Automatic Segmentation of the Corpus Callosum Using a Cell-Competition Algorithm

2015 ◽  
Vol 39 (5) ◽  
pp. 781-786 ◽  
Author(s):  
Shiou-Ping Lee ◽  
Chien-Sheng Wu ◽  
Jie-Zhi Cheng ◽  
Chung-Ming Chen ◽  
Yu-Chiang Chen ◽  
...  
Keyword(s):  
Corpus Callosum ◽  
Automatic Segmentation ◽  
Cell Competition ◽  
A Cell

scholarly journals Ephrin-B3 controls excitatory synapse density through cell-cell competition for EphBs

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Nathan T Henderson ◽  
Sylvain J Le Marchand ◽  
Martin Hruska ◽  
Simon Hippenmeyer ◽  
Liqun Luo ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Spine Density ◽  
Cell Competition ◽  
Intrinsic Factors ◽  
Genetic Mouse Model ◽  
Synapse Density ◽  
A Cell ◽  
Cell Cell

Cortical networks are characterized by sparse connectivity, with synapses found at only a subset of axo-dendritic contacts. Yet within these networks, neurons can exhibit high connection probabilities, suggesting that cell-intrinsic factors, not proximity, determine connectivity. Here, we identify ephrin-B3 (eB3) as a factor that determines synapse density by mediating a cell-cell competition that requires ephrin-B-EphB signaling. In a microisland culture system designed to isolate cell-cell competition, we find that eB3 determines winning and losing neurons in a contest for synapses. In a Mosaic Analysis with Double Markers (MADM) genetic mouse model system in vivo the relative levels of eB3 control spine density in layer 5 and 6 neurons. MADM cortical neurons in vitro reveal that eB3 controls synapse density independently of action potential-driven activity. Our findings illustrate a new class of competitive mechanism mediated by trans-synaptic organizing proteins which control the number of synapses neurons receive relative to neighboring neurons.

scholarly journals Neuroepithelial cell competition triggers loss of cellular juvenescence

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Faidruz Azura Jam ◽  
Takao Morimune ◽  
Atsushi Tsukamura ◽  
Ayami Tano ◽  
Yuya Tanaka ◽  
...  
Keyword(s):  
Interaction Mechanism ◽  
Cell Interaction ◽  
Neuroepithelial Cell ◽  
Cell Competition ◽  
Early Brain Development ◽  
Associated Proteins ◽  
Model Cell ◽  
A Cell ◽  
Model Expression

Abstract Cell competition is a cell–cell interaction mechanism which maintains tissue homeostasis through selective elimination of unfit cells. During early brain development, cells are eliminated through apoptosis. How cells are selected to undergo elimination remains unclear. Here we aimed to identify a role for cell competition in the elimination of suboptimal cells using an in vitro neuroepithelial model. Cell competition was observed when neural progenitor HypoE-N1 cells expressing RASV12 were surrounded by normal cells in the co-culture. The elimination through apoptosis was observed by cellular changes of RASV12 cells with rounding/fragmented morphology, by SYTOX blue-positivity, and by expression of apoptotic markers active caspase-3 and cleaved PARP. In this model, expression of juvenility-associated genes Srsf7 and Ezh2 were suppressed under cell-competitive conditions. Srsf7 depletion led to loss of cellular juvenescence characterized by suppression of Ezh2, cell growth impairment and enhancement of senescence-associated proteins. The cell bodies of eliminated cells were engulfed by the surrounding cells through phagocytosis. Our data indicates that neuroepithelial cell competition may have an important role for maintaining homeostasis in the neuroepithelium by eliminating suboptimal cells through loss of cellular juvenescence.

A Mathematical Model for Stem Cell Competition to Maintain a Cell Pool Injured by Radiation

2020 ◽  
Vol 194 (4) ◽  
Author(s):  
Kouki Uchinomiya ◽  
Kazuo Yoshida ◽  
Masahiro Kondo ◽  
Masanori Tomita ◽  
Toshiyasu Iwasaki
Keyword(s):  
Mathematical Model ◽  
Stem Cell ◽  
Cell Competition ◽  
Cell Pool ◽  
A Cell

scholarly journals Cell competition corrects noisy Wnt morphogen gradients to achieve robust patterning in the zebrafish embryo

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Yuki Akieda ◽  
Shohei Ogamino ◽  
Hironobu Furuie ◽  
Shizuka Ishitani ◽  
Ryutaro Akiyoshi ◽  
...  
Keyword(s):  
Zebrafish Embryo ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Cell Competition ◽  
Related System ◽  
Morphogen Gradients ◽  
Gradient Formation ◽  
A Cell ◽  
Species Production ◽  
Anterior Posterior

Abstract Morphogen signalling forms an activity gradient and instructs cell identities in a signalling strength-dependent manner to pattern developing tissues. However, developing tissues also undergo dynamic morphogenesis, which may produce cells with unfit morphogen signalling and consequent noisy morphogen gradients. Here we show that a cell competition-related system corrects such noisy morphogen gradients. Zebrafish imaging analyses of the Wnt/β-catenin signalling gradient, which acts as a morphogen to establish embryonic anterior-posterior patterning, identify that unfit cells with abnormal Wnt/β-catenin activity spontaneously appear and produce noise in the gradient. Communication between unfit and neighbouring fit cells via cadherin proteins stimulates apoptosis of the unfit cells by activating Smad signalling and reactive oxygen species production. This unfit cell elimination is required for proper Wnt/β-catenin gradient formation and consequent anterior-posterior patterning. Because this gradient controls patterning not only in the embryo but also in adult tissues, this system may support tissue robustness and disease prevention.

scholarly journals Cell competition corrects noisy Wnt morphogen gradients to achieve robust patterning

2018 ◽  
Author(s):  
Yuki Akieda ◽  
Shohei Ogamino ◽  
Hironobu Furuie ◽  
Shizuka Ishitani ◽  
Ryutaro Akiyoshi ◽  
...  
Keyword(s):  
Reactive Oxygen Species Production ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Cell Competition ◽  
Related System ◽  
Morphogen Gradients ◽  
Gradient Formation ◽  
A Cell ◽  
Species Production ◽  
Anterior Posterior

SUMMARYMorphogen signaling forms an activity gradient and instructs cell identities in a signaling strength-dependent manner to pattern developing tissues. However, developing tissues also undergo dynamic morphogenesis, which may produce cells with unfit morphogen signaling and consequent noisy morphogen gradient. Here we show that a cell competition-related system corrects such noisy morphogen gradients. Zebrafish imaging analyses of the Wnt/β-catenin signaling-gradient, which acts as a morphogen to establish embryonic anterior-posterior patterning, revealed that unfit cells with abnormal Wnt/β-catenin activity spontaneously appear and produce noise in the Wnt/β-catenin-gradient. Communication between the unfit and neighboring fit cells via cadherin proteins stimulates the apoptosis of the unfit cells by activating Smad signaling and reactive oxygen species production. This unfit cell elimination is required for proper Wnt/β-catenin-gradient formation and consequent anterior-posterior patterning. Because this gradient controls patterning not only in the embryo but also in adult tissues, this system may support tissue robustness and disease prevention.

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