I send you a concrete example of differentiating model: the very early commitment of the embryonic cells to trophoblast or inner cell mass.

The early development of mammalian embryo has, from this point of view, three stages.

Stage one: up to the eight cell stage, each blastomere is still totipotent and can go to form at least both foetus and trophoblast; stage three: above 32 cells stage of development: the trophoblast and inner cell mass are differentiated and determined; stage two(a temporary stage)from 8 to 16 cell stage, when distinction between inside and outside cells first becomes manifest suggesting that it is this event which begins to limit totipotency. But in this stage at least some blastomeres remains totipotent, and if remove from the embryo or displace within, it may alter their ultimate fate.

The distinction between trophoblast and inner cell mass are represented by:

-biochemical parameters(the inner cells divide faster as judged by the rate of incorporation of tritiated thimidine into DNA-Barlow)

-surface cell receptors: when isolated and grown in culture the outer cells are found to form closed multicellular vesicles cells from the inside of the blastocyst never show this property. Outside cells develop tight intercellular junction, in contrast, tight junction are not found between the inner cells.

The fecundation moment started synthesis of two types of nonhistonic proteins (in inactive state) and of interface proteins (which are connected two by two)-see Pagina.The differentation begins when the interface protein connect with an hypothetic X site (its position in genome are not known) Because there is only one site the probability of connecting depend on concentration level of interface protein. In the very early stage the embryonic volume did not grow too much, so the probability of connecting depends almost entirely on the number of mythosis. So, after 3-4 mythosis (8-16 cell stage) the concentration of interface protein is high enough to make the connecting between interface protein and X site-see Pagina.Each of two daughter cell, which result from each mythosis, will have different nonhistonic protein (as an active protein-see Pagina) and will active different genes. These will synthesize different receptors for each of two types of cells and different proteins for chemotaxis and cellular movement. The inner cells receptors are synthesized earlier, so that these cells are located inside the blastocyst. This stage is the stage two: these two types of cells are not actually determined because the nonhistonic proteins are only temporary activated; these are unstable proteins and these are quickly inactivated. So, in this stage, it is very important for every cell to move to and interacts with the same type of cell to form a compact population made up by the same type of cells-see Imagine 2 and Imagine 3.This is a crucial moment: the interaction between the same type of receptors will start the synthesis of nonhistonic proteins (as an active protein), like a feed-back regulation-see Imagine2.In this way the state of differentation are maintain and the cells are determined (stage three: above 32-64 cell stage).

Each of these proteins will activate the genes which synthesizing the nonhistonic proteins of the next differentation step. And so on to the higly differentiated cells, in which specific nonhistonic proteins will activate(connecting with specific introns sequences-see Pagina)the specific genes for a certain tissue. The interface protein is the same, but will be synthesized by allelic genes. The only differences is how fast will be synthesized this protein. This will decide, as we could see, when the differentiating phenomenon will start.

An important mechanism will be the inductor factors (proteins and mRNA, as an external factors) that appear in the next step of development. This is very important but it is not the only one mechanism, which can induce the differentation. The intrinsic mechanism must be present even in the latter stages of differentiation (when the very specialized tissues will appear) The ability of the original embryonic cell of teratoma and of stem cell line of teratocarcinomas to differentiate into a variety of identifiable highly differentiated cell type in the very limited environment of the tumora site sustain this assertion.