‘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.

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

Fracture pattern formation in frictional, cohesive, granular material

2010 ◽  
Vol 368 (1910) ◽  
pp. 95-118 ◽  
Author(s):  
Alison Ord ◽  
Bruce E. Hobbs
Keyword(s):  
Pattern Formation ◽  
Granular Media ◽  
Large Scale ◽  
High Stress ◽  
Reaction Diffusion ◽  
Fracture Pattern ◽  
Reaction Diffusion Equations ◽  
Three Dimensions ◽  
Localized Deformation

Naturally, deformed rocks commonly contain crack arrays (joints) forming patterns with systematic relationships to the large-scale deformation. Kinematically, joints can be mode-1, -2 or -3 or combinations of these, but there is no overarching theory for the development of the patterns. We develop a model motivated by dislocation pattern formation in metals. The problem is formulated in one dimension in terms of coupled reaction–diffusion equations, based on computer simulations of crack development in deformed granular media with cohesion. The cracks are treated as interacting defects, and the densities of defects diffuse through the rock mass. Of particular importance is the formation of cracks at high stresses associated with force-chain buckling and variants of this configuration; these cracks play the role of ‘inhibitors’ in reaction–diffusion relationships. Cracks forming at lower stresses act as relatively mobile defects. Patterns of localized deformation result from (i) competition between the growth of the density of ‘mobile’ defects and the inhibition of these defects by crack configurations forming at high stress and (ii) the diffusion of damage arising from these two populations each characterized by a different diffusion coefficient. The extension of this work to two and three dimensions is discussed.

scholarly journals Model analogies between pattern formation in deforming engineering materials & morphogenesis in ageing human brains

2019 ◽  
Vol 28 (1) ◽  
pp. 95-106
Author(s):  
Apostolos C. Tsolakis ◽  
George Petsos ◽  
Olga Kapetanou ◽  
Ioannis N. Nikolaidis ◽  
Elias C. Aifantis
Keyword(s):  
Pattern Formation ◽  
Reaction Diffusion ◽  
Reaction Diffusion Model ◽  
Biochemical Systems ◽  
Model Cell ◽  
Material Physics ◽  
Engineering Materials ◽  
Human Brains ◽  
Ageing Brain

AbstractMathematical models developed within the material mechanics and material physics communities have been routinely adapted to interpret and further understand physiological and biological processes. The field of biomechanics, in particular, has emerged from a direct application of elasticity and fluid mechanics theories to model cell and tissue behavior, as well as bone fracture and blood flow. On the other hand, Turing’s reaction-diffusion model of morphogenesis for biochemical systems has been adapted to interpret pattern formation in deforming materials. An important aspect, however, that has not been sufficiently examined is to investigate the role of an externally applied or internally developed stress. Another, equally interesting issue that has not been adequately explored, concerns the development of a common effective methodology to analyze signals and images for both humanmade and naturemade systems, especially when differential equations are not available to use for this purpose. The article is an initial modest effort to discuss such common features between nonliving and living materials. It focuses, in particular, to modeling analogies between pattern formation of defects in deforming engineering materials under application of external stress and morphogenesis of cellular structures in ageing brain tissue under development of internal stress.

scholarly journals Effects of (–)-Loliolide against Fine Dust Preconditioned Keratinocyte Media-Induced Dermal Fibroblast Inflammation

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 675
Author(s):  
Ilekuttige Priyan Shanura Fernando ◽  
Mawalle Kankanamge Hasitha Madhawa Dias ◽  
Dissanayaka Mudiyanselage Dinesh Madusanka ◽  
Hyun-Soo Kim ◽  
Eui-Jeong Han ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Dermal Fibroblast ◽  
Pulmonary Complications ◽  
Mitogen Activated Protein Kinase ◽  
Tissue Inhibitors Of Metalloproteinases ◽  
Fine Dust ◽  
Elastase Activity ◽  
Therapeutic Role ◽  
Extracellular Matrix Components

At present air pollution in parts of East Asia is at an alarming level due to elevated levels of fine dust (FD). Other than pulmonary complications, FD was found to affect the pathogenesis of ROS-dependent inflammatory responses via penetrating barrier-disrupted skin, leading to degradation of extracellular matrix components through the keratinocyte-fibroblast axis. The present study discloses the evaluation of human dermal fibroblast (HDF) responses to FD preconditioned human keratinocyte media (HPM) primed without and with (-)-loliolide (HTT). HPM-FD treatment increased the ROS level in HDFs and activated mitogen-activated protein kinase-derived nuclear factor (NF)-κB inflammatory signaling pathways with a minor reduction of viability. The above events led to cell differentiation and production of matrix metalloproteinases (MMP), increasing collagenase and elastase activity despite the increase of tissue inhibitors of metalloproteinases (TIMP). Media from HTT primed keratinocytes stimulated with FD indicated ameliorated levels of MMPs, inflammatory cytokines, and chemokines in HDFs with suppressed collagenase and elastase activity. Present observations help to understand the factors that affect HDFs in the microenvironment of FD exposed keratinocytes and the therapeutic role of HTT as a suppressor of skin aging. Further studies using organotypic skin culture models could broaden the understanding of the effects of FD and the therapeutic role of HTT.

