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to its normal development (Michaelson, 1993; Penaloza et al .,
2006). Conceived conventionally, this cell death is said to be dic-
tated by the genetic programme, with programmes existing to
control it. However, this theory comes up against the same problem
as cell differentiation. How can these programmes function with non-
specific molecules? In the context of a deterministic view of the cell
based on specific signals leading to very precise regulation, the very
existence of this cell death is problematical. Why would the genetic
programme create cells and subsequently destroy them? If cell dif-
ferentiation is a selective process, on the other hand, it is normal for
cells to die from the moment when they are not adapted to their
microenvironment or if there are too many of them relative to the
resources available (Kupiec, 1986; Glisse et al ., in press).
Several observations corroborate this interpretation. Growth
factors very frequently act as trophic factors necessary for survival.
They do not stimulate multiplication of the cells but their presence
is essential to avoid the death of cells. During embryogenesis of the
brain of vertebrates, 20 to 80% of the neural cells die (Gordon,
1995). A major proportion of this cell death is connected with the
rarity of growth factors, only the neurons that have an adequate
quantity of them survive (Vyas et al ., 2002).
Experiments performed on the development of the wing of the fly
Drosophila melanogaster confirm the Darwinian explanation of cell
death . In flies with two types of genetically different cells, some meta-
bolically more active than others, the cells compete during develop-
ment of the wing to avoid cell death. This competition is related to
a 'decapentaplegic' survival factor and is an integral part of the
embryogenesis process of the wing. This factor is usually considered
a signal but for the Darwinian mechanism it really acts as a resource.
In this competition, the cells with the more active metabolism
monopolise the decapentaplegic factor, proliferate more rapidly and
take it up to the detriment of the less active cells, which die (Moreno
et al ., 2002; Moreno and Basler, 2004; Diaz and Moreno, 2005).
The stabilising role of signals is equally supported by experi-
mental data. Wnt proteins are growth factors which play a major
role during embryonic development (Logan and Nusse, 2004). In the
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