Hysteresis in cell biology often follows bistable systems where the same input state can lead to two different, stable outputs. Where bistability can lead to digital, switch-like outputs from the continuous inputs of chemical concentrations and activities, hysteresis makes these systems more resistant to noise. These systems are often characterized by higher values of the input required to switch into a particular state as compared to the input required to stay in the state, allowing for a transition that is not continuously reversible, and thus less susceptible to noise. 
Cells undergoing cell division exhibit hysteresis in that it takes a higher concentration of cyclins to switch them from G2 phase into mitosis than to stay in mitosis once begun.
Biochemical systems can also show hysteresis-like output when slowly varying states that are not directly monitored are involved, as in the case of the cell cycle arrest in yeast exposed to mating pheromone. Here, the duration of cell cycle arrest depends not only on the final level of input Fus3, but also on the previously achieved Fus3 levels. This effect is achieved due to the slower time scales involved in the transcription of intermediate Far1, such that the total Far1 activity reaches its equilibrium value slowly, and for transient changes in Fus3 concentration, the response of the system depends on the Far1 concentration achieved with the transient value. Experiments in this type of hysteresis benefit from the ability to change the concentration of the inputs with time. The mechanisms are often elucidated by allowing independent control of the concentration of the key intermediate, for instance, by using an inducible promoter.
Darlington in his classic works on genetics discussed hysteresis of the chromosomes, by which he meant "failure of the external form of the chromosomes to respond immediately to the internal stresses due to changes in their molecular spiral", as they lie in a somewhat rigid medium in the limited space of the cell nucleus.
In developmental biology, cell type diversity is regulated by long range-acting signaling molecules called morphogens that pattern uniform pools of cells in a concentration- and time-dependent manner. The morphogen sonic hedgehog (Shh), for example, acts on limb bud and neural progenitors to induce expression of a set of homeodomain-containing transcription factors to subdivide these tissues into distinct domains. It has been shown that these tissues have a memory of previous exposure to Shh.
In neural tissue, this hysteresis is regulated by a homeodomain (HD) feedback circuit that amplifies Shh signaling. In this circuit, expression of Gli transcription factors, the executors of the Shh pathway, is suppressed. Glis are processed to repressor forms (GliR) in the absence of Shh, but in the presence of Shh, a proportion of Glis are maintained as full-length proteins allowed to translocate to the nucleus, where they act as activators (GliA) of transcription. By reducing Gli expression then, the HD transcription factors reduce the total amount of Gli (GliT), so a higher proportion of GliT can be stabilized as GliA for the same concentration of Shh.