scholarly journals Syndecans and Pancreatic Ductal Adenocarcinoma

Biomolecules ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 349
Author(s):  
Nausika Betriu ◽  
Juan Bertran-Mas ◽  
Anna Andreeva ◽  
Carlos E. Semino
Keyword(s):  
Extracellular Matrix ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Cell Types ◽  
Ductal Adenocarcinoma ◽  
Physiological Processes ◽  
Extracellular Matrix Components ◽  
Detection And Diagnosis ◽  
And Migration ◽  
Early Detection And Diagnosis

Pancreatic Ductal Adenocarcinoma (PDAC) is a fatal disease with poor prognosis because patients rarely express symptoms in initial stages, which prevents early detection and diagnosis. Syndecans, a subfamily of proteoglycans, are involved in many physiological processes including cell proliferation, adhesion, and migration. Syndecans are physiologically found in many cell types and their interactions with other macromolecules enhance many pathways. In particular, extracellular matrix components, growth factors, and integrins collect the majority of syndecans associations acting as biochemical, physical, and mechanical transducers. Syndecans are transmembrane glycoproteins, but occasionally their extracellular domain can be released from the cell surface by the action of matrix metalloproteinases, converting them into soluble molecules that are capable of binding distant molecules such as extracellular matrix (ECM) components, growth factor receptors, and integrins from other cells. In this review, we explore the role of syndecans in tumorigenesis as well as their potential as therapeutic targets. Finally, this work reviews the contribution of syndecan-1 and syndecan-2 in PDAC progression and illustrates its potential to be targeted in future treatments for this devastating disease.

scholarly journals Osteoarthritis: Insights Offered by the Study of Bone Mass Genetics

2021 ◽  
Vol 19 (2) ◽  
pp. 115-122
Author(s):  
A. Hartley ◽  
C. L. Gregson ◽  
L. Paternoster ◽  
J. H. Tobias
Keyword(s):  
Bone Mass ◽  
Causal Effect ◽  
Mendelian Randomisation ◽  
Mineral Density ◽  
High Bone Mass ◽  
Increased Risk ◽  
High Bone ◽  
Genetic Mechanisms ◽  
Additional Support

Abstract Purpose of Review This paper reviews how bone genetics has contributed to our understanding of the pathogenesis of osteoarthritis. As well as identifying specific genetic mechanisms involved in osteoporosis which also contribute to osteoarthritis, we review whether bone mineral density (BMD) plays a causal role in OA development. Recent Findings We examined whether those genetically predisposed to elevated BMD are at increased risk of developing OA, using our high bone mass (HBM) cohort. HBM individuals were found to have a greater prevalence of OA compared with family controls and greater development of radiographic features of OA over 8 years, with predominantly osteophytic OA. Initial Mendelian randomisation analysis provided additional support for a causal effect of increased BMD on increased OA risk. In contrast, more recent investigation estimates this relationship to be bi-directional. However, both these findings could be explained instead by shared biological pathways. Summary Pathways which contribute to BMD appear to play an important role in OA development, likely reflecting shared common mechanisms as opposed to a causal effect of raised BMD on OA. Studies in HBM individuals suggest this reflects an important role of mechanisms involved in bone formation in OA development; however further work is required to establish whether the same applies to more common forms of OA within the general population.

scholarly journals Loss of RET Promotes Mesenchymal Identity in Neuroblastoma Cells

Cancers ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1909
Author(s):  
Joachim T. Siaw ◽  
Jonatan L. Gabre ◽  
Ezgi Uçkun ◽  
Marc Vigny ◽  
Wancun Zhang ◽  
...  
Keyword(s):  
Genome Engineering ◽  
Neuroblastoma Cells ◽  
Gene Signature ◽  
Additional Insight ◽  
Downstream Target ◽  
Anaplastic Lymphoma ◽  
Extracellular Matrix Components ◽  
Transforming Gene ◽  
Insight Into

Aberrant activation of anaplastic lymphoma kinase (ALK) drives neuroblastoma (NB). Previous work identified the RET receptor tyrosine kinase (RTK) as a downstream target of ALK activity in NB models. We show here that ALK activation in response to ALKAL2 ligand results in the rapid phosphorylation of RET in NB cells, providing additional insight into the contribution of RET to the ALK-driven gene signature in NB. To further address the role of RET in NB, RET knockout (KO) SK-N-AS cells were generated by CRISPR/Cas9 genome engineering. Gene expression analysis of RET KO NB cells identified a reprogramming of NB cells to a mesenchymal (MES) phenotype that was characterized by increased migration and upregulation of the AXL and MNNG HOS transforming gene (MET) RTKs, as well as integrins and extracellular matrix components. Strikingly, the upregulation of AXL in the absence of RET reflects the development timeline observed in the neural crest as progenitor cells undergo differentiation during embryonic development. Together, these findings suggest that a MES phenotype is promoted in mesenchymal NB cells in the absence of RET, reflective of a less differentiated developmental status.

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