  The protein p53 has a well established role in protecting genomic integrity
in human cells. When DNA is damaged p53 induces the cell cycle arrest to
prevent the transmission of the damage to cell progeny, triggers the production
of proteins for DNA repair and ultimately calls for apoptosis. In particular,
the p53-Mdm2 feedback loop seems to be the key circuit in this response of
cells to damage. For many years, based on measurements over populations of
cells it was believed that the p53-Mdm2 feedback loop was the responsible for
the existence of damped oscillations in the levels of p53 and Mdm2 after DNA
damage. However, recent measurements in individual human cells have shown that
p53 and its regulator Mdm2 develop sustained oscillations over long periods of
time even in the absence of stress. These results have attracted a lot of
interest, first because they open a new experimental framework to study the p53
and its interactions and second because they challenge years of mathematical
models with new and accurate data on single cells. Inspired by these
experiments standard models of the p53-Mdm2 circuit were modified introducing
ad-hoc some biologically motivated noise that becomes responsible for the
stability of the oscillations. Here, we follow an alternative approach
proposing that the noise that stabilizes the fluctuations is the intrinsic
noise due to the finite nature of the populations of p53 and Mdm2 in a single
cell.
