Work on how transposable elements are maintained and spread by virtue of their transposition processes have produced many theoretical studies of their evolutionary dynamics. But recent studies, which have experimentally identified some of these mechanisms, have not been taken into account. We present an integrated model of P transposable element regulation. It includes, at an individual level, the various mechanisms of regulation and the transposition events, that have been experimentally identified, recording specifically the chromosomal localisations of the inserted copies. It attempts to define the minimum conditions for explaining the regulation and spread of the P transposable element in Drosophila melanogaster natural populations. One test of this model is that it must explain the different population states found in the wild. A program that simulates the changes in Drosophila populations during the invasion of P elements was developed; the simulated populations were then compared to natural population data at the molecular and genetic levels. The model was validated by testing the dynamics of P element invasion in populations. It could explain the different natural population states with a recurrent invasion process. The simulations show that migration reduces the total number of copies, increases the number of defective copies, decreases P-activity and increases P-susceptibility, shifting equilibrium states from P to M'. They also show that the copies determining P-cytotype regulation spread faster by selection when located on the X chromosome. This result could account for the unexplained accumulation of P copies on the X chromosomes of some natural populations. Moreover the simulations predict a novel equilibrium state, called P', not yet characterized in natural populations but that can be found in natural population data.