Biology Reference
In-Depth Information
cells, the transduction of signals and the differential expression of
genes. Secondly, a deterministic model might seem perfectly relevant
at first sight for accounting for the precision in the way an organism
functions. However, if we analyse it in more detail, it reveals diffi-
culties which must lead us to challenge it.
6.2.3
The instructive model trips up against
the contradiction in genetic determinism
By definition, the signals must be specific since this is a determin-
istic model. In Fig. 19, cell B reacts in a unique way to signal
d
,
and it is the same for cell A in relation to signal
c
. This necessarily
presupposes that these signals also induce specific reactions within
cells. If this condition is not fulfilled, the model can no longer func-
tion because several cell reactions are possible for a single signal.
Now, despite intense research efforts undertaken since Spemann's
work was published, these specific signals have never been discov-
ered. Of course, very many molecules implicated in embryogenesis
have been isolated, but as we saw earlier, they do not exhibit this
character of specificity predicted by the model (see chapter 4). To
overcome this difficulty, adherents to the deterministic model usu-
ally argue that it is not just one molecule that transmits the spe-
cific signal, but a combination of cofactors. Considering again the
example in Fig. 19, this means that the signals
d
and
c
no longer
correspond to single molecules synthesised by cells A and B, but to
sets of molecules synthesised by these cells. In reality, this is an
unsatisfactory palliative explanation for it only moves the problem
elsewhere. Indeed, if cells A and B already synthesise sets of differ-
ent molecules, it means that they are already differentiated whereas
this is precisely what the model is supposed to be explaining. Once
again we stumble against the contradiction in genetic determinism
which consists in reversing the cause and effect. This contradiction
is moreover inherent in the model itself which is based on initial
asymmetry between cells which synthesise different signals. The
model must therefore presume a diversity of cells, the appearance of
which it is supposed to explain. The usual practice for resolving this
