codium Fragile ◽  
Rhizoid Formation

AbstractRegeneration is a widely observed phenomenon by which the integrity of an organism is recovered after damage. So far, studies on the molecular and cellular mechanisms of regeneration have been limited to a handful of model multicellular organisms. Here, we systematically surveyed the regeneration ability of marine macroalgae (Rhodophyta, Phaeophyceae, Chlorophyta) after thallus severing and applied live cell microscopy on them to uncover the cellular response to the damage. We observed three types of responses – budding, rhizoid formation and/or sporulation – in 25 species among 66 examined, demonstrating the high potential of regeneration of macroalgae. In contrast, callus formation, which often accompanies plant regeneration, was never observed. We monitored the cellular and nuclear dynamics during cell repair or rhizoid formation of four phylogenetically diverged Rhodophyta and Chlorophyta species (Colaconema sp., Dasya sessilis, Cladophora albida, Codium fragile). We observed tip growth of the cells near the damaged site as a common response, despite the difference in the number of nuclei and cells across species. Nuclear translocation follows tip growth, enabling overall uniform distribution of multinuclei (Dasya sessilis, Cladophora albida, Codium fragile) or central positioning of the mononucleus (Colaconema sp.). In contrast, the control of cell cycle events, such as nuclear division and septation, varied in these species. In Dasya sessilis, the division of multinuclei was synchronised, whereas it was not the case in Cladophora albida. Septation was tightly coupled with nuclear division in Colaconema and Dasya but not in others. These observations show that marine macroalgae utilise a variety of regeneration pathways, with some common features. This study also provides a novel methodology of live cell biology in macroalgae, offering a foundation for the future of this under-studied taxon.

scholarly journals Impact of Protein Kinase PKR in Cell Biology: from Antiviral to Antiproliferative Action

2006 ◽  
Vol 70 (4) ◽  
pp. 1032-1060 ◽  
Author(s):  
M. A. García ◽  
J. Gil ◽  
I. Ventoso ◽  
S. Guerra ◽  
E. Domingo ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Cell Fate ◽  
Cell Biology ◽  
Cellular Response ◽  
Nuclear Translocation ◽  
Receptor Activation ◽  
Initiation Factor ◽  
Viral Mrnas ◽  
Double Stranded Rna ◽  
Antiproliferative Action

SUMMARY The double-stranded RNA-dependent protein kinase PKR is a critical mediator of the antiproliferative and antiviral effects exerted by interferons. Not only is PKR an effector molecule on the cellular response to double-stranded RNA, but it also integrates signals in response to Toll-like receptor activation, growth factors, and diverse cellular stresses. In this review, we provide a detailed picture on how signaling downstream of PKR unfolds and what are the ultimate consequences for the cell fate. PKR activation affects both transcription and translation. PKR phosphorylation of the alpha subunit of eukaryotic initiation factor 2 results in a blockade on translation initiation. However, PKR cannot avoid the translation of some cellular and viral mRNAs bearing special features in their 5′ untranslated regions. In addition, PKR affects diverse transcriptional factors such as interferon regulatory factor 1, STATs, p53, activating transcription factor 3, and NF-κB. In particular, how PKR triggers a cascade of events involving IKK phosphorylation of IκB and NF-κB nuclear translocation has been intensively studied. At the cellular and organism levels PKR exerts antiproliferative effects, and it is a key antiviral agent. A point of convergence in both effects is that PKR activation results in apoptosis induction. The extent and strength of the antiviral action of PKR are clearly understood by the findings that unrelated viral proteins of animal viruses have evolved to inhibit PKR action by using diverse strategies. The case for the pathological consequences of the antiproliferative action of PKR is less understood, but therapeutic strategies aimed at targeting PKR are beginning to offer promising results.

Effect of caffeine on the growth and photosynthetic efficiency of marine macroalgae

2021 ◽  
Vol 64 (1) ◽  
pp. 13-18
Author(s):  
Ira Gray ◽  
Lindsay A. Green-Gavrielidis ◽  
Carol Thornber
Keyword(s):  
Growth Rate ◽  
Photosynthetic Efficiency ◽  
Sublethal Effects ◽  
Marine Species ◽  
Marine Organisms ◽  
Marine Macroalgae ◽  
Chondrus Crispus ◽  
Coastal Environments ◽  
Codium Fragile ◽  
High Concentrations

Abstract Caffeine is present in coastal environments worldwide and there is a need to assess its impact on marine organisms. Here, we exposed two species of ecologically important marine macroalgae (Chondrus crispus and Codium fragile subsp. fragile) to a suite of caffeine concentrations and measured their response. Caffeine concentrations of 10–100 ng L−1 had no significant effect on the growth rate or photosynthetic efficiency of either algae. Extremely high concentrations (100–200 mg L−1), which may occur acutely, produced sublethal effects for both species and mortality in C. fragile subsp. fragile. Our results highlight the need to understand how caffeine impacts marine species.

Role of the ligand in intracellular receptor function: receptor affinity determines activation in vitro of the latent dioxin receptor to a DNA-binding form

1991 ◽  
Vol 11 (1) ◽  
pp. 401-411
Author(s):  
S Cuthill ◽  
A Wilhelmsson ◽  
L Poellinger
Keyword(s):  
Dna Binding ◽  
Cellular Response ◽  
Molecular Mechanisms ◽  
Nuclear Translocation ◽  
Rank Order ◽  
Receptor Ligands ◽  
Free System ◽  
Dioxin Receptor

To reconstitute the molecular mechanisms underlying the cellular response to soluble receptor ligands, we have exploited a cell-free system that exhibits signal- (dioxin-)induced activation of the latent cytosolic dioxin receptor to an active DNA-binding species. The DNA-binding properties of the in vitro-activated form were qualitatively indistinguishable from those of in vivo-activated nuclear receptor extracted from dioxin-treated cells. In vitro activation of the receptor by dioxin was dose dependent and was mimicked by other dioxin receptor ligands in a manner that followed the rank order of their relative affinities for the receptor in vitro and their relative potencies to induce target gene transcription in vivo. Thus, in addition to triggering the initial release of inhibition of DNA binding and presumably allowing nuclear translocation, the ligand appears to play a crucial role in the direct control of the level of functional activity of a given ligand-receptor complex.

scholarly journals p85α Acts as a Novel Signal Transducer for Mediation of Cellular Apoptotic Response to UV Radiation

2007 ◽  
Vol 27 (7) ◽  
pp. 2713-2731 ◽  
Author(s):  
Lun Song ◽  
Jingxia Li ◽  
Jianping Ye ◽  
Gang Yu ◽  
Jin Ding ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Uv Radiation ◽  
Gene Transcription ◽  
Cell Apoptosis ◽  
Cellular Response ◽  
Nuclear Translocation ◽  
Site Directed Mutagenesis ◽  
Regulatory Subunit ◽  
Special Effect ◽  
Tnf Α

ABSTRACT Apoptosis is an important cellular response to UV radiation (UVR), but the corresponding mechanisms remain largely unknown. Here we report that the p85α regulatory subunit of phosphatidylinositol 3-kinase (PI-3K) exerted a proapoptotic role in response to UVR through the induction of tumor necrosis factor alpha (TNF-α) gene expression. This special effect of p85α was unrelated to the PI-3K-dependent signaling pathway. Further evidence demonstrated that the inducible transcription factor NFAT3 was the major downstream target of p85α for the mediation of UVR-induced apoptosis and TNF-α gene transcription. p85α regulated UVR-induced NFAT3 activation by modulation of its nuclear translocation and DNA binding and the relevant transcriptional activities. Gel shift assays and site-directed mutagenesis allowed the identification of two regions in the TNF-α gene promoter that served as the NFAT3 recognition sequences. Chromatin immunoprecipitation assays further confirmed that the recruitment of NFAT3 to the endogenous TNF-α promoter was regulated by p85α upon UVR exposure. Finally, the knockdown of the NFAT3 level by its specific small interfering RNA decreased UVR-induced TNF-α gene transcription and cell apoptosis. The knockdown of endogenous p85α blocked NFAT activity and TNF-α gene transcription, as well as cell apoptosis. Thus, we demonstrated p85α-associated but PI-3K-independent cell death in response to UVR and identified a novel p85α/NFAT3/TNF-α signaling pathway for the mediation of cellular apoptotic responses under certain stress conditions such as UVR.

scholarly journals Cytoskeleton reorganization of spreading cells on micro-patterned islands: a functional model

2010 ◽  
Vol 368 (1920) ◽  
pp. 2629-2652 ◽  
Author(s):  
Y. Loosli ◽  
R. Luginbuehl ◽  
J. G. Snedeker
Keyword(s):  
Cell Biology ◽  
Cellular Response ◽  
Cell Model ◽  
Numerical Models ◽  
Mechanistic Model ◽  
Functional Model ◽  
Cell Spreading ◽  
Cellular Interaction

Predictive numerical models of cellular response to biophysical cues have emerged as a useful quantitative tool for cell biology research. Cellular experiments in silico can augment in vitro and in vivo investigations by filling gaps in what is possible to achieve through ‘wet work’. Biophysics-based numerical models can be used to verify the plausibility of mechanisms regulating tissue homeostasis derived from experiments. They can also be used to explore potential targets for therapeutic intervention. In this perspective article we introduce a single cell model developed towards the design of novel biomaterials to elicit a regenerative cellular response for the repair of diseased tissues. The model is governed by basic mechanisms of cell spreading (lamellipodial and filopodial extension, formation of cell–matrix adhesions, actin reinforcement) and is developed in the context of cellular interaction with functionalized substrates that present defined points of potential adhesion. To provide adequate context, we first review the biophysical underpinnings of the model as well as reviewing existing cell spreading models. We then present preliminary benchmarking of the model against published experiments of cell spreading on micro-patterned substrates. Initial results indicate that our mechanistic model may represent a potentially useful approach in a better understanding of cell interactions with the extracellular matrix.

scholarly journals A drug-compatible and temperature-controlled microfluidic device for live-cell imaging

Open Biology ◽  
2016 ◽  
Vol 6 (8) ◽  
pp. 160156 ◽  
Author(s):  
Tong Chen ◽  
Blanca Gomez-Escoda ◽  
Javier Munoz-Garcia ◽  
Julien Babic ◽  
Laurent Griscom ◽  
...  
Keyword(s):  
Cell Biology ◽  
Live Cell Imaging ◽  
Cell Imaging ◽  
Critical Issue ◽  
Growth Conditions ◽  
Medium Composition ◽  
Live Cell ◽  
Model Systems ◽  
Dynamic Regulation ◽  
Cellular Environment

Monitoring cellular responses to changes in growth conditions and perturbation of targeted pathways is integral to the investigation of biological processes. However, manipulating cells and their environment during live-cell-imaging experiments still represents a major challenge. While the coupling of microfluidics with microscopy has emerged as a powerful solution to this problem, this approach remains severely underexploited. Indeed, most microdevices rely on the polymer polydimethylsiloxane (PDMS), which strongly absorbs a variety of molecules commonly used in cell biology. This effect of the microsystems on the cellular environment hampers our capacity to accurately modulate the composition of the medium and the concentration of specific compounds within the microchips, with implications for the reliability of these experiments. To overcome this critical issue, we developed new PDMS-free microdevices dedicated to live-cell imaging that show no interference with small molecules. They also integrate a module for maintaining precise sample temperature both above and below ambient as well as for rapid temperature shifts. Importantly, changes in medium composition and temperature can be efficiently achieved within the chips while recording cell behaviour by microscopy. Compatible with different model systems, our platforms provide a versatile solution for the dynamic regulation of the cellular environment during live-cell imaging.

scholarly journals From imaging to understanding: Frontiers in Live Cell Imaging, Bethesda, MD, April 19–21, 2006

2006 ◽  
Vol 174 (4) ◽  
pp. 481-484 ◽  
Author(s):  
Yu-li Wang ◽  
Klaus M. Hahn ◽  
Robert F. Murphy ◽  
Alan F. Horwitz
Keyword(s):  
Cell Biology ◽  
Live Cell Imaging ◽  
Recent Progress ◽  
Cell Imaging ◽  
Live Cell ◽  
The Other ◽  
Biological Applications ◽  
Research Fields ◽  
Recent Meeting ◽  
The One

A recent meeting entitled Frontiers in Live Cell Imaging was attended by more than 400 cell biologists, physicists, chemists, mathematicians, and engineers. Unlike typical special topics meetings, which bring together investigators in a defined field primarily to review recent progress, the purpose of this meeting was to promote cross-disciplinary interactions by introducing emerging methods on the one hand and important biological applications on the other. The goal was to turn live cell imaging from a “technique” used in cell biology into a new exploratory science that combines a number of research fields.

scholarly journals p66 Shc Couples Mechanical Signals to RhoA through Focal Adhesion Kinase-Dependent Recruitment of p115-RhoGEF and GEF-H1

2016 ◽  
Vol 36 (22) ◽  
pp. 2824-2837 ◽  
Author(s):  
Ru-Feng Wu ◽  
Chengxu Liao ◽  
Guosheng Fu ◽  
Heather N. Hayenga ◽  
Kejia Yang ◽  
...  
Keyword(s):  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Cellular Response ◽  
Nuclear Translocation ◽  
Mechanical Stimuli ◽  
Rhoa Activation ◽  
Ras Activation ◽  
P115 Rhogef ◽  
Necessary And Sufficient ◽  
Rho Gef

Tissue cells respond to changes in tensional forces with proliferation or death through the control of RhoA. However, the response coupling mechanisms that link force with RhoA activation are poorly understood. We found that tension applied to fibronectin-coated microbeads caused recruitment of all three isoforms of the Shc adapter (p66 Shc , p52 Shc , and p46 Shc ) to adhesion complexes. The Shc PTB domain was necessary and sufficient for this recruitment, and screening studies revealed the direct interactions with the FERM domain of focal adhesion kinase (FAK) that were required for Shc translocation to adhesion complexes. The FAK/p66 Shc complex specifically bound and activated the Rho guanyl exchange factors (GEFs) p115-RhoGEF and GEF-H1, leading to tension-induced RhoA activation. In contrast, the FAK/p52 Shc complex bound SOS1 but not the Rho GEFs to mediate tension-induced Ras activation. Nuclear translocation and activation of the YAP/TAZ transcription factors on firm substrates required the FAK/p66 Shc /Rho GEF complex, and both proliferation on firm substrates and anoikis in suspension required signaling through p66 Shc and its associated Rho GEFs. These studies reveal the binary and exclusive assignment of p66 Shc and p52 Shc to tension-induced Rho or Ras signals, respectively, and suggest an integrated role for the two Shc isoforms in coordinating the cellular response to mechanical stimuli.

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