scholarly journals Cell-Fate Determination from Embryo to Cancer Development: Genomic Mechanism Elucidated

2020 ◽  
Vol 21 (13) ◽  
pp. 4581 ◽  
Author(s):  
Masa Tsuchiya ◽  
Alessandro Giuliani ◽  
Kenichi Yoshikawa
Keyword(s):  
Critical Point ◽  
Cell Fate ◽  
Critical State ◽  
Local Level ◽  
Stochastic Perturbation ◽  
Physical Principle ◽  
Cancer Development ◽  
Biological Regulation ◽  
Organizing Center ◽  
Whole Genome Expression

Elucidation of the genomic mechanism that guides the cell-fate change is one of the fundamental issues of biology. We previously demonstrated that whole genome expression is coordinated by the emergence of a critical point at both the cell-population and single-cell levels through the physical principle of self-organized criticality. In this paper, we further examine the genomic mechanism that determines the cell-fate changes from embryo to cancer development. The state of the critical point, acting as the organizing center of the cell fate, determines whether the genome resides in a super- or sub-critical state. In the super-critical state, a specific stochastic perturbation can spread over the entire system through the “genome engine”, an autonomous critical-control genomic system, whereas in the sub-critical state, the perturbation remains at a local level. The cell-fate changes when the genome becomes super-critical. We provide a consistent framework to develop a time-evolutional transition theory for the biological regulation of the cell-fate change.

scholarly journals Cell-Fate Determination from Embryo to Cancer Development: Genomic Mechanism Elucidated

2019 ◽  
Author(s):  
Masa Tsuchiya ◽  
Alessandro Giuliani ◽  
Kenichi Yoshikawa
Keyword(s):  
Critical Point ◽  
Cell Fate ◽  
Critical State ◽  
Local Level ◽  
Stochastic Perturbation ◽  
Physical Principle ◽  
Cancer Development ◽  
Biological Regulation ◽  
Self Organized ◽  
Organizing Center

AbstractThe elucidation of the how and when of a cell-fate change asks for a physically reasonable mechanism allowing to achieve a coordinated switching of thousands of genes within a small and highly packed cell nucleus. We previously demonstrated that whole genome expression is dynamically self-organized through the emergence of a critical point. Furthermore, it has been confirmed that this happens at both the cell-population and single-cell level through the physical principle of self-organized criticality.In this paper, we further examine the genomic mechanism which determines cell-fate changes from embryo to cancer development. The state of the critical point, acting as the organizing center of cell-fate, determines whether the genome resides in a super- or sub-critical state. In the super-critical state, a specific stochastic perturbation can spread over the entire system through the ‘genome engine’ - an autonomous critical-control genomic system, whereas in the sub-critical state, the perturbation remains at a local level. We provide a consistent framework to develop a biological regulation transition theory demonstrating the cell-fate change.

scholarly journals Finite-size transitions in complex membranes

2020 ◽  
Author(s):  
M. Girard ◽  
T. Bereau
Keyword(s):  
Experimental Evidence ◽  
Critical Point ◽  
Finite Size ◽  
Underlying Mechanism ◽  
Large Temperature ◽  
Strong Argument ◽  
Biological Regulation ◽  
Critical Manifold ◽  
Critical Composition ◽  
Dynamics Simulations

ABSTRACTThe lipid raft hypothesis postulates that cell membranes possess some degree of lateral organization. The last decade has seen a large amount of experimental evidence for rafts. Yet, the underlying mechanism remains elusive. One hypothesis that supports rafts relies on the membrane to lie near a critical point. While supported by experimental evidence, the role of regulation is unclear. Using both a lattice model and molecular dynamics simulations, we show that lipid regulation of a many-component membrane can lead to critical behavior over a large temperature range. Across this range, the membrane displays a critical composition due to finite-size effects. This mechanism provides a rationale as to how cells tune their composition without the need for specific sensing mechanisms. It is robust and reproduces important experimentally verified biological trends: membrane-demixing temperature closely follows cell growth temperature, and the composition evolves along a critical manifold. The simplicity of the mechanism provides a strong argument in favor of the critical membrane hypothesis.SIGNIFICANCEWe show that biological regulation of a large amount of phospholipids in membranes naturally leads to a critical composition for finite-size systems. This suggests that regulating a system near a critical point is trivial for cells. These effects vanish logarithmically and therefore can be present in micron-sized systems.

scholarly journals The molecular scattering of light in vapours and in liquids and its relation to the opalescence observed in the critical state

1922 ◽  
Vol 102 (715) ◽  
pp. 151-161 ◽  
Keyword(s):  
Critical Point ◽  
Critical State ◽  
Incident Light ◽  
Wave Length ◽  
Molecular Scattering ◽  
Avogadro’S Number ◽  
Quantitative Manner ◽  
The Mean ◽  
Good Agreement ◽  
Molecular Scattering Of Light

