Background: Few genome-scale models of organisms focus on the regulatory networks and none of them integrates all known levels of regulation. In particular, the regulations involving metabolite pools are often neglected. However, metabolite pools link the metabolic to the genetic network through genetic regulations, including those involving effectors of transcription factors or riboswitches. Consequently, they play pivotal roles in the global organization of the genetic and metabolic regulatory networks.

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Summary 1.Soil organisms, such as earthworms, accelerate mineralization of soil organic matter and are thought to be beneficial for plant growth. This has been shown in short-term microcosm experiments. It is thus legitimate to ask whether these increases in plant growth are due to brief pulses of mineralization or whether these increases are long-lasting. 2. This question was addressed using a system of differential equations modelling the effects of decomposers on nutrient cycling via trophic (nutrient assimilation) and nontrophic effects (through their ecosystem engineering activities). 3. The analytical study of this model showed that these processes increase primary production in the long term when they recycle nutrients efficiently, allowing a small fraction of the recycled nutrients to be leached out of the ecosystem. 4. Mineralization by the ecosystem engineering activities of decomposers seems to deprive them of a resource. However, it was shown that a decomposer may increase its own biomass, through its ecosystem engineering activities, provided the created recycling loop is efficient enough. 5. Mechanisms through which earthworms may modify the efficiency of nutrient cycling are discussed. The necessity of measuring the effect of earthworms on the nutrient input-output balance of ecosystems under field conditions is emphasized.

We present a nonlinear model of the dynamics of a cell population divided into proliferative and quiescent compartments. The proliferative phase represents the complete cell cycle (G (1)-S-G (2)-M) of a population committed to divide at its end. The model is structured by the time spent by a cell in the proliferative phase, and by the amount of Cyclin D/(CDK4 or 6) complexes. Cells can transit from one compartment to the other, following transition rules which differ according to the tissue state: healthy or tumoral. The asymptotic behaviour of solutions of the nonlinear model is analysed in two cases, exhibiting tissue homeostasis or tumour exponential growth. The model is simulated and its analytic predictions are confirmed numerically.