scholarly journals Microtubule-based localization of a synaptic calcium-signaling complex is required for left-right neuronal asymmetry in C. elegans

Development ◽  
2011 ◽  
Vol 138 (16) ◽  
pp. 3509-3518 ◽  
Author(s):  
Chieh Chang ◽  
Yi-Wen Hsieh ◽  
Bluma J. Lesch ◽  
Cornelia I. Bargmann ◽  
Chiou-Fen Chuang
Keyword(s):  
Calcium Signaling ◽  
C Elegans ◽  
Signaling Complex ◽  
Neuronal Asymmetry

scholarly journals Stochastic left–right neuronal asymmetry in Caenorhabditis elegans

2016 ◽  
Vol 371 (1710) ◽  
pp. 20150407 ◽  
Author(s):  
Amel Alqadah ◽  
Yi-Wen Hsieh ◽  
Rui Xiong ◽  
Chiou-Fen Chuang
Keyword(s):  
Caenorhabditis Elegans ◽  
Molecular Mechanisms ◽  
Neurological Diseases ◽  
Calcium Signalling ◽  
Model Organism ◽  
Brain Asymmetry ◽  
C Elegans ◽  
Left And Right ◽  
Left Right Asymmetry ◽  
Neuronal Asymmetry

Left–right asymmetry in the nervous system is observed across species. Defects in left–right cerebral asymmetry are linked to several neurological diseases, but the molecular mechanisms underlying brain asymmetry in vertebrates are still not very well understood. The Caenorhabditis elegans left and right amphid wing ‘C’ (AWC) olfactory neurons communicate through intercellular calcium signalling in a transient embryonic gap junction neural network to specify two asymmetric subtypes, AWC OFF (default) and AWC ON (induced), in a stochastic manner. Here, we highlight the molecular mechanisms that establish and maintain stochastic AWC asymmetry. As the components of the AWC asymmetry pathway are highly conserved, insights from the model organism C. elegans may provide a window onto how brain asymmetry develops in humans. This article is part of the themed issue ‘Provocative questions in left–right asymmetry’.

scholarly journals Engagement of the Human Pre-B Cell Receptor Generates a Lipid Raft–Dependent Calcium Signaling Complex

Immunity ◽  
2000 ◽  
Vol 13 (2) ◽  
pp. 243-253 ◽  
Author(s):  
Beichu Guo ◽  
Roberta M Kato ◽  
Maria Garcia-Lloret ◽  
Matthew I Wahl ◽  
David J Rawlings
Keyword(s):  
Calcium Signaling ◽  
B Cell ◽  
Lipid Raft ◽  
Cell Receptor ◽  
B Cell Receptor ◽  
Signaling Complex

scholarly journals Kinase Suppressor of Ras Forms a Multiprotein Signaling Complex and Modulates MEK Localization

1999 ◽  
Vol 19 (8) ◽  
pp. 5523-5534 ◽  
Author(s):  
Scott Stewart ◽  
Meera Sundaram ◽  
Yanping Zhang ◽  
Jeeyong Lee ◽  
Min Han ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Mitogen Activated Protein Kinase ◽  
Scaffolding Protein ◽  
Ras Signaling ◽  
Loss Of Function ◽  
C Elegans ◽  
Signaling Complex ◽  
Independent Functions ◽  
Kinase Suppressor Of Ras ◽  
Mitogen Activated Protein

ABSTRACT Genetic screens for modifiers of activated Ras phenotypes have identified a novel protein, kinase suppressor of Ras (KSR), which shares significant sequence homology with Raf family protein kinases. Studies using Drosophila melanogaster andCaenorhabditis elegans predict that KSR positively regulates Ras signaling; however, the function of mammalian KSR is not well understood. We show here that two predicted kinase-dead mutants of KSR retain the ability to complement ksr-1 loss-of-function alleles in C. elegans, suggesting that KSR may have physiological, kinase-independent functions. Furthermore, we observe that murine KSR forms a multimolecular signaling complex in human embryonic kidney 293T cells composed of HSP90, HSP70, HSP68, p50CDC37, MEK1, MEK2, 14-3-3, and several other, unidentified proteins. Treatment of cells with geldanamycin, an inhibitor of HSP90, decreases the half-life of KSR, suggesting that HSPs may serve to stabilize KSR. Both nematode and mammalian KSRs are capable of binding to MEKs, and three-point mutants of KSR, corresponding to C. elegans loss-of-function alleles, are specifically compromised in MEK binding. KSR did not alter MEK activity or activation. However, KSR-MEK binding shifts the apparent molecular mass of MEK from 44 to >700 kDa, and this results in the appearance of MEK in membrane-associated fractions. Together, these results suggest that KSR may act as a scaffolding protein for the Ras-mitogen-activated protein kinase pathway.

