Symmetry-breaking in mammalian cell cohort migration during tissue pattern formation: Role of random-walk persistence

2005 ◽  
Vol 61 (4) ◽  
pp. 201-213 ◽  
Author(s):  
S. Huang ◽  
C.P. Brangwynne ◽  
K.K. Parker ◽  
D.E. Ingber
Keyword(s):  
Random Walk ◽  
Pattern Formation ◽  
Symmetry Breaking ◽  
Mammalian Cell

Centrosome Aurora A gradient ensures single polarity axis in C. elegans embryos

2020 ◽  
Vol 48 (3) ◽  
pp. 1243-1253 ◽  
Author(s):  
Sukriti Kapoor ◽  
Sachin Kotak
Keyword(s):  
Symmetry Breaking ◽  
Cell Fate ◽  
Cell Cortex ◽  
Axis Formation ◽  
Aurora A Kinase ◽  
Aurora A ◽  
C Elegans ◽  
Cell Embryo ◽  
Polarity Establishment

Cellular asymmetries are vital for generating cell fate diversity during development and in stem cells. In the newly fertilized Caenorhabditis elegans embryo, centrosomes are responsible for polarity establishment, i.e. anterior–posterior body axis formation. The signal for polarity originates from the centrosomes and is transmitted to the cell cortex, where it disassembles the actomyosin network. This event leads to symmetry breaking and the establishment of distinct domains of evolutionarily conserved PAR proteins. However, the identity of an essential component that localizes to the centrosomes and promotes symmetry breaking was unknown. Recent work has uncovered that the loss of Aurora A kinase (AIR-1 in C. elegans and hereafter referred to as Aurora A) in the one-cell embryo disrupts stereotypical actomyosin-based cortical flows that occur at the time of polarity establishment. This misregulation of actomyosin flow dynamics results in the occurrence of two polarity axes. Notably, the role of Aurora A in ensuring a single polarity axis is independent of its well-established function in centrosome maturation. The mechanism by which Aurora A directs symmetry breaking is likely through direct regulation of Rho-dependent contractility. In this mini-review, we will discuss the unconventional role of Aurora A kinase in polarity establishment in C. elegans embryos and propose a refined model of centrosome-dependent symmetry breaking.

scholarly journals Instability of the marginal commutative model of tunneling centers interacting with a metallic environment: Role of the electron-hole symmetry breaking

1997 ◽  
Vol 56 (20) ◽  
pp. 12947-12960 ◽  
Author(s):  
A. Zawadowski ◽  
G. Zaránd ◽  
P. Nozières ◽  
K. Vladár ◽  
G. T. Zimányi
Keyword(s):  
Symmetry Breaking ◽  
Electron Hole ◽  
Tunneling Centers

Role of Nuclei in Liesegang Pattern Formation: Insights from Experiment and Reaction-Diffusion Simulation

2018 ◽  
Vol 122 (6) ◽  
pp. 3669-3676 ◽  
Author(s):  
Masaki Itatani ◽  
Qing Fang ◽  
Kei Unoura ◽  
Hideki Nabika
Keyword(s):  
Pattern Formation ◽  
Reaction Diffusion ◽  
Diffusion Simulation

Citral, an inhibitor of retinoic acid synthesis, modifies pattern formation during limb regeneration in the axolotl Ambystoma mexicanum

1999 ◽  
Vol 77 (11) ◽  
pp. 1835-1837 ◽  
Author(s):  
Steven R Scadding
Keyword(s):  
Retinoic Acid ◽  
Pattern Formation ◽  
Limb Regeneration ◽  
Acid Synthesis ◽  
Ambystoma Mexicanum

While the effects of exogenous retinoids on amphibian limb regeneration have been studied extensively, the role of endogenous retinoids is not clear. Hence, I wished to investigate the role of endogenous retinoic acid during axolotl limb regeneration. Citral is a known inhibitor of retinoic acid synthesis. Thus, I treated regenerating limbs of the larval axolotl Ambystoma mexicanum with citral. The result of this inhibition of retinoic acid synthesis was that limb regeneration became extremely irregular and hypomorphic, with serious pattern defects, or was inhibited altogether. I conclude that endogenous retinoic acid plays an important role in pattern formation during limb regeneration.

‘Generic’ physical mechanisms of morphogenesis and pattern formation

Development ◽  
1990 ◽  
Vol 110 (1) ◽  
pp. 1-18 ◽  
Author(s):  
S.A. Newman ◽  
W.D. Comper
Keyword(s):  
Pattern Formation ◽  
Reaction Diffusion ◽  
Physical Mechanisms ◽  
Extracellular Matrix Components ◽  
Genetic Mechanisms ◽  
Chemical Waves ◽  
Phylogenetic Lineages ◽  
Living Tissues ◽  
Highly Evolved

The role of ‘generic’ physical mechanisms in morphogenesis and pattern formation of tissues is considered. Generic mechanisms are defined as those physical processes that are broadly applicable to living and non-living systems, such as adhesion, surface tension and gravitational effects, viscosity, phase separation, convection and reaction-diffusion coupling. They are contrasted with ‘genetic’ mechanisms, a term reserved for highly evolved, machine-like, biomolecular processes. Generic mechanisms acting upon living tissues are capable of giving rise to morphogenetic rearrangements of cytoplasmic, tissue and extracellular matrix components, sometimes leading to ‘microfingers’, and to chemical waves or stripes. We suggest that many morphogenetic and patterning effects are the inevitable outcome of recognized physical properties of tissues, and that generic physical mechanisms that act on these properties are complementary to, and interdependent with genetic mechanisms. We also suggest that major morphological reorganizations in phylogenetic lineages may arise by the action of generic physical mechanisms on developing embryos. Subsequent evolution of genetic mechanisms could stabilize and refine developmental outcomes originally guided by generic effects.

Reorganization of membrane contacts prior to apoptosis in the Drosophila retina: the role of the IrreC-rst protein

Development ◽  
1996 ◽  
Vol 122 (6) ◽  
pp. 1931-1940 ◽  
Author(s):  
C. Reiter ◽  
T. Schimansky ◽  
Z. Nie ◽  
K.F. Fischbach
Keyword(s):  
Pattern Formation ◽  
Pigment Cells ◽  
Immunoglobulin Superfamily ◽  
Specific Cell ◽  
Axonal Pathfinding ◽  
Single Row ◽  
Cell Contacts ◽  
Regulated Expression ◽  
Membrane Contacts

The final step of pattern formation in the developing retina of Drosophila is the elimination of excess cells between ommatidia and the differentiation of the remaining cells into secondary and tertiary pigment cells. Temporally and spatially highly regulated expression of the irregular chiasmC-roughest protein, an adhesion molecule of the immunoglobulin superfamily known to be involved in axonal pathfinding, is essential for correct sorting of cell-cell contacts in the pupal retina without which the ensuing wave of apoptosis does not occur. Irregular chiasmC-roughest accumulates strongly at the borders between primary pigment and interommatidial cells. Mutant and misexpression analysis show that this accumulation of the irregular chiasmC-roughest protein is necessary for aligning interommatidial cells in a single row. This reorganisation is a prerequisite for the identification of death candidates. Irregular chiasmC-roughest function in retinal development demonstrates the importance of specific cell contacts for assignment of the apoptotic fate.

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