  Decisions in the cell that lead to its ultimate fate are important for
cellular functions such as proliferation, growth, differentiation, development
and death. Understanding this decision process is imperative for advancements
in the treatment of diseases such as cancer. It is clear that underlying gene
regulatory networks and surrounding environments of the cells are crucial for
function. The self-repressor is a very abundant gene regulatory motif, and is
often believed to have only one cell fate. In this study, we elucidate the
effects of microenvironments mimicking the epigenetic effects on cell fates
through the introduction of inducers capable of binding to a self-repressing
gene product (protein), thus regulating the associated gene. This alters the
effective regulatory binding speed of the self-repressor regulatory protein to
its destination DNA without changing the gene itself. The steady state
observations and real time monitoring of the self-repressor expression dynamics
reveal the emergence of the two cell fates, The simulations are consistent with
the experimental findings. We provide physical and quantitative explanations
for the origin of the two phenotypic cell fates. We find that two cell fates,
rather than a single fate, and their associated switching dynamics emerge from
a change in effective gene regulation strengths. The switching time scale is
quantified. Our results reveal a new mechanism for the emergence of multiple
cell fates. This provides an origin for the heterogeneity often observed among
cell states, while illustrating the influence of microenvironments on cell
fates and their decision-making processes without genetic changes
