scholarly journals An Innexin-Dependent Cell Network Establishes Left-Right Neuronal Asymmetry in C. elegans

Cell ◽  
2007 ◽  
Vol 129 (4) ◽  
pp. 787-799 ◽  
Author(s):  
Chiou-Fen Chuang ◽  
Miri K. VanHoven ◽  
Richard D. Fetter ◽  
Vytas K. Verselis ◽  
Cornelia I. Bargmann
Keyword(s):  
C Elegans ◽  
Cell Network ◽  
Dependent Cell ◽  
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 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 Function of the Tetraspanin CD151–α6β1 Integrin Complex during Cellular Morphogenesis

2002 ◽  
Vol 13 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Xin A. Zhang ◽  
Alexander R. Kazarov ◽  
Xiuwei Yang ◽  
Alexa L. Bontrager ◽  
Christopher S. Stipp ◽  
...  
Keyword(s):  
Network Formation ◽  
Functional Unit ◽  
Dominant Negative ◽  
Dominant Negative Effect ◽  
Nih3t3 Cells ◽  
Cell Network ◽  
Cellular Morphogenesis ◽  
Negative Effect ◽  
Dependent Cell ◽  
Laminin 1

Upon plating on basement membrane Matrigel, NIH3T3 cells formed an anastomosing network of cord-like structures, inhibitable by anti-α6β1 integrin antibodies. For NIH3T3 cells transfected with human CD151 protein, the formation of a cord-like network was also inhibitable by anti-CD151 antibodies. Furthermore, CD151 and α6β1 were physically associated within NIH3T3 cells. On removal of the short 8-amino acid C-terminal CD151 tail (by deletion or exchange), exogenous CD151 exerted a dominant negative effect, as it almost completely suppressed α6β1-dependent cell network formation and NIH3T3 cell spreading on laminin-1 (an α6β1 ligand). Importantly, mutant CD151 retained α6β1 association and did not alter α6β1-mediated cell adhesion to Matrigel. In conclusion, the CD151–α6β1 integrin complex acts as a functional unit that markedly influences cellular morphogenesis, with the CD151 tail being of particular importance in determining the “outside-in” functions of α6β1-integrin that follow ligand engagement. Also, antibodies to α6β1 and CD151 inhibited formation of endothelial cell cord-like networks, thus pointing to possible relevance of CD151–α6β1 complexes during angiogenesis.

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 Lysoptosis is an evolutionarily conserved cell death pathway moderated by intracellular serpins

2022 ◽  
Vol 5 (1) ◽  
Author(s):  
Cliff J. Luke ◽  
Stephanie Markovina ◽  
Misty Good ◽  
Ira E. Wight ◽  
Brian J. Thomas ◽  
...  
Keyword(s):  
Cell Death ◽  
Cathepsin L ◽  
Cysteine Protease Inhibitor ◽  
C Elegans ◽  
Cell Death Pathways ◽  
Cell Death Pathway ◽  
Endogenous Inhibitors ◽  
Regulated Cell Death ◽  
Evolutionarily Conserved ◽  
Dependent Cell

AbstractLysosomal membrane permeabilization (LMP) and cathepsin release typifies lysosome-dependent cell death (LDCD). However, LMP occurs in most regulated cell death programs suggesting LDCD is not an independent cell death pathway, but is conscripted to facilitate the final cellular demise by other cell death routines. Previously, we demonstrated that Caenorhabditis elegans (C. elegans) null for a cysteine protease inhibitor, srp-6, undergo a specific LDCD pathway characterized by LMP and cathepsin-dependent cytoplasmic proteolysis. We designated this cell death routine, lysoptosis, to distinguish it from other pathways employing LMP. In this study, mouse and human epithelial cells lacking srp-6 homologues, mSerpinb3a and SERPINB3, respectively, demonstrated a lysoptosis phenotype distinct from other cell death pathways. Like in C. elegans, this pathway depended on LMP and released cathepsins, predominantly cathepsin L. These studies suggested that lysoptosis is an evolutionarily-conserved eukaryotic LDCD that predominates in the absence of neutralizing endogenous inhibitors.

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