Aim of the study was to evaluate the relationship between the mitogeni
c stimulus interleukin-3 to normal murine mast cells and the cell cycl
e dependent expression of the nuclear c-myc protein. In order to do th
at on a cell by cell basis, we measured the nuclear c-myc protein simu
ltaneously by flow cytometry, via specific monoclonal antibodies, and
the DNA content via the intercalating dye propidium iodide. When cells
were deprived from interleukin-3 (IL-3), proliferation was inhibited
and the majority of cells arrested in early G1 (G1A, characterized by
low c-myc content). Readdition of IL-3 resulted in a slow transition o
f cells from G1A to late G1 (G1B, at higher c-myc content) before DNA
synthesis started. G1A cells with low c-myc content do not undertake D
NA synthesis. Using a stathmokinetic methodology we confirmed that the
G1A cells are early postmitotic G1 phase cells. The low content of c-
myc within these cells appears a direct consequence of reduced c-myc l
evels during mitosis. Cumulatively, the data suggest that c-myc protei
n levels of murine mast cells fall at mitosis and that these levels mu
st rise before cells can traverse the G1 phase. Our data are compatibl
e with a model in which c-myc protein content of G1 phase cells has to
reach a critical threshold before the cells can move further into the
cell cycle.