scholarly journals Hypoxia-induced Acidosis Uncouples the STIM-Orai Calcium Signaling Complex

2011 ◽  
Vol 286 (52) ◽  
pp. 44788-44798 ◽  
Author(s):  
Salvatore Mancarella ◽  
Youjun Wang ◽  
Xiaoxiang Deng ◽  
Gavin Landesberg ◽  
Rosario Scalia ◽  
...  
Keyword(s):  
Calcium Signaling ◽  
Signaling Complex

scholarly journals Intercellular calcium signaling in a gap junction-coupled cell network establishes asymmetric neuronal fates in C. elegans

Development ◽  
2012 ◽  
Vol 139 (22) ◽  
pp. 4191-4201 ◽  
Author(s):  
J. A. Schumacher ◽  
Y.-W. Hsieh ◽  
S. Chen ◽  
J. K. Pirri ◽  
M. J. Alkema ◽  
...  
Keyword(s):  
Calcium Signaling ◽  
Gap Junction ◽  
C Elegans ◽  
Cell Network

scholarly journals Rictor/TORC2 mediates gut-to-brain signaling in the regulation of phenotypic plasticity in C. elegans

2017 ◽  
Author(s):  
Michael P. O’Donnell ◽  
Pin-Hao Chao ◽  
Jan E. Kammenga ◽  
Piali Sengupta
Keyword(s):  
Nervous System ◽  
Internal State ◽  
Environmental Signals ◽  
C Elegans ◽  
Signaling Complex ◽  
External Cues ◽  
Nervous System Function ◽  
Sensory Nervous System ◽  
Neuronal Functions ◽  
Available Information

ABSTRACTAnimals integrate external cues with information about internal conditions such as metabolic state to execute the appropriate behavioral and developmental decisions. Information about food quality and quantity is assessed by the intestine and transmitted to modulate neuronal functions via mechanisms that are not fully understood. The conserved Target of Rapamycin complex 2 (TORC2) controls multiple processes in response to cellular stressors and growth factors. Here we show that TORC2 coordinates larval development and adult behaviors in response to environmental cues and feeding state in the bacterivorous nematode C. elegans. During development, pheromone, bacterial food, and temperature regulate expression of the daf-7 TGF-β and daf-28 insulin-like peptide in sensory neurons to promote a binary decision between reproductive growth and entry into the alternate dauer larval stage. We find that TORC2 acts in the intestine to regulate neuronal expression of both daf-7 and daf-28, which together reflect bacterial-diet dependent feeding status, thus providing a mechanism for integration of food signals with external cues in the regulation of neuroendocrine gene expression. In the adult, TORC2 similarly acts in the intestine to modulate food-regulated foraging behaviors via the PDFR-1 neuropeptide receptor. We also demonstrate that genetic variation affects food-dependent larval and adult phenotypes, and identify quantitative trait loci (QTL) associated with these traits.Together, these results suggest that TORC2 acts as a hub for communication of feeding state information from the gut to the brain, thereby contributing to modulation of neuronal function by internal state.AUTHOR SUMMARYDecision-making in all animals, including humans, involves weighing available information about the external environment as well as the animals’ internal conditions. Information about the environment is obtained via the sensory nervous system, whereas internal state can be assessed via cues such as levels of hormones or nutrients. How multiple external and internal inputs are processed in the nervous system to drive behavior or development is not fully understood. In this study, we examine how the nematode C. elegans integrates dietary information received by the gut with environmental signals to alter nervous system function. We have found that a signaling complex, called TORC2, acts in the gut to relay nutrition signals to alter hormonal signaling by the nervous system in C. elegans. Altered neuronal signaling in turn affects a food-dependent binary developmental decision in larvae, as well as food-dependent foraging behaviors in adults. Our results provide a mechanism by which animals prioritize specific signals such as feeding status to appropriately alter their development and/or behavior.

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