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pathway. The latter are then compelled to react with each other
because of their proximity. The signalling pathway is thus prefer-
entially activated.
Signal transduction via a combination of intracellular pathways
is another mechanism conferring specificity. Two signals share a
mutual pathway but at the same time they each activate other dif-
ferent pathways. In this case, specificity is conferred by the combi-
nation of different pathways activated by each signal. In the same
way, in gene expression it is the combinations of transcription fac-
tors which appear to ensure regulation.
Crossed inhibition may equally restrict the effects of molecular
non-specificity, with an element unique to one of the two pathways
possibly inhibiting an element unique to the other, even though
they have elements in common. From the moment there is an
imbalance in favour of one of the two pathways, for example owing
to the presence of a scaffold protein, this pathway will totally
inhibit the other.
Finally, the intensity of the signal could also play a part.
Depending whether a pathway is activated by one signal or another,
the magnitude and period of activation of a single intracellular path-
way could be different and thus end in producing different effects.
All these mechanisms are supported by solid experimental data
which explain how appropriate regulation occurs despite molecular
non-specificity.
However, there is no denying that this shakes genetic determin-
ism to the roots and that we have arrived at a contradiction.
Indeed, for all the suggested mechanisms to be effective, it has to
be assumed that cellular organisation and a state of macroscopic
differentiation already exists to ensure compartmentalisation and
the very precise expression of certain proteins. It is this differenti-
ated state, specific to one cell, which must explain why certain
molecular interactions occur specifically in this cell and not in oth-
ers. Yet in genetic determinism, the macroscopic state of a cell is
precisely what the molecular interactions are supposed to determine
(Fig. 10) and what a theory of ontogenesis must explain. We also
arrive at the idea that the effect of a signal does not depend on its
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