scholarly journals Reaction-Diffusion Model for the Arrest of Oscillations in the Somitogenesis Segmentation Clock

2020 ◽  
Author(s):  
Jesús Pantoja-Hernández ◽  
Víctor F. Breña-medina ◽  
Moisés Santillán

AbstractThe clock and wavefront model is one of the most accepted models for explaining the embryonic process of somitogenesis. According to this model, somitogenesis is based upon the interaction between a genetic oscillator, known as segmentation clock, and a moving wavefront, which provides the positional information indicating where each pair of somites is formed. Recently, Cotterell et al. (2015) reported a conceptually different mathematical model for somitogenesis. The authors called it a progressive oscillatory reaction-diffusion (PORD) model. In this model, somitogenesis is driven by short-range interactions and the posterior movement of the front is a local, emergent phenomenon, which is not controlled by global positional information. With the PORD model, it was possible to explain some experimental observations that are incompatible with the clock and wavefront model. However the PORD model has the disadvantage of being quite sensitive to fluctuations. In this work, we propose a modified version of the PORD model in order to overcome this and others inconveniences. By means of numerical simulations and a numerical stability analysis, we demonstrate that the modified PORD model achieves the robustness characteristic of somitogenesis, when the effect of the wavefront is included.

1994 ◽  
Vol 02 (01) ◽  
pp. 1-12 ◽  
Author(s):  
J. CHATTOPADHYAY ◽  
P.K. TAPASWI

Intercellular diffusion of mitosis inhibiting factors, maintained by proper intercellular contact, is one of the means of transferring “positional information”—a message to peripheral cells of a growing normal tissue instructing them where (at what size of the tissue) to stop their further proliferation by mitotic cell division. This property is commonly known as “contact cell inhibition of mitosis” in biology. In a growing tumor tissue, this regulatory mechanism is absent and as a result, peripheral cells of a tumor tissue, being devoid of any “positional information”, go on dividing successively, increasing the size of the tumor (uncontrolled growth). In this paper, the above idea has been captured in a reaction-diffusion model of tumor tissue growth with a spatially decreasing diffusion coefficient, D(r), of the mitotic inhibitor. This model merely provides an alternative explanation of certain observations on normal and tumor tissue growth. The solutions of the simple model (with (i) D=constant for normal tissue growth and (ii) D=D(r) for tumor tissue growth), discussed in this paper, quite reasonably agree with the characteristic patterns of normal and tumor tissue growth.


2020 ◽  
Vol 19 ◽  
pp. 103462 ◽  
Author(s):  
Hijaz Ahmad ◽  
Tufail A. Khan ◽  
Imtiaz Ahmad ◽  
Predrag S. Stanimirović ◽  
Yu-Ming Chu

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