It has long been known that in the immediate vicinity of the critical state, many substances exhibit a strong and characteristic opalescence. In recent years, the phenomenon has been studied by Travers and Usher in the case of carefully purified CS 2 , SO 2 , and ether, by S. Young, by F. B. Young in the case of ether, and in a quantitative manner by Kammerlingh Onnes and Keesom in the case of ethylene. An explanation of the phenomenon on thermodynamic principles as due to the accidental deviations of density arising in the substance was put forward by Smoluchowski. He obtained an expression for the mean fluctuation of density in terms of the compressibility of the substance, and later, Einstein applied Maxwell’s equations of the electromagnetic field to obtain an expression for the intensity of the light scattered in consequence of such deviations of density. He showed that the fraction α of the incident energy scattered in the substance per unit volume is 8 π 3 /27 RT β ( μ 2 – 1) 2 ( μ 2 + 2) 2 /N λ 4 (1) In this, R and N are the gas constant and Avogadro’s number per grammolecule, β is the isothermal compressibility of the substance, μ is the refractive index and λ is the wave-length of the incident light. Keesom tested this formula over a range of 2·35° above the critical point of ethylene and found good agreement except very close to the critical point.

scholarly journals II. On the critical state of gases

1880 ◽  
Vol 30 (200-205) ◽  
pp. 323-329 ◽  
Keyword(s):  
Critical Point ◽  
Critical Points ◽  
Critical State ◽  
Atmospheric Pressure ◽  
Boiling Point ◽  
Chemical Society ◽  
Boiling Points ◽  
Intermediate Condition ◽  
Specific Volumes

In a paper read before the Chemical Society, in May, 1879, I gave an account of a method of determining what is termed by Kopp the “specific volumes” of liquids; that was shown to be the volume of liquid at its boiling-point, at ordinary atmospheric pressure, obtainable from 22,326 volumes of its gas, supposed to exist at 0°. Being desirous of extending these researches, with the view of ascertaining such relations at higher temperatures, since April, 1879, I have made numerous experiments, the results of, and deductions from which I hope to publish before long. The temperatures observed vary from the boiling-points of the liquids examined, to about 50° above their critical points; and in course of these experiments I have noticed some curious facts, which may not be unworthy of the attention of the Society. It is well known that at temperatures above that which produces what is termed by Dr. Andrews the “critical point” of a liquid, the substance is supposed to exist in a peculiar condition, and Dr Andrews purposely abstained from speculating on the nature of the matter, whether it be liquid or gaseous, or in an intermediate condition, to which no name has been given. As my observations bear directly on this point, it may be advisable first to describe the experiments I have made, and then to draw the deductions which appear to follow from them.

scholarly journals Cell- and non-cell-autonomous ARF3 coordinates meristem proliferation and organ patterning in Arabidopsis

2022 ◽  
Author(s):  
Xigang Liu ◽  
Ke Zhang ◽  
Hao Zhang ◽  
Yanyun Pan ◽  
Lin Guo ◽  
...  
Keyword(s):  
Cell Fate ◽  
Cell Communication ◽  
Coordination Mechanism ◽  
Cytokinin Activity ◽  
Cytokinin Signaling ◽  
Expression Domain ◽  
Accumulation Pattern ◽  
Organizing Center ◽  
Meristem Maintenance ◽  
Cell Cell

In cell-cell communication, non-cell-autonomous transcription factors play vital roles in controlling plant stem cell fate. We previously reported that AUXIN RESPONSE FACTOR 3 (ARF3), a member of the ARF family with critical roles in floral meristem maintenance and determinacy, has a distinct accumulation pattern that differs from the expression domain of its encoding gene in the shoot apical meristem (SAM). However, the biological meaning of this difference is obscure. Here, we demonstrate that ARF3 expression is mainly activated at the periphery of the SAM by auxin, where ARF3 cell-autonomously regulates the expression of meristem-organ boundary-specific genes, such as CUP-SHAPED COTYLEDON1-3 (CUC1-3), BLADE ON PETIOLE1-2 (BOP1-2) and TARGETS UNDER ETTIN CONTROL3 (TEC3) to determine organ patterning. We also show that ARF3 is translocated into the organizing center, where it represses cytokinin activity and WUSCHEL expression to regulate meristem activity non-cell-autonomously. Therefore, ARF3 acts as a molecular link that mediates the interaction of auxin and cytokinin signaling in the SAM while coordinating the balance between meristem maintenance and organogenesis. Our findings reveal an ARF3-mediated coordination mechanism through cell-cell communication in dynamic SAM maintenance.

scholarly journals A Unified Genomic Mechanism of Cell-Fate Change

2021 ◽  
Author(s):  
Masa Tsuchiya ◽  
Alessandro Giuliani ◽  
Giovanna Zimatore ◽  
Jekaterina Erenpreisa ◽  
Kenichi Yoshikawa
Keyword(s):  
Cell Fate ◽  
Hot Spots ◽  
Center Of Mass ◽  
Local Perturbation ◽  
Whole Genome ◽  
Entire Genome ◽  
Collective Behaviors ◽  
Genome Expression ◽  
Temporal Variance ◽  
Whole Genome Expression

The purpose of our studies is to elucidate the nature of massive control of whole genome expression with a particular emphasis on cell-fate change. Whole genome expression is coordinated by the emergence of a critical point (CP: a peculiar set of bi-phasic genes) through the genome-engine. In response to stimuli, the genome expression self-organizes three critical states, each exhibiting distinct collective behaviors with its center of mass acting as a local attractor, coexisting with whole genome attractor (GA). Genome-engine mechanism accounts for local attractors interaction in phase space. The CP acts as the organizing center of cell-fate change, and its activation makes local perturbation spread over the genome affecting GA. The activation of CP is in turn elicited by hot-spots genes with elevated temporal variance, normally in charge to keep genome expression at pace with microenvironment fluctuations. When hot-spots oscillation exceeds a given threshold, the CP synchronizes with the GA driving genome expression state transition. The expression synchronization wave invading the entire genome depends on the power law fusion-bursting dynamics of silencing pericentromere-associated heterochromatin domains and the consequent folding-unfolding status of transcribing euchromatin domains. The proposed mechanism is a unified step toward a time-evolutional transition theory of biological regulation.

scholarly journals Cell Fate Decision as High-Dimensional Critical State Transition

PLoS Biology ◽  
2016 ◽  
Vol 14 (12) ◽  
pp. e2000640 ◽  
Author(s):  
Mitra Mojtahedi ◽  
Alexander Skupin ◽  
Joseph Zhou ◽  
Ivan G. Castaño ◽  
Rebecca Y. Y. Leong-Quong ◽  
...  
Keyword(s):  
Cell Fate ◽  
Critical State ◽  
State Transition ◽  
High Dimensional ◽  
Cell Fate Decision ◽  
Fate Decision

scholarly journals Plant stem-cell organization and differentiation at single-cell resolution

2020 ◽  
Vol 117 (52) ◽  
pp. 33689-33699
Author(s):  
James W. Satterlee ◽  
Josh Strable ◽  
Michael J. Scanlon
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Cell Differentiation ◽  
Single Cell ◽  
Cell Fate ◽  
Cell Function ◽  
Ectopic Expression ◽  
Cellular Level ◽  
Organizing Center ◽  
Cell Niche

Plants maintain populations of pluripotent stem cells in shoot apical meristems (SAMs), which continuously produce new aboveground organs. We used single-cell RNA sequencing (scRNA-seq) to achieve an unbiased characterization of the transcriptional landscape of the maize shoot stem-cell niche and its differentiating cellular descendants. Stem cells housed in the SAM tip are engaged in genome integrity maintenance and exhibit a low rate of cell division, consistent with their contributions to germline and somatic cell fates. Surprisingly, we find no evidence for a canonical stem-cell organizing center subtending these cells. In addition, trajectory inference was used to trace the gene expression changes that accompany cell differentiation, revealing that ectopic expression of KNOTTED1 (KN1) accelerates cell differentiation and promotes development of the sheathing maize leaf base. These single-cell transcriptomic analyses of the shoot apex yield insight into the processes of stem-cell function and cell-fate acquisition in the maize seedling and provide a valuable scaffold on which to better dissect the genetic control of plant shoot morphogenesis at the cellular level.

scholarly journals Nf2 fine-tunes proliferation and tissue alignment during closure of the optic fissure in the embryonic mouse eye

2020 ◽  
Author(s):  
Wesley R. Sun ◽  
Sara Ramirez ◽  
Kelly E. Spiller ◽  
Yan Zhao ◽  
Sabine Fuhrmann
Keyword(s):  
Cell Fate ◽  
Hippo Pathway ◽  
Cell Number ◽  
Cancer Development ◽  
Developmentally Regulated ◽  
Ferm Domain ◽  
Embryonic Mouse ◽  
Ocular Abnormalities ◽  
Optic Cup ◽  
Eye Morphogenesis

AbstractUveal coloboma represents one of the most common congenital ocular malformations accounting for up to 10% of childhood blindness (1~ in 5,000 live birth). Coloboma originates from defective fusion of the optic fissure (OF), a transient gap that forms during eye morphogenesis by asymmetric, ventral invagination. Genetic heterogeneity combined with the activity of developmentally regulated genes suggest multiple mechanisms regulating OF closure. The tumor suppressor and FERM domain protein neurofibromin 2 (NF2) controls diverse processes in cancer, development and regeneration, via Hippo pathway and cytoskeleton regulation. In humans, NF2 mutations can cause ocular abnormalities, including coloboma, however, its actual role in OF closure is unknown. Using conditional inactivation in the embryonic mouse eye, our data indicates that loss of Nf2 function results in a novel underlying cause for coloboma. In particular, mutant eyes show substantially increased RPE proliferation in the fissure region with concomitant acquisition of RPE cell fate. Cells lining the OF margin can maintain RPE fate ectopically and fail to transition from neuroepithelial to cuboidal shape. In the dorsal RPE of the optic cup, Nf2 inactivation leads to a robust increase in cell number, with local disorganization of the cytoskeleton components F-actin and pMLC2. We propose that RPE hyperproliferation is the primary cause for the observed defects causing insufficient alignment of the OF margins in Nf2 mutants and failure to fuse properly, resulting in persistent coloboma. Our findings indicate that limiting proliferation particularly in the RPE layer is a critical mechanism during optic fissure closure.

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