Eleutheroside E Enhances the Long-Term Memory of Radiation-Damaged C. elegans through G-Protein-Coupled Receptor and Neuropeptide Signaling Pathways

2020 ◽  
Vol 83 (11) ◽  
pp. 3315-3323
Author(s):  
Mengyao Liu ◽  
Yi Xiong ◽  
Shan Shan ◽  
Yuanbing Zhu ◽  
Deyong Zeng ◽  
...  
2003 ◽  
Vol 31 (5) ◽  
pp. 1001-1005 ◽  
Author(s):  
F. Daumas ◽  
N. Destainville ◽  
C. Millot ◽  
A. Lopez ◽  
D. Dean ◽  
...  

The monitoring of the movements of membrane proteins (or lipids) by single-particle tracking enables one to obtain reliable insights into the complex dynamic organization of the plasma membrane constituents. Using this technique, we investigated the diffusional behaviour of a G-protein-coupled receptor. The trajectories of the receptors revealed a diffusion mode combining a short-term rapid confined diffusion with a long-term slow diffusion. A detailed statistical analysis shows that the receptors have a diffusion confined to a domain which itself diffuses, the confinement being due to long-range attractive inter-protein interactions. The existing models of the dynamic organization of the cell membrane cannot explain our results. We propose a theoretical Brownian model of interacting proteins that is consistent with the experimental observations and accounts for the variations found as a function of the domain size of the short-term and long-term diffusion coefficients.


2018 ◽  
Vol 6 (4) ◽  
pp. 28 ◽  
Author(s):  
Daniel Matúš ◽  
Simone Prömel

Many vital processes during C. elegans development, especially the establishment and maintenance of cell polarity in embryogenesis, are controlled by complex signaling pathways. G protein-coupled receptors (GPCRs), such as the four Frizzled family Wnt receptors, are linchpins in regulating and orchestrating several of these mechanisms. However, despite being GPCRs, which usually couple to G proteins, these receptors do not seem to activate classical heterotrimeric G protein-mediated signaling cascades. The view on signaling during embryogenesis is further complicated by the fact that heterotrimeric G proteins do play essential roles in cell polarity during embryogenesis, but their activity is modulated in a predominantly GPCR-independent manner via G protein regulators such as GEFs GAPs and GDIs. Further, the triggered downstream effectors are not typical. Only very few GPCR-dependent and G protein-mediated signaling pathways have been unambiguously defined in this context. This unusual and highly intriguing concept of separating GPCR function and G-protein activity, which is not restricted to embryogenesis in C. elegans but can also be found in other organisms, allows for essential and multi-faceted ways of regulating cellular communication and response. Although its relevance cannot be debated, its impact is still poorly discussed, and C. elegans is an ideal model to understand the underlying principles.


2020 ◽  
Author(s):  
Miguel A. Casal ◽  
Santiago Galella ◽  
Oscar Vilarroya ◽  
Jordi Garcia-Ojalvo

Neuronal networks provide living organisms with the ability to process information. They are also characterized by abundant recurrent connections, which give rise to strong feed-back that dictates their dynamics and endows them with fading (short-term) memory. The role of recurrence in long-term memory, on the other hand, is still unclear. Here we use the neuronal network of the roundworm C. elegans to show that recurrent architectures in living organisms can exhibit long-term memory without relying on specific hard-wired modules. A genetic algorithm reveals that the experimentally observed dynamics of the worm’s neuronal network exhibits maximal complexity (as measured by permutation entropy). In that complex regime, the response of the system to repeated presentations of a time-varying stimulus reveals a consistent behavior that can be interpreted as soft-wired long-term memory.A common manifestation of our ability to remember the past is the consistence of our responses to repeated presentations of stimuli across time. Complex chaotic dynamics is known to produce such reliable responses in spite of its characteristic sensitive dependence on initial conditions. In neuronal networks, complex behavior is known to result from a combination of (i) recurrent connections and (ii) a balance between excitation and inhibition. Here we show that those features concur in the neuronal network of a living organism, namely C. elegans. This enables long-term memory to arise in an on-line manner, without having to be hard-wired in the brain.


Neurosignals ◽  
2002 ◽  
Vol 11 (1) ◽  
pp. 34-44 ◽  
Author(s):  
Mariana M. Belcheva ◽  
Carmine J. Coscia

2016 ◽  
Vol 291 (15) ◽  
pp. 7809-7820 ◽  
Author(s):  
Jianxin Hu ◽  
Matthew Stern ◽  
Luis E. Gimenez ◽  
Lizzy Wanka ◽  
Lu Zhu ◽  
...  

2009 ◽  
Vol 83 (16) ◽  
pp. 8141-8152 ◽  
Author(s):  
Joseph D. Sherrill ◽  
Melissa P. Stropes ◽  
Olivia D. Schneider ◽  
Diana E. Koch ◽  
Fabiola M. Bittencourt ◽  
...  

ABSTRACT The presence of numerous G protein-coupled receptor (GPCR) homologs within the herpesvirus genomes suggests an essential role for these genes in viral replication in the infected host. Such is the case for murine cytomegalovirus (MCMV), where deletion of the M33 GPCR or replacement of M33 with a signaling defective mutant has been shown to severely attenuate replication in vivo. In the present study we utilized a genetically altered version of M33 (termed R131A) in combination with pharmacological inhibitors to further characterize the mechanisms by which M33 activates downstream signaling pathways. This R131A mutant of M33 fails to support salivary gland replication in vivo and, as such, is an important tool that can be used to examine the signaling activities of M33. We show that M33 stimulates the transcription factor CREB via heterotrimeric Gq/11 proteins and not through promiscuous coupling of M33 to the Gs pathway. Using inhibitors of signaling molecules downstream of Gq/11, we demonstrate that M33 stimulates CREB transcriptional activity in a phospholipase C-β and protein kinase C (PKC)-dependent manner. Finally, utilizing wild-type and R131A versions of M33, we show that M33-mediated activation of other signaling nodes, including the mitogen-activated protein kinase family member p38α and transcription factor NF-κB, occurs in the absence of Gq/11 and PKC signaling. The results from the present study indicate that M33 utilizes multiple mechanisms to modulate intracellular signaling cascades and suggest that signaling through PLC-β and PKC plays a central role in MCMV pathogenesis in vivo